[Severe metabolic alkalosis following hypokalemia from a paraneoplastic Cushing syndrome].

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Dubé, L; Daenen, S; Kouatchet, A; Soltner, C; Alquier, P

2001-12-01

Metabolic alkalosis is frequently observed in critically ill patients. Etiologies are numerous but endocrinal causes are rare. We report a case of a patient with severe respiratory insufficiency, metabolic alkalosis and hypokalemia. The evolution was fatal. Further explorations revealed an ectopic Adrenocorticotropine Hormone syndrome. The initial tumor was probably a small cell lung carcinoma.

Respiratory alkalosis in children with febrile seizures.

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Schuchmann, Sebastian; Hauck, Sarah; Henning, Stephan; Grüters-Kieslich, Annette; Vanhatalo, Sampsa; Schmitz, Dietmar; Kaila, Kai

2011-11-01

Febrile seizures (FS) are the most common type of convulsive events in children. FS are suggested to result from a combination of genetic and environmental factors. However, the pathophysiologic mechanisms underlying FS remain unclear. Using an animal model of experimental FS, it was demonstrated that hyperthermia causes respiratory alkalosis with consequent brain alkalosis and seizures. Here we examine the acid-base status of children who were admitted to the hospital for FS. Children who were admitted because of gastroenteritis (GE), a condition known to promote acidosis, were examined to investigate a possible protective effect of acidosis against FS. We enrolled 433 age-matched children with similar levels of fever from two groups presented to the emergency department. One group was admitted for FS (n = 213) and the other for GE (n = 220). In the FS group, the etiology of fever was respiratory tract infection (74.2%), otitis media (7%), GE (7%), tonsillitis (4.2%), scarlet fever (2.3%) chickenpox (1.4%), urinary tract infection (1.4%), postvaccination reaction (0.9%), or unidentified (1.4%). In all patients, capillary pH and blood Pco(2) were measured immediately on admission to the hospital. Respiratory alkalosis was found in children with FS (pH 7.46 ± 0.04, [mean ± standard deviation] Pco(2) 29.5 ± 5.5 mmHg), whereas a metabolic acidosis was seen in all children admitted for GE (pH 7.31 ± 0.03, Pco(2) 37.7 ± 4.3 mmHg; p respiratory alkalosis, irrespective of the severity of the underlying infection as indicated by the level of fever. The lack of FS in GE patients is attributable to low pH, which also explains the fact that children with a susceptibility to FS do not have seizures when they have GE-induced fever that is associated with acidosis. The present demonstration of a close link between FS and respiratory alkalosis may pave the way for further clinical studies and attempts to design novel therapies for the treatment of FS by controlling the

Pulmonary vascular responses during acute and sustained respiratory alkalosis or acidosis in intact newborn piglets.

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Gordon, J B; Rehorst-Paea, L A; Hoffman, G M; Nelin, L D

1999-12-01

Acute alkalosis-induced pulmonary vasodilation and acidosis-induced pulmonary vasoconstriction have been well described, but responses were generally measured within 5-30 min of changing pH. In contrast, several in vitro studies have found that relatively brief periods of sustained alkalosis can enhance, and sustained acidosis can decrease, vascular reactivity. In this study of intact newborn piglets, effects of acute (20 min) and sustained (60-80 min) alkalosis or acidosis on baseline (35% O2) and hypoxic (12% O2) pulmonary vascular resistance (PVR) were compared with control piglets exposed only to eucapnia. Acute alkalosis decreased hypoxic PVR, but sustained alkalosis failed to attenuate either baseline PVR or the subsequent hypoxic response. Acute acidosis did not significantly increase hypoxic PVR, but sustained acidosis markedly increased both baseline PVR and the subsequent hypoxic response. Baseline PVR was similar in all piglets after resumption of eucapnic ventilation, but the final hypoxic response was greater in piglets previously exposed to alkalosis than in controls. Thus, hypoxic pulmonary vasoconstriction was not attenuated during sustained alkalosis, but was accentuated during sustained acidosis and after the resumption of eucapnia in alkalosis-treated piglets. Although extrapolation of data from normal piglets to infants and children with pulmonary hypertension must be done with caution, this study suggests that sustained alkalosis may be of limited efficacy in treating acute hypoxia-induced pulmonary hypertension and the risks of pulmonary hypertension must be considered when using ventilator strategies resulting in permissive hypercapnic acidosis.

Hyperventilation of pregnancy presenting with flaccid quadriparesis due to hypokalaemia secondary to respiratory alkalosis.

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Santra, Gouranga; Paul, Rudrajit; Das, Shubhabrata; Pradhan, Sourav

2014-06-01

Hyperventilation in pregnancy is a cause of chronic respiratory alkalosis. Alkalosis either metabolic or respiratory may cause intracellular shift of potassium ions that may lead to hypokalaemia. However, the resultant hypokalaemia in respiratory alkalosis is usually mild and does not cause much clinical features. A five-months-pregnant female of the age 25 years presented with sudden onset flaccid weakness of both lower limbs associated with thigh muscle pain followed by weakness of both upper limbs within three days. Subsequent investigation revealed severe hypokalaemia due to acute exacerbation of chronic respiratory alkalosis secondary to hyperventilation of pregnancy, other causes of hypokalaemia being ruled out. Respiratory alkalosis causes tetany and other clinical manifestations. But hypokalaemia and such weakness is rarely found. Thisis probably the first report of this type from India.

Metabolic Alkalosis in Adults with Stable Cystic Fibrosis

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Al-Ghimlas, Fahad; Faughnan, Marie E; Tullis, Elizabeth

2012-01-01

Background: The frequency of metabolic alkalosis among adults with stable severe CF-lung disease is unknown. Methods: Retrospective chart review. Results: Fourteen CF and 6 COPD (controls) patients were included. FEV1 was similar between the two groups. PaO2 was significantly higher in the COPD (mean ± 2 SD is 72.0 ± 6.8 mmHg,) than in the CF group (56.1 ± 4.1 mmHg). The frequency of metabolic alkalosis in CF patients (12/14, 86%) was significantly greater (p=0.04) than in the COPD group (2/6...

A patient with foot ulcer and severe metabolic alkalosis.

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John, Ruby Samuel; Simoes, Sonia; Reddi, Alluru S

2012-01-01

We report a case of triple acid-base disorder with metabolic alkalosis as the primary disorder in a 65-year-old man due to ingestion and application to leg ulcers of baking soda (calcium bicarbonate). The blood pH was 7.65 with hypochloremia, hypokalemia, and prerenal azotemia. He was treated with isotonic saline with K replacement, and the patient improved without any adverse clinical consequences. We discuss the causes, mechanisms, and management of Cl-responsive (depletion) metabolic alkalosis.

Hyperthermic-induced hyperventilation and associated respiratory alkalosis in humans.

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Abbiss, Chris R; Nosaka, Kazunori; Laursen, Paul B

2007-05-01

The purpose of this study was to determine if increased environmental heat leads to hyperthermic-induced hypocapnia and associated alkalosis during prolonged self-paced cycling. Nine male cyclists completed three 100 km stochastic time trials in hot (34 degrees C), neutral (22 degrees C) and cold (10 degrees C) environments. Intermittent measurements of rectal and skin temperature, expired gases, blood pH, PaCO(2), PaO(2), and bicarbonate were made throughout. Rectal temperature increased significantly throughout all trials (P respiratory alkalosis.

Metabolic alkalosis from unsuspected ingestion: use of urine pH and anion gap.

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Yi, Joo-Hark; Han, Sang-Woong; Song, June-Seok; Kim, Ho-Jung

2012-04-01

Underlying causes of metabolic alkalosis may be evident from history, evaluation of effective circulatory volume, and measurement of urine chloride concentration. However, identification of causes may be difficult for certain conditions associated with clandestine behaviors, such as surreptitious vomiting, use of drugs or herbal supplements with mineralocorticoid activity, abuse of laxatives or diuretics, and long-term use of alkalis. In these circumstances, clinicians often are bewildered by unexplained metabolic alkalosis from an incomplete history or persistent deception by the patient, leading to misdiagnosis and poor outcome. We present a case of severe metabolic alkalosis and hypokalemia with a borderline urine chloride concentration in an alcoholic patient treated with a thiazide. The cause of the patient's metabolic alkalosis eventually was linked to surreptitious ingestion of baking soda. This case highlights the necessity of a high index of suspicion for the diverse clandestine behaviors that can cause metabolic alkalosis and the usefulness of urine pH and anion gap in its differential diagnosis. Copyright © 2012 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

A case report of uncompensated alkalosis induced by daily plasmapheresis in a patient with thrombotic thrombocytopenic purpura.

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Nagai, Yoshiko; Itabashi, Mitsuyo; Mizutani, Mayuko; Ogawa, Tetsuya; Yumura, Wako; Tsuchiya, Ken; Nitta, Kosaku

2008-02-01

Plasmapheresis (PP) is widely known as the standard therapy for thrombotic thrombocytopenic purpura (TTP). Citrate is used as an anticoagulant in fresh frozen plasma, and the large amount of citrate infused during PP induces metabolic alkalosis. A 29-year-old woman was diagnosed with TTP associated with systemic lupus erythematosus, and was treated by daily PP in addition to a steroid, an immunosuppressant, vincristine, and cyclophosphamide. Uncompensated alkalosis caused by a combination of metabolic and respiratory alkalosis developed after artificial ventilation was discontinued. Her metabolic status improved after controlling her respiratory status and the activity of the TTP. Metabolic alkalosis is a common complication in TTP patients treated by frequent PP, but several factors that affect metabolic status may aggravate the alkalosis and induce uncompensated alkalosis.

Cerebrospinal fluid ionic regulation, cerebral blood flow, and glucose use during chronic metabolic alkalosis

International Nuclear Information System (INIS)

Schroeck, H.K.; Kuschinsky, W.

1989-01-01

Chronic metabolic alkalosis was induced in rats by combining a low K+ diet with a 0.2 M NaHCO3 solution as drinking fluid for either 15 or 27 days. Local cerebral blood flow and local cerebral glucose utilization were measured in 31 different structures of the brain in conscious animals by means of the iodo-[14C]antipyrine and 2-[14C]deoxy-D-glucose method. The treatment induced moderate [15 days, base excess (BE) 16 mM] to severe (27 days, BE 25 mM) hypochloremic metabolic alkalosis and K+ depletion. During moderate metabolic alkalosis no change in cerebral glucose utilization and blood flow was detectable in most brain structures when compared with controls. Cerebrospinal fluid (CSF) K+ and H+ concentrations were significantly decreased. During severe hypochloremic alkalosis, cerebral blood flow was decreased by 19% and cerebral glucose utilization by 24% when compared with the control values. The decrease in cerebral blood flow during severe metabolic alkalosis is attributed mainly to the decreased cerebral metabolism and to a lesser extent to a further decrease of the CSF H+ concentration. CSF K+ concentration was not further decreased. The results show an unaltered cerebral blood flow and glucose utilization together with a decrease in CSF H+ and K+ concentrations at moderate metabolic alkalosis and a decrease in cerebral blood flow and glucose utilization together with a further decreased CSF H+ concentration at severe metabolic alkalosis

Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis.

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Li, Kai; Xu, Yuan

2015-01-01

Metabolic alkalosis commonly results from excessive hydrochloric acid (HCl), potassium (K(+)) and water (H2O) loss from the stomach or through the urine. The plasma anion gap increases in non-hypoproteinemic metabolic alkalosis due to an increased negative charge equivalent on albumin and the free ionized calcium (Ca(++)) content of plasma decreases. The mean citrate load in all patients was 8740±7027 mg from 6937±6603 mL of transfused blood products. The citrate load was significantly higher in patients with alkalosis (9164±4870 vs. 7809±3967, P alkalosis + respiratory acidosis and electrolyte imbalance may develop, blood transfusions may result in certain complications.

Clinical presentation of metabolic alkalosis in an adult patient with cystic fibrosis.

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Sweetser, Lisel J; Douglas, James A; Riha, Renata L; Bell, Scott C

2005-03-01

In subtropical and tropical climates, dehydration is common in cystic fibrosis patients with respiratory exacerbations. This may lead to a clinical presentation of metabolic alkalosis with associated hyponatraemia and hypochloraemia. An adult cystic fibrosis patient who presented with a severe respiratory exacerbation accompanied by metabolic alkalosis is presented and the effects of volume correction are reported.

Metabolic alkalosis in children: Study of patients admitted to pediatrics center

OpenAIRE

Sobhani A; Radmehr B; Raji AR

2001-01-01

Metabolic alkalosis is characterized by high HCO3- as it is seen in chronic respiratory acidosis, but PH differentiates the two disorders. There is no characteristic symptom or sign. Orthostatic hypotension may be encountered. Weakness and hyporeflexia occur if serum K+ is markerdly low. Tetany and neuromuscular irritability occur rarely. We report the results of retrospective data analysis of metabolic alkalosis in 15463 patients hospitalized Pediatric Medical Center in Tehran during years 1...

Ectopic adrenocorticotropic hormone syndrome presenting as hypokalemic metabolic alkalosis and hypertension

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Mansoor C Abdulla

2016-01-01

Full Text Available The ectopic adrenocorticotropic hormone (ACTH syndrome is an uncommon cause of hypercortisolism, which should be considered in patients with hypokalemic metabolic alkalosis and hypertension in the context of lung neoplasm. We report a 60-year-old male patient with severe hypertension, metabolic alkalosis, and hypokalemia as the initial manifestations of an ACTH-secreting small cell lung carcinoma. Ectopic Cushing's syndrome should always be ruled out in patients with severe hypertension and hypokalemia.

Acetazolamide Therapy for Metabolic Alkalosis in Pediatric Intensive Care Patients.

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López, Carolina; Alcaraz, Andrés José; Toledo, Blanca; Cortejoso, Lucía; Gil-Ruiz, Maite Augusta

2016-12-01

Patients in PICUs frequently present hypochloremic metabolic alkalosis secondary to loop diuretic treatment, especially those undergoing cardiac surgery. This study evaluates the effectiveness of acetazolamide therapy for metabolic alkalosis in PICU patients. Retrospective, observational study. A tertiary care children's hospital PICU. Children receiving at least a 2-day course of enteral acetazolamide. None. Demographic variables, diuretic treatment and doses of acetazolamide, urine output, serum electrolytes, urea and creatinine, acid-base excess, pH, and use of mechanical ventilation during treatment were collected. Patients were studied according to their pathology (postoperative cardiac surgery, decompensated heart failure, or respiratory disease). A total of 78 episodes in 58 patients were identified: 48 were carried out in cardiac postoperative patients, 22 in decompensated heart failure, and eight in respiratory patients. All patients received loop diuretics. A decrease in pH and PCO2 in the first 72 hours, a decrease in serum HCO3 (mean, 4.65 ± 4.83; p alkalosis secondary to diuretic therapy. Cardiac postoperative patients present a significant increase in urine output after acetazolamide treatment.

Metabolic alkalosis contributes to acute hypercapnic respiratory failure in adult cystic fibrosis.

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Holland, Anne E; Wilson, John W; Kotsimbos, Thomas C; Naughton, Matthew T

2003-08-01

and study objectives: Patients with end-stage cystic fibrosis (CF) develop respiratory failure and hypercapnia. In contrast to COPD patients, altered electrolyte transport and malnutrition in CF patients may predispose them to metabolic alkalosis and, therefore, may contribute to hypercapnia. The aim of this study was to determine the prevalence of metabolic alkalosis in adults with hypercapnic respiratory failure in the setting of acute exacerbations of CF compared with COPD. Levels of arterial blood gases, plasma electrolytes, and serum albumin from 14 consecutive hypercapnic CF patients who had been admitted to the hospital with a respiratory exacerbation were compared with 49 consecutive hypercapnic patients with exacerbations of COPD. Hypercapnia was defined as a PaCO(2) of > or = 45 mm Hg. Despite similar PaCO(2) values, patients in the CF group were significantly more alkalotic than were those in the COPD group (mean [+/- SD] pH, 7.43 +/- 0.03 vs 7.37 +/- 0.05, respectively; p respiratory acidosis and metabolic alkalosis was evident in 71% of CF patients and 22% of COPD patients (p alkalosis contributes to hypercapnic respiratory failure in adults with acute exacerbations of CF. This acid-base disturbance occurs in conjunction with reduced total body salt levels and hypoalbuminemia.

Acute respiratory alkalosis occurring after endoscopic third ventriculostomy -A case report-.

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Sung, Hui-Jin; Sohn, Ju-Tae; Kim, Jae-Gak; Shin, Il-Woo; Ok, Seong-Ho; Lee, Heon-Keun; Chung, Young-Kyun

2010-12-01

An endoscopic third ventriculostomy was performed in a 55-year-old man with an obstructive hydrocephalus due to aqueductal stenosis. The vital signs and laboratory studies upon admission were within the normal limits. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The patient received irrigation with approximately 3,000 ml normal saline during the procedure. Anesthesia and operation were uneventful. However, he developed postoperative hyperventilation in the recovery room, and arterial blood gas analysis revealed acute respiratory alkalosis. We report a rare respiratory alkalosis that occurred after an endoscopic third ventriculostomy.

Severe metabolic alkalosis due to baking soda ingestion: case reports of two patients with unsuspected antacid overdose.

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Fitzgibbons, L J; Snoey, E R

1999-01-01

Oral ingestion of baking soda (sodium bicarbonate) has been used for decades as a home remedy for acid indigestion. Excessive bicarbonate ingestion places patients at risk for a variety of metabolic derangements including metabolic alkalosis, hypokalemia, hypernatremia, and even hypoxia. The clinical presentation is highly variable but can include seizures, dysrhythmias, and cardiopulmonary arrest. We present two cases of severe metabolic alkalosis in patients with unsuspected antacid overdose. The presentation and pathophysiology of antacid-related metabolic alkalosis is reviewed.

Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap.

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Batlle, Daniel; Chin-Theodorou, Jamie; Tucker, Bryan M

2017-09-01

Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is a finding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, arterial blood gas, and clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as a surrogate marker of urine ammonium excretion, in the evaluation of a patient with low plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urine acid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap) to evaluate urine acidification are discussed. Copyright © 2017 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

Acetazolamide improves oxygenation in patients with respiratory failure and metabolic alkalosis.

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Gulsvik, Ragnhild; Skjørten, Ingunn; Undhjem, Kenneth; Holø, Lars; Frostad, Anne; Saure, Eirunn Waatevik; Lejlic, Vasvija; Humerfelt, Sjur; Hansen, Gunnar; Bruun Wyller, Torgeir

2013-10-01

Coexistent respiratory failure and metabolic alkalosis is a common finding. Acidotic diuretics cause a fall in pH that may stimulate respiration. The purpose of the study was to evaluate the effectiveness of short-term treatment with acetazolamide for combined respiratory failure and metabolic alkalosis. A randomised, placebo-controlled and double-blind parallel group trial where oral acetazolamide 250 mg three times a day for 5 days were administered to patients hospitalised for respiratory failure because of a pulmonary disease (Pa O2 ≤ 8 kPa and/or Pa CO2 ≥ 7 kPa) who had concurrent metabolic alkalosis [base excess (BE) ≥ 8 mmol/L]. Pa O2 after 5 days was the primary effect variable. Secondary effect variables were Pa CO2 , BE and pH on day 5, and the total number of days in hospital. Of 70 patients enrolled (35 in each group), data from 54 were analysed per protocol, while last observation carried forward was used for the remaining 16. During the 5-day treatment, Pa O2 increased on average 0.81 kPa in the placebo group and 1.41 kPa in the acetazolamide group. After adjustment for baseline skewness, the difference was statistically significant (adjusted mean difference 0.55 kPa, 95% confidence interval 0.03-1.06). Pa CO2 decreased in both groups, but the difference was not statistically significant. As expected, pH and BE decreased markedly in the acetazolamide group. Acetazolamide may constitute a useful adjuvant treatment mainly to be considered in selected patients with respiratory failure combined with prominent metabolic alkalosis or where non-invasive ventilation is insufficient or infeasible. © 2013 John Wiley & Sons Ltd.

Reversed electrogenic sodium bicarbonate cotransporter 1 is the major acid loader during recovery from cytosolic alkalosis in mouse cortical astrocytes.

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Theparambil, Shefeeq M; Naoshin, Zinnia; Thyssen, Anne; Deitmer, Joachim W

2015-08-15

The regulation of H(+) i from cytosolic alkalosis has generally been attributed to the activity of Cl(-) -coupled acid loaders/base extruders in most cell types, including brain cells. The present study demonstrates that outwardly-directed sodium bicarbonate cotransport via electrogenic sodium bicarbonate cotransporter 1 (NBCe1) mediates the major fraction of H(+) i regulation from cytosolic alkalosis in mouse cortical astrocytes. Cl(-) -coupled acid-loading transporters play only a minor role in the regulation of H(+) i from alkalosis in mouse cortical astrocytes. NBCe1-mediated H(+) i regulation from alkalosis was dominant, with the support of intracellular carbonic anhydrase II, even when the intra- and extracellular [HCO3 (-) ] was very low (sodium bicarbonate cotransporter 1 (NBCe1) and for carbonic anhydrase (CA) isoform II. An acute cytosolic alkalosis was induced by the removal of either CO2 /HCO3 (-) or butyric acid, and the subsequent acid loading was analysed by monitoring changes in cytosolic H(+) or Na(+) using ion-sensitive fluorescent dyes. We have identified that NBCe1 reverses during alkalosis and contributes more than 70% to the rate of recovery from alkalosis by extruding Na(+) and HCO3 (-) . After CA inhibition or in CAII-knockout (KO) cells, the rate of recovery was reduced by 40%, and even by 70% in the nominal absence of CO2 /HCO3 (-) . Increasing the extracellular K(+) concentration modulated the rate of acid loading in wild-type cells, but not in NBCe1-KO cells. Removing chloride had only a minor effect on the recovery from alkalosis. Reversal of NBCe1 by reducing pH/[HCO3 (-) ] was demonstrated in astrocytes and in Xenopus oocytes, in which human NBCe1 was heterologously expressed. The results obtained suggest that reversed NBCe1, supported by CAII activity, plays a major role in acid-loading cortical astrocytes to support recovery from cytosolic alkalosis. © 2015 The Authors. The Journal of Physiology © 2015 The Physiological Society.

Girl with hypokaliemia and metabolic alkalosis: a case report

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Ksenja Marguč Kirn

2013-04-01

Conclusions: In cases of unexplained hypokalemia and metabolic alkalosis associated with a normal or low blood pressure a tubulopathy, e.g., Gitelman syndrome, must be excluded. The identification and recognition of correct diagnosis is extremely important since a proper treatment can reduce the risk of life-threatening events, e.g. arrhythmias.

[An unexpected stage of alkalosis in the dynamics of the early posthemorrhagic period].

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Beliaev, A V

2000-01-01

A study was made on acid-base metabolism in early posthemorrhagic period as exemplified by examination of patients presenting with gastrointestinal hemorrhage. It has been ascertained that hemorrhage is accompanied by a mixed variant of the acid-base state (ABS) deviation, namely metabolic lactate-acidosis and respiratory alkalosis. In the time-related course of posthemorrhagic period such deviations persist in patients with lethal outcome; with the disease running a favourable course the above deviations are found to return to normal quite soon. The development of complications leads to staging in ABC, its stages being as follows: stage I--the initial stage, stage II--persisting metabolic acidosis and respiratory alkalosis, stage III--alkalosis, stage IV--normalization, with stage III of ABS being encouraged by hypocapnia caused by function disorders of the lungs in early posthemorrhagic period, normalization of cell metabolism, increase in the rate of urination as a reflection of the third earlier identified stage of water metabolism, with the H+ excretion in the urine at the previous level. The identified ABS stage III threatens coming trouble, being accompanied by metabolic deviations together with a risk of function disorder of the myocardium.

Acidosis, but Not Alkalosis, Affects Anaerobic Metabolism and Performance in a 4-km Time Trial.

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Correia-Oliveira, Carlos Rafaell; Lopes-Silva, João Paulo; Bertuzzi, Romulo; McConell, Glenn K; Bishop, David John; Lima-Silva, Adriano Eduardo; Kiss, Maria Augusta Peduti Dal'molin

2017-09-01

This study aimed to determine the effect of preexercise metabolic acidosis and alkalosis on power output (PO) and aerobic and anaerobic energy expenditure during a 4-km cycling time trial (TT). Eleven recreationally trained cyclists (V˙O2peak 54.1 ± 9.3 mL·kg·min) performed a 4-km TT 100 min after ingesting in a double-blind matter 0.15 g·kg of body mass of ammonium chloride (NH4Cl, acidosis), 0.3 g·kg of sodium bicarbonate (NaHCO3, alkalosis), or 0.15 g·kg of CaCO3 (placebo). A preliminary study (n = 7) was conducted to establish the optimal doses to promote the desirable preexercise blood pH alterations without gastrointestinal distress. Data for PO, aerobic and anaerobic energy expenditure, and blood and respiratory parameters were averaged for each 1 km and compared between conditions using two-way repeated-measures ANOVA (condition and distance factors). Gastrointestinal discomfort was analyzed qualitatively. Compared with placebo (pH 7.37 ± 0.02, [HCO3]: 27.5 ± 2.6 mmol·L), the NaHCO3 ingestion resulted in a preexercise blood alkalosis (pH +0.06 ± 0.04, [HCO3]: +4.4 ± 2.0 mmol·L, P 0.05). Minimal gastrointestinal distress was noted in all conditions. Preexercise acidosis, but not alkalosis, affects anaerobic metabolism and PO during a 4-km cycling TT.

Mechanisms controlling the oxygen consumption in experimentally induced hypochloremic alkalosis in calves.

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Cambier, Carole; Clerbaux, Thierry; Amory, Hélène; Detry, Bruno; Florquin, Sandra; Marville, Vincent; Frans, Albert; Gustin, Pascal

2002-01-01

The study was carried out on healthy Friesian calves (n = 10) aged between 10 and 30 days. Hypochloremia and alkalosis were induced by intravenous administration of furosemide and isotonic sodium bicarbonate. The venous and arterial blood samples were collected repeatedly. 2,3-diphosphoglycerate (2,3-DPG), hemoglobin and plasmatic chloride concentrations were determined. The red blood cell chloride concentration was also calculated. pH, PCO2 and PO2 were measured in arterial and mixed venous blood. The oxygen equilibrium curve (OEC) was measured in standard conditions. The correspondence of the OEC to the arterial and mixed venous compartments was calculated, taking blood temperature, pH and PCO2 values into account. The oxygen exchange fraction (OEF%), corresponding to the degree of blood desaturation between the arterial and mixed venous compartments and the amount of oxygen released at the tissue level by 100 mL of blood (OEF Vol%) were calculated from the arterial and mixed venous OEC, combined with PO2 and hemoglobin concentration. Oxygen delivery (DO2) was calculated using the arterial oxygen content, the cardiac output measured by thermodilution, and the body weight of the animal. The oxygen consumption (VO2) was derived from the cardiac output, OEF Vol% and body weight values. Despite the plasma hypochloremia, the erythrocyte chloride concentration was not influenced by furosemide and sodium bicarbonate infusion. Due to the alkalosis-induced increase in the 2,3-DPG, the standard OEC was shifted to the right, allowing oxygen to dissociate from hemoglobin more rapidly. These changes opposed the increased affinity of hemoglobin for oxygen induced by alkalosis. Moreover, respiratory acidosis, hemoconcentration, and the slight decrease in the partial oxygen pressure in mixed venous blood (Pvo2) tended to improve the OEF Vol% and maintain the oxygen consumption in a physiological range while the cardiac output, and the oxygen delivery were significantly decreased

[Cardiac arrest in chronic metabolic alkalosis due to sodium bicarbonate abuse].

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Niewiński, Grzegorz; Korta, Teresa; Debowska, Małgorzata; Kosiński, Cezary; Kubik, Tomasz; Romanik, Wojciech; Kański, Andrzej

2008-01-01

Moderate metabolic alkalosis has not been considered as a life-threatening situation by many authors, but when it persists and pH increases above 7.65, the situation may become critical. We present a case of a 61-yr-old alcoholic male patient, who had been consuming approximately 200 g of sodium bicarbonate daily for twenty years, due to persisitent heartburn and abdominal pains. The patient was admitted to the ITU after home cardiac arrest and resuscitation. On admission he was unconscious and in respiratory distress, with a GCS of 5. Blood gases revealed that his pH was 7.64, HCO3 44 mmol L(-1), K+ 2.4 mmol L(-1)l, Cl- 44 mmol L(-1), and lactate concentration over 15 mmol L(-1). He was treated with controlled hypercapnia, up to a PaCO2 of 63 mm Hg, sedation, and administration of a large amount of chloride (864 mmol during the first day). The patient regained consciousness after 48 h, was extubated and transferred to the internal medicine department where he died 3 days later. Chronic alkali abuse can lead to various metabolic disturbances, neurologic disturbances and cardiovascular compromise. In the described case, the exact cause of cardiac arrest remained unknown, but may have been caused by alkalosis combined with hypoxia, hypokalemia and poor general condition. The extreme metabolic alkalosis (pH 7.8) could also have been enhanced by the administration of i.v. sodium bicarbonate during resuscitation. The treatment of choice in such cases should consist of vigorous chloride containing fluid resuscitation, ammonium chloride and hemodialysis.

The effect of metabolic alkalosis on the ventilatory response in healthy subjects

NARCIS (Netherlands)

Mos-Oppersma, Eline; Doorduin, Jonne; van der Hoeven, J.G.; Veltink, Petrus H.; van Hees, H.W.H.; Heunks, L.M.A.

Background Patients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma

Metabolic alkalosis with multiple salt unbalance: an atypical onset of cystic fibrosis in a child

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Dimitri Poddighe

2017-12-01

Full Text Available Dehydration with multiple salt abnormalities is frequently encountered in the paediatric emergency department, during acute illnesses complicated by loss of body fluids. Metabolic alkalosis is not a common finding in dehydrated children. The presence of unusual electrolyte unbalance, such as metabolic alkalosis, hyponatremia, hypochloremia and hypokalemia, without evidence of renal tubular defects, is named as pseudo-Bartter syndrome. It can occur in several clinical settings and, in infancy, it is described as a potential complication of cystic fibrosis. We report a case of pseudo-Bartter syndrome representing the onset of cystic fibrosis in childhood.

Experimental febrile seizures are precipitated by a hyperthermia-induced respiratory alkalosis.

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Schuchmann, Sebastian; Schmitz, Dietmar; Rivera, Claudio; Vanhatalo, Sampsa; Salmen, Benedikt; Mackie, Ken; Sipilä, Sampsa T; Voipio, Juha; Kaila, Kai

2006-07-01

Febrile seizures are frequent during early childhood, and prolonged (complex) febrile seizures are associated with an increased susceptibility to temporal lobe epilepsy. The pathophysiological consequences of febrile seizures have been extensively studied in rat pups exposed to hyperthermia. The mechanisms that trigger these seizures are unknown, however. A rise in brain pH is known to enhance neuronal excitability. Here we show that hyperthermia causes respiratory alkalosis in the immature brain, with a threshold of 0.2-0.3 pH units for seizure induction. Suppressing alkalosis with 5% ambient CO2 abolished seizures within 20 s. CO2 also prevented two long-term effects of hyperthermic seizures in the hippocampus: the upregulation of the I(h) current and the upregulation of CB1 receptor expression. The effects of hyperthermia were closely mimicked by intraperitoneal injection of bicarbonate. Our work indicates a mechanism for triggering hyperthermic seizures and suggests new strategies in the research and therapy of fever-related epileptic syndromes.

Sleep apnoea during upper respiratory infection and metabolic alkalosis in infancy.

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Abreu e Silva, F A; MacFadyen, U M; Williams, A; Simpson, H

1986-01-01

Three to four hour polygraphic sleep studies were carried out in 10 infants, five with upper respiratory infection and five with metabolic alkalosis secondary to vomiting during and after recovery from illness. During upper respiratory infection, the main abnormality detected was brief (greater than 3 less than 6 seconds) or prolonged (greater than 6 seconds) attacks of obstructive apnoea. Other indices of apnoea were similar to recovery data. Gross body movements were also increased. In infants with metabolic alkalosis indices of central apnoea were significantly increased when compared with recovery or case control data. Prolonged (greater than 15 seconds) attacks of central apnoea and obstructive apnoea (greater than 6 seconds) were only observed during illness. Gross body movements and periodic breathing were also increased. These findings suggest that the functional consequences of apparently 'mild' illnesses in young infants may be greater than is generally suspected and perhaps relevant to mechanism(s) of death in sudden infant death syndrome. PMID:3789786

Acetazolamide for the management of chronic metabolic alkalosis in neonates and infants.

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Tam, Bonnie; Chhay, Annie; Yen, Lilly; Tesoriero, Linda; Ramanathan, Rangasamy; Seri, Istvan; Friedlich, Philippe S

2014-01-01

In this study, we evaluated the efficacy and safety of acetazolamide in the management of chronic metabolic alkalosis in neonates and infants with chronic respiratory insufficiency. A retrospective chart review of 90 patients treated with acetazolamide between 2006 and 2007 admitted to the neonatal intensive care unit was performed. Blood gases and electrolytes obtained at baseline and by 24 hours after acetazolamide administration were compared. Compared with baseline and after 24 hours of acetazolamide, mean measured serum bicarbonate (29.5±3.7 vs. 26.9±3.8 mEq/L, Prespiratory acidosis developed in 4 (3.1%) treatment courses. Acetazolamide may be effective in decreasing serum bicarbonate in carefully selected patients. Its use and safety as an adjunctive therapy for chronic metabolic alkalosis in neonates and infants with chronic respiratory insufficiency needs further study.

Metformin-associated respiratory alkalosis.

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Bryant, Sean M; Cumpston, Kirk; Lipsky, Martin S; Patel, Nirali; Leikin, Jerrold B

2004-01-01

We present an 84-year-old man with a history of chronic obstructive pulmonary disease, type 2 diabetes, hypertension, glaucoma, and bladder cancer who presented to the emergency department after the police found him disoriented and confused. Metformin therapy began 3 days before, and he denied any overdose or suicidal ideation. Other daily medications included glipizide, fluticasone, prednisone, aspirin, furosemide, insulin, and potassium supplements. In the emergency department, his vital signs were significant for hypertension (168/90), tachycardia (120 bpm), and Kussmaul respirations at 24 breaths per minute. Oxygen saturation was 99% on room air, and a fingerstick glucose was 307 mg/dL. He was disoriented to time and answered questions slowly. Metformin was discontinued, and by day 3, the patient's vital signs and laboratory test results normalized. He has been asymptomatic at subsequent follow-up visits. Metformin-associated lactic acidosis is a well-known phenomenon. Respiratory alkalosis may be an early adverse event induced by metformin prior to the development of lactic acidosis.

Low sodium intake does not impair renal compensation of hypoxia-induced respiratory alkalosis.

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Höhne, Claudia; Boemke, Willehad; Schleyer, Nora; Francis, Roland C; Krebs, Martin O; Kaczmarczyk, Gabriele

2002-05-01

Acute hypoxia causes hyperventilation and respiratory alkalosis, often combined with increased diuresis and sodium, potassium, and bicarbonate excretion. With a low sodium intake, the excretion of the anion bicarbonate may be limited by the lower excretion rate of the cation sodium through activated sodium-retaining mechanisms. This study investigates whether the short-term renal compensation of hypoxia-induced respiratory alkalosis is impaired by a low sodium intake. Nine conscious, tracheotomized dogs were studied twice either on a low-sodium (LS = 0.5 mmol sodium x kg body wt-1 x day-1) or high-sodium (HS = 7.5 mmol sodium x kg body wt-1 x day-1) diet. The dogs breathed spontaneously via a ventilator circuit during the experiments: first hour, normoxia (inspiratory oxygen fraction = 0.21); second to fourth hour, hypoxia (inspiratory oxygen fraction = 0.1). During hypoxia (arterial PO2 34.4 +/- 2.1 Torr), plasma pH increased from 7.37 +/- 0.01 to 7.48 +/- 0.01 (P respiratory alkalosis was not impaired by a low sodium intake. The increased sodium excretion during hypoxia seems to be combined with a decrease in plasma aldosterone and angiotensin II in LS as well as in HS dogs. Other factors, e.g., increased mean arterial blood pressure, minute ventilation, and renal blood flow, may have contributed.

Exaggerated compensatory response to acute respiratory alkalosis in panic disorder is induced by increased lactic acid production.

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Ueda, Yoshiyasu; Aizawa, Masayo; Takahashi, Atsushi; Fujii, Masamitsu; Isaka, Yoshitaka

2009-03-01

In acute respiratory alkalosis, the severity of alkalaemia is ameliorated by a decrease in plasma [HCO(3)(-)] of 0.2 mEq/L for each 1 mmHg decrease in PaCO(2). Although hyperventilation in panic disorder patients is frequently encountered in outpatients, the drop in plasma [HCO(3)(-)] sometimes surpasses the expectation calculated from the above formula. The quantitative relationship between reduced PaCO(2) and plasma [HCO(3)(-)] in acute respiratory alkalosis has not been studied in panic disorder patients. Our objective was to provide reference data for the compensatory metabolic changes in acute respiratory alkalosis in panic disorder patients. In 34 panic disorder patients with hyperventilation attacks, we measured arterial pH, PaCO(2), plasma [HCO(3)(-)] and lactate on arrival at the emergency room. For each decrease of 1 mmHg in PaCO(2), plasma [HCO(3)(-)] decreased by 0.41 mEq/L. During hypocapnia, panic disorder patients exhibited larger increases in serum lactate levels (mean +/- SD; 2.59 +/- 1.50 mmol/L, range; 0.78-7.78 mmol/L) than previously reported in non-panic disorder subjects. Plasma lactate accumulation was correlated with PaCO(2) (P respiratory alkalosis is exaggerated by increased lactic acid production in panic disorder patients. Here, we call attention to the diagnosis of acid-base derangements by means of plasma [HCO(3)(-)] and lactate concentration in panic disorder patients.

Respiratory alkalosis and metabolic acidosis in a child treated with sulthiame.

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Weissbach, Avichai; Tirosh, Irit; Scheuerman, Oded; Hoffer, Vered; Garty, Ben Zion

2010-10-01

To report on severe acid-base disturbance in a child with symptomatic epilepsy treated with sulthiame. A 9.5-year-old boy with chronic generalized tonic-clonic seizures was treated with carbamazepine and valproic acid. Because of poor seizure control, sulthiame was added to the treatment. Two months later, he presented at the emergency department with severe weakness, headache, dizziness, dyspnea, anorexia, and confusional state. Arterial blood gas analysis showed mixed respiratory alkalosis with high anion gap metabolic acidosis. Sulthiame-induced acid-base disturbance was suspected. The drug was withheld for the first 24 hours and then restarted at a reduced dosage. The arterial blood gases gradually normalized, the confusion disappeared, and the patient was discharged home.Three months later, 4 weeks after an increase in sulthiame dosage, the patient was once again admitted with the same clinical picture. Improvement was noted after the drug dosage was reduced. This is the first report of mixed respiratory alkalosis and metabolic acidosis in a child treated with sulthiame. Monitoring of the acid-base status should be considered in patients treated with sulthiame.

Baking soda pica: a case of hypokalemic metabolic alkalosis and rhabdomyolysis in pregnancy.

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Grotegut, Chad A; Dandolu, Vani; Katari, Sunita; Whiteman, Valerie E; Geifman-Holtzman, Ossie; Teitelman, Melissa

2006-02-01

We report a case of baking soda pica in a woman at 31 weeks of pregnancy causing severe hypokalemic metabolic alkalosis and rhabdomyolysis. A multigravida at 31 weeks of gestation presented with weakness and muscle pain. She was found to have severe hypokalemic metabolic alkalosis and rhabdomyolysis, with elevation in serum transaminases and hypertension. We initially thought the patient had an atypical presentation of preeclampsia until it was realized that she was ingesting 1 full box of baking soda (454 g sodium bicarbonate) per day. Symptoms and abnormal laboratory findings resolved with discontinuation of the patient's pica practices. Pica is a common but often overlooked practice that can potentially lead to life-threatening disorders. A thorough evaluation of a patient's dietary intake is extremely important, especially in the setting of atypical presentations of disease in pregnancy.

Effectiveness of acetazolamide for reversal of metabolic alkalosis in weaning COPD patients from mechanical ventilation.

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Faisy, Christophe; Mokline, Amel; Sanchez, Olivier; Tadié, Jean-Marc; Fagon, Jean-Yves

2010-05-01

To evaluate the effects of a single daily dose of acetazolamide (ACET) on metabolic alkalosis and respiratory parameters in weaning chronic obstructive pulmonary disease (COPD) patients from invasive mechanical ventilation. Case-control study. An 18-bed intensive care unit (ICU) in a university hospital. Twenty-six intubated COPD patients with mixed metabolic alkalosis (serum bicarbonate >26 mmol/l and arterial pH >or=7.38) were compared with a historical control group (n = 26) matched for serum bicarbonate, arterial pH, age, and severity of illness at admission to ICU. ACET administration (500 mg intravenously) was monitored daily according to arterial blood gas analysis from readiness to wean until extubation. ACET was administered 4 (1-11) days throughout the weaning period. Patients with ACET treatment significantly decreased their serum bicarbonate (p = 0.01 versus baseline) and arterial blood pH (p respiratory parameters except PaO(2)/FiO(2) ratio (p = 0.03). ACET patients and their matched controls had similar duration of weaning. Extubation success rate was not significantly different between groups, and causes of reintubation were comparable. ACET used at the dosage of 500 mg per day reduces metabolic alkalosis but has no benefit in terms of improving PaCO(2) or respiratory parameters in weaning COPD patients from mechanical ventilation.

[Dehydration and metabolic alkalosis: an unusual presentation of cystic fibrosis in an infant].

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Aranzamendi, Roberto J; Breitman, Fanny; Asciutto, Carolina; Delgado, Norma; Castaños, Claudio

2008-10-01

Cystic fibrosis (CF) may present during neonatal period with classic clinic symptoms related to the disease. The severity of the disease is multifactorial, one of the factors depends on the level of activity of the CFTR protein, which is related with the mutation type that affects the patient. An infant is presented who developed recurrent episodes of vomiting, anorexia, weight loss, dehydration and electrolyte abnormalities, such as metabolic alkalosis, hyponatremia, hypokalemia and hypochloremia. CF was diagnosed after the third episode showing an unusual and not very publicized presentation of the disease. Mutations !F 508 and 2789+5G-A were found. CF should be considered in patients of any age, but particularly in infants, presenting with anorexia, vomiting, failure to thrive, that are associated with recurrent episodes of hyponatremic hypochloremic, dehydration with metabolic alkalosis unexplained by other causes, even in the absence of respiratory or gastrointestinal symptoms or failure to thrive.

Citrate metabolism and its complications in non-massive blood transfusions: association with decompensated metabolic alkalosis+respiratory acidosis and serum electrolyte levels.

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Bıçakçı, Zafer; Olcay, Lale

2014-06-01

Metabolic alkalosis, which is a non-massive blood transfusion complication, is not reported in the literature although metabolic alkalosis dependent on citrate metabolism is reported to be a massive blood transfusion complication. The aim of this study was to investigate the effect of elevated carbon dioxide production due to citrate metabolism and serum electrolyte imbalance in patients who received frequent non-massive blood transfusions. Fifteen inpatients who were diagnosed with different conditions and who received frequent blood transfusions (10-30 ml/kg/day) were prospectively evaluated. Patients who had initial metabolic alkalosis (bicarbonate>26 mmol/l), who needed at least one intensive blood transfusion in one-to-three days for a period of at least 15 days, and whose total transfusion amount did not fit the massive blood transfusion definition (alkalosis+respiratory acidosis developed as a result of citrate metabolism. There was a positive correlation between cumulative amount of citrate and the use of fresh frozen plasma, venous blood pH, ionized calcium, serum-blood gas sodium and mortality, whereas there was a negative correlation between cumulative amount of citrate and serum calcium levels, serum phosphorus levels and amount of urine chloride. In non-massive, but frequent blood transfusions, elevated carbon dioxide production due to citrate metabolism causes intracellular acidosis. As a result of intracellular acidosis compensation, decompensated metabolic alkalosis+respiratory acidosis and electrolyte imbalance may develop. This situation may contribute to the increase in mortality. In conclusion, it should be noted that non-massive, but frequent blood transfusions may result in certain complications. Copyright © 2014 Elsevier Ltd. All rights reserved.

Changes in bone sodium and carbonate in metabolic acidosis and alkalosis in the dog

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Burnell, James M.

1971-01-01

Metabolic acidosis and alkalosis were produced in adult dogs over 5- to 10-day periods. Midtibial cortical bone was analyzed for calcium, sodium, phosphorus, and carbonate. In acidosis bone CO3/Ca decreased 9.5% and bone Na/Ca decreased 6.3%. In alkalosis bone CO3/Ca increased 3.1% and bone Na/Ca increased 3.0%. Previous attempts to account for changes in net acid balance by summation of extra- and intracellular acid-base changes have uniformly resulted in about 40-60% of acid gained or lost being “unaccounted for.” If it is assumed that changes in tibial cortex reflect changes in the entire skeletal system, changes in bone CO3= are sufficiently large to account for the “unaccounted for” acid change without postulating changes in cellular metabolic acid production. PMID:5540172

A short-term supranutritional vitamin E supplementation alleviated respiratory alkalosis but did not reduce oxidative stress in heat stressed pigs.

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Liu, Fan; Celi, Pietro; Chauhan, Surinder Singh; Cottrell, Jeremy James; Leury, Brian Joseph; Dunshea, Frank Rowland

2018-02-01

Heat stress (HS) triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE) can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. A total of 24 pigs were given either a control diet (17 IU/kg VE) or a high VE (200 IU/kg VE; HiVE) diet for 14 d, then exposed to thermoneutral (TN; 20°C, 45% humidity) or HS (35°C, 35% to 45% humidity, 8 h daily) conditions for 7 d. Respiration rate and rectal temperature were measured three times daily during the thermal exposure. Blood gas variables and oxidative stress markers were studied in blood samples collected on d 7. Although HiVE diet did not affect the elevated rectal temperature or respiration rate observed during HS, it alleviated (all prespiratory alkalosis but did not reduce oxidative stress in heat-stressed pigs.

The effect of metabolic alkalosis on the ventilatory response in healthy subjects.

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Oppersma, E; Doorduin, J; van der Hoeven, J G; Veltink, P H; van Hees, H W H; Heunks, L M A

2018-02-01

Patients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma bicarbonate levels decrease respiratory drive and minute ventilation. In an intervention study in 10 healthy subjects the ventilatory response using a hypercapnic ventilatory response (HCVR) test was assessed, before and after administration of high dose sodium bicarbonate. Total dose of sodiumbicarbonate was 1000 ml 8.4% in 3 days. Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO 2 pressure during the HCVR test, RR, V t , Pdi, EAdi and V E increased. The clinical ratio ΔV E /ΔP et CO 2 remained unchanged, but Pdi, EAdi and V E were significantly lower after bicarbonate administration for similar levels of inspired CO 2 . This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO 2 . Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

Metabolic alkalosis secondary to baking soda treatment of a diaper rash.

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Gonzalez, J; Hogg, R J

1981-06-01

A 4-month-old infant was seen with hypokalemic metabolic alkalosis that was associated with prior application of liberal amounts of sodium bicarbonate (baking soda) to a diaper rash. After exclusion of other etiologies of the infant's acid-base disturbance, a complete resolution occurred following discontinuation of the baking soda applications. This case report provides a reminder of the significant side effects that may result from the excessive use of a seemingly harmless household substance.

Acute respiratory acidosis and alkalosis – A modern quantitative interpretation

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Andraž Stožer

2014-03-01

Full Text Available Background: Three different approaches for assessing the acid-base status of a patient exist, i.e. the Boston, Copenhagen, and Stewart´s approach, and they employ different parameters to assess a given acid-base disturbance. Students, researchers, and clinicians are getting confused by heated debates about which of these performs best and by the fact that during their curricula, they typically get acquainted with one of the approaches only, which prevents them to understand sources employing other approaches and to critically evaluate the advantages and drawbacks of each approach. In this paper, the authors introduce and define the basic parameters characterizing each of the approaches and point out differences and similarities between them. Special attention is devoted to how the different approaches assess the degree of change in the concentration of plasma bicarbonate that occurs during primary respiratory changes; proper understanding of these is necessary to correctly interpret chronic respiratory and metabolic acid-base changes.Conclusion: During acute respiratory acidosis the concentration of bicarbonate rises and during acute respiratory alkalosis it falls, depending on the buffering strength of non-bicarbonate buffers. During acute respiratory acid-base disturbances, buffer base (employed by the Copenhagen approach, apparent and effective strong ion difference, as well as strong ion gap (employed by the Stewart approach remain unchanged; the anion gap (employed by the Boston and Copenhagen approach falls during acute respiratory acidosis and rises during acute respiratory alkalosis.

Metabolic alkalosis during immobilization in monkeys (M. nemestrina)

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Young, D. R.; Yeh, I.; Swenson, R. S.

1983-01-01

The systemic and renal acid-base response of monkeys during ten weeks of immobilization was studied. By three weeks of immobilization, arterial pH and bicarbonate concentrations were elevated (chronic metabolic alkalosis). Net urinary acid excretion increased in immobilized animals. Urinary bicarbonate excretion decreased during the first three weeks of immobilization, and then returned to control levels. Sustained increases in urinary ammonium excretion were seen throughout the time duration of immobilization. Neither potassium depletion nor hypokalemia was observed. Most parameters returned promptly to the normal range during the first week of recovery. Factors tentatively associated with changes in acid-base status of monkeys include contraction of extracellular fluid volume, retention of bicarbonate, increased acid excretion, and possible participation of extrarenal buffers.

An infant with poor weight gain and hypochloremic metabolic alkalosis: a case report

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Alhammadi AH

2014-07-01

Full Text Available Ahmed H Alhammadi, Mohamed Khalifa, Lolwa Alnaimi Department of Pediatrics, Division of General Pediatrics, Hamad Medical Corporation, Doha, Qatar Abstract: Bartter syndrome is an autosomal recessive disease manifested by a defect in chloride transport in the thick loop of Henle, with different genetic origins and molecular pathophysiology. Children with Bartter syndrome generally present in early infancy with persistent polyuria and associated dehydration, electrolyte imbalance, and failure to thrive. Although early diagnosis and appropriate treatment of Bartter syndrome may improve the outcome, some children will progress to renal failure. We report a case of an 8-week-old infant who was admitted for electrolyte imbalance and failure to thrive. Laboratory studies revealed hypochloremic metabolic alkalosis with severe hypokalemia. Health care providers should consider Bartter syndrome when excessive chloride losses appear to be renal in origin and the patient has normal blood pressure and high levels of serum renin and aldosterone. Treatments, including indomethacin, spironolactone, and aggressive fluid and electrolyte replacement, may prevent renal failure in children with Bartter syndrome. Molecular genetics studies are indicated to identify the primary genetic defect. Keywords: Bartter syndrome, failure to thrive, metabolic alkalosis 

Clinical characterization and diagnosis of cystic fibrosis through exome sequencing in Chinese infants with Bartter-syndrome-like hypokalemia alkalosis.

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Qiu, Liru; Yang, Fengjie; He, Yonghua; Yuan, Huiqing; Zhou, Jianhua

2018-03-09

Cystic fibrosis (CF) is a fatal autosomal-recessive disease caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. CF is characterized by recurrent pulmonary infection with obstructive pulmonary disease. CF is common in the Caucasian population but is rare in the Chinese population. The symptoms of early-stage CF are often untypical and may sometimes manifest as Bartter syndrome (BS)-like hypokalemic alkalosis. Therefore, the ability of doctors to differentiate CF from BS-like hypokalemic alkalosis in Chinese infants is a great challenge in the timely and accurate diagnosis of CF. In China, sporadic CF has not been diagnosed in children younger than three years of age to date. Three infants, who were initially admitted to our hospital over the period of June 2013 to September 2014 with BS-like hypokalemic alkalosis, were diagnosed with CF through exome sequencing and sweat chloride measurement. The compound heterozygous mutations of the CFTR gene were detected in two infants, and a homozygous missense mutation was found in one infant. Among the six identified mutations, two are novel point mutations (c.1526G > C and c.3062C > T) that are possibly pathogenic. The three infants are the youngest Chinese patients to have been diagnosed with sporadic CF at a very early stage. Follow-up examination showed that all of the cases remained symptom-free after early intervention, indicating the potential benefit of very early diagnosis and timely intervention in children with CF. Our results demonstrate the necessity of distinguishing CF from BS in Chinese infants with hypokalemic alkalosis and the significant diagnostic value of powerful exome sequencing for rare genetic diseases. Furthermore, our findings expand the CFTR mutation spectrum associated with CF.

Dopamine enhances the phosphaturic effect of PTH during acute respiratory alkalosis.

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Berndt, T J; Tucker, R R; Kent, P D; Streiff, P C; Tyce, G M; Knox, F G

1999-12-01

The phosphaturic response to parathyroid hormone (PTH) is blunted during acute respiratory alkalosis. The objective of the present study was to determine the effect of dopamine on the blunted phosphaturic response to PTH during acute respiratory alkalosis. The phosphaturic response to PTH was determined in thyroparathyroidectomized (TPTX) normocapnic and respiratory alkalotic rats in the absence and presence of the infusion of exogenous dopamine (25 microg/kg/min) or of 3,4-dihydroxyphenylalanine (L-DOPA, 250 microg/kg/min) to increase endogenous dopamine synthesis. In normocapnic rats, PTH infusion (33 U/kg plus 1 U/kg/min) significantly increased the fractional excretion of phosphate (FE(Pi)), from 1.5%+/-0.5% to 28.4%+/-4.0%, (deltaFE(Pi) 26.9%+/-4.1%, n = 11, Prespiratory alkalotic rats, the increase was from 0.4%+/-0.1% to 11.4%+/-1.7% (deltaFE(Pi) 11.0%+/-1.8%, n = 13, Prespiratory alkalotic rats (deltaFE(Pi) 26.9%+/-4.1% vs 11.0%+/-1.9%, Prespiratory alkalotic rats, in the presence of dopamine infusion, PTH significantly increased the FE(Pi), from 0.6%+/-0.2% to 19.3%+/-3.3% (deltaFE(Pi) 18.7%+/-3.3%, n = 6); in the presence of L-DOPA infusion it increased from 1.0%+/-0.3% to 20.5%+/-2.8% (deltaFE(Pi) 19.5%+/-2.9%, n = 8, Prespiratory alkalotic rats was enhanced by stimulation of endogenous dopamine synthesis by the infusion of L-DOPA.

Hypernatremia and metabolic alkalosis as a consequence of the therapeutic misuse of baking soda.

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Fuchs, S; Listernick, R

1987-12-01

When used appropriately, baking soda (sodium bicarbonate, USP) is a nontoxic, readily available, multipurpose product found in many households. We report an infant who presented with hypernatremia and metabolic alkalosis due to the addition of baking soda to her water. This case represents the possible dangerous use of a common household product in infants owing to the lack of proper warning labels.

[Self-treatment with baking soda can lead to severe metabolic alkalosis].

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Jensen, Sara; Skriver, Signe

2014-12-15

This case report describes a 66-year-old man, previously healthy besides mild hypertension. He ingested a self-made folk remedy consisting of baking soda and water against acid reflux in dosages that resulted in severe metabolic alkalosis (pH 7.8). Diagnosing and treating MA is easy and cheap, but if the condition is not treated, consequences can be severe. The challenge is to uncover patients' use of non prescription medications and folk remedies in the diagnostic process. Having this information it is possible to prevent MA in both high- and low-risk patients.

Respiratory acidosis prolongs, while alkalosis shortens, the duration and recovery time of vecuronium in humans.

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Yamauchi, Masanori; Takahashi, Hiromi; Iwasaki, Hiroshi; Namiki, Akiyoshi

2002-03-01

To determine the effects of respiratory acidosis and alkalosis by mechanical ventilation on the onset, duration, and recovery times of vecuronium. Randomized, prospective study. Operating rooms in the Sapporo Medical University Hospital and Kitami Red Cross Hospital. 90 ASA physical status I and II patients undergoing lower abdominal surgery. Patients were randomly allocated to one of three groups by arterial carbon dioxide tension level (PaCO2; mmHg) after induction: hyperventilation group (PaCO2 = 25-35), normoventilation group (PaCO2 = 35-45), and hypoventilation group (PaCO2 = 45-55). Anesthesia was maintained by spinal block with inhalation of 50% to 66% nitrous oxide in oxygen and intermittent intravenous administration of fentanyl and midazolam with tracheal intubation. After vecuronium 0.08 mg/kg was given, onset, duration, and recovery time were measured by mechanomyography (Biometer Myograph 2,000, Odense, Denmark). There were significant differences in the duration and recovery time of vecuronium among the normoventilation group (12.7 +/- 3.3 min and 11.8 +/- 2.8 min, respectively), the hyperventilation group (10.6 +/- 3.5 min and 9.2 +/- 2.7 min, respectively; p respiratory acidosis and shortened in respiratory alkalosis.

Effects of respiratory alkalosis on human skeletal muscle metabolism at the onset of submaximal exercise.

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LeBlanc, P J; Parolin, M L; Jones, N L; Heigenhauser, G J F

2002-10-01

The purpose of this study was to examine the effects of respiratory alkalosis on human skeletal muscle metabolism at rest and during submaximal exercise. Subjects exercised on two occasions for 15 min at 55 % of their maximal oxygen uptake while either hyperventilating (R-Alk) or breathing normally (Con). Muscle biopsies were taken at rest and after 1 and 15 min of exercise. At rest, no effects on muscle metabolism were observed in response to R-Alk. In the first minute of exercise, there was a delayed activation of pyruvate dehydrogenase (PDH) in R-Alk compared with Con, resulting in a reduced rate of pyruvate oxidation. Also, glycogenolysis was higher in R-Alk compared with Con, which was attributed to a higher availability of the monoprotonated form of inorganic phosphate (P(i)), resulting in an elevated rate of pyruvate production. The mismatch between pyruvate production and its oxidation resulted in net lactate accumulation. These effects were not seen after 15 min of exercise, with no further differences in muscle metabolism between conditions. The results from the present study suggest that respiratory alkalosis may play an important role in lactate accumulation during the transition from rest to exercise in acute hypoxic conditions, but that other factors mediate lactate accumulation during steady-state exercise.

Renal responses of trout to chronic respiratory and metabolic acidoses and metabolic alkalosis.

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Wood, C M; Milligan, C L; Walsh, P J

1999-08-01

Exposure to hyperoxia (500-600 torr) or low pH (4.5) for 72 h or NaHCO(3) infusion for 48 h were used to create chronic respiratory (RA) or metabolic acidosis (MA) or metabolic alkalosis in freshwater rainbow trout. During alkalosis, urine pH increased, and [titratable acidity (TA) - HCO(-)(3)] and net H(+) excretion became negative (net base excretion) with unchanged NH(+)(4) efflux. During RA, urine pH did not change, but net H(+) excretion increased as a result of a modest rise in NH(+)(4) and substantial elevation in [TA - HCO(-)(3)] efflux accompanied by a large increase in inorganic phosphate excretion. However, during MA, urine pH fell, and net H(+) excretion was 3.3-fold greater than during RA, reflecting a similar increase in [TA - HCO(-)(3)] and a smaller elevation in phosphate but a sevenfold greater increase in NH(+)(4) efflux. In urine samples of the same pH, [TA - HCO(-)(3)] was greater during RA (reflecting phosphate secretion), and [NH(+)(4)] was greater during MA (reflecting renal ammoniagenesis). Renal activities of potential ammoniagenic enzymes (phosphate-dependent glutaminase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, alanine aminotransferase, phosphoenolpyruvate carboxykinase) and plasma levels of cortisol, phosphate, ammonia, and most amino acids (including glutamine and alanine) increased during MA but not during RA, when only alanine aminotransferase increased. The differential responses to RA vs. MA parallel those in mammals; in fish they may be keyed to activation of phosphate secretion by RA and cortisol mobilization by MA.

Anesthetic management of a patient with sustained severe metabolic alkalosis and electrolyte abnormalities caused by ingestion of baking soda.

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Soliz, Jose; Lim, Jeffrey; Zheng, Gang

2014-01-01

The use of alternative medicine is prevalent worldwide. However, its effect on intraoperative anesthetic care is underreported. We report the anesthetic management of a patient who underwent an extensive head and neck cancer surgery and presented with a severe intraoperative metabolic alkalosis from the long term ingestion of baking soda and other herbal remedies.

A short-term supranutritional vitamin E supplementation alleviated respiratory alkalosis but did not reduce oxidative stress in heat stressed pigs

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Fan Liu

2018-02-01

Full Text Available Objective Heat stress (HS triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. Methods A total of 24 pigs were given either a control diet (17 IU/kg VE or a high VE (200 IU/kg VE; HiVE diet for 14 d, then exposed to thermoneutral (TN; 20°C, 45% humidity or HS (35°C, 35% to 45% humidity, 8 h daily conditions for 7 d. Respiration rate and rectal temperature were measured three times daily during the thermal exposure. Blood gas variables and oxidative stress markers were studied in blood samples collected on d 7. Results Although HiVE diet did not affect the elevated rectal temperature or respiration rate observed during HS, it alleviated (all p<0.05 for diet×temperature the loss of blood CO2 partial pressure and bicarbonate, as well as the increase in blood pH in the heat-stressed pigs. The HS reduced (p = 0.003 plasma biological antioxidant potential (BAP and tended to increase (p = 0.067 advanced oxidized protein products (AOPP in the heat-stressed pigs, suggesting HS triggers oxidative stress. The HiVE diet did not affect plasma BAP or AOPP. Only under TN conditions the HiVE diet reduced the plasma reactive oxygen metabolites (p<0.05 for diet× temperature. Conclusion A short-term supplementation with 200 IU/kg VE partially alleviated respiratory alkalosis but did not reduce oxidative stress in heat-stressed pigs.

Anesthetic Management of a Patient with Sustained Severe Metabolic Alkalosis and Electrolyte Abnormalities Caused by Ingestion of Baking Soda

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Jose Soliz

2014-01-01

Full Text Available The use of alternative medicine is prevalent worldwide. However, its effect on intraoperative anesthetic care is underreported. We report the anesthetic management of a patient who underwent an extensive head and neck cancer surgery and presented with a severe intraoperative metabolic alkalosis from the long term ingestion of baking soda and other herbal remedies.

Respiratory alkalosis and primary hypocapnia in Labrador Retrievers participating in field trials in high-ambient-temperature conditions.

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Steiss, Janet E; Wright, James C

2008-10-01

To determine whether Labrador Retrievers participating in field trials develop respiratory alkalosis and hypocapnia primarily in conditions of high ambient temperatures. 16 Labrador Retrievers. At each of 5 field trials, 5 to 10 dogs were monitored during a test (retrieval of birds over a variable distance on land [1,076 to 2,200 m]; 36 assessments); ambient temperatures ranged from 2.2 degrees to 29.4 degrees C. For each dog, rectal temperature was measured and a venous blood sample was collected in a heparinized syringe within 5 minutes of test completion. Blood samples were analyzed on site for Hct; pH; sodium, potassium, ionized calcium, glucose, lactate, bicarbonate, and total CO2 concentrations; and values of PvO2 and PvCO2. Scatterplots of each variable versus ambient temperature were reviewed. Regression analysis was used to evaluate the effect of ambient temperature ( 21 degrees C) on each variable. Compared with findings at ambient temperatures 21 degrees C; rectal temperature did not differ. Two dogs developed signs of heat stress in 1 test at an ambient temperature of 29 degrees C; their rectal temperatures were higher and PvCO2 values were lower than findings in other dogs. When running distances frequently encountered at field trials, healthy Labrador Retrievers developed hyperthermia regardless of ambient temperature. Dogs developed respiratory alkalosis and hypocapnia at ambient temperatures > 21 degrees C.

Delay in onset of metabolic alkalosis during regional citrate anti-coagulation in continous renal replacement therapy with calcium-free replacement solution

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See Kay

2009-01-01

Full Text Available Regional citrate anti-coagulation for continuous renal replacement therapy chelates calcium to produce the anti- coagulation effect. We hypothesise that a calcium-free replacement solution will require less citrate and produce fewer metabolic side effects. Fifty patients, in a Medical Intensive Care Unit of a tertiary teaching hospital (25 in each group, received continuous venovenous hemofiltration using either calcium-containing or calcium-free replacement solutions. Both groups had no significant differences in filter life, metabolic alkalosis, hypernatremia, hypocalcemia, and hypercalcemia. However, patients using calcium-containing solution developed metabolic alkalosis earlier, compared to patients using calcium-free solution (mean 24.6 hours,CI 0.8-48.4 vs. 37.2 hours, CI 9.4-65, P = 0.020. When calcium-containing replacement solution was used, more citrate was required (mean 280ml/h, CI 227.2-332.8 vs. 265ml/h, CI 203.4-326.6, P = 0.069, but less calcium was infused (mean 21.2 ml/h, CI 1.2-21.2 vs 51.6ml/h, CI 26.8-76.4, P ≤ 0.0001.

Central lactic acidosis, hyperventilation, and respiratory alkalosis: leading clinical features in a 3-year-old boy with malignant meningeal melanoma.

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Blüher, Susann; Schulz, Manuela; Bierbach, Uta; Meixensberger, Jürgen; Tröbs, Ralf-Bodo; Hirsch, Wolfgang; Schober, Ralf; Kiess, Wieland; Siekmeyer, Werner

2008-04-01

Meningeal tumors are extremely rare in children and are diagnostically as well as therapeutically challenging. Among the least common types of malignancies in childhood is malignant melanoma, counting for less than 1% of pediatric tumors. Due to the rarity and the wide spectrum of appearance, initial clinical features may be misleading. A 3-year-old boy was referred to our hospital with symptoms of hyperventilation, dyspnoea, tachycardia, respiratory alkalosis, inarticulate speech, and fatigue. Measurement of pH in cerebrospinal fluid (CSF) yielded central lactic acidosis despite alkalosis in peripheral blood. Diagnostic imaging procedures as well as histology and immunohistochemistry revealed the diagnosis of a malignant meningeal melanoma. We hypothesize that central lactate production of the tumor nests might have induced central acidification, thus inducing hyperventilation by stimulation of central chemoreceptors. This case is a model example of the key role of central pH as an inducer/suppressor of ventilation in humans and illustrates the critical importance of central pH for regulating both ventilation and acid-base homeostasis. Thus, pH of CSF should be measured whenever a malignant brain tumor is suspected.

[Metabolic alkalosis despite hyperlactatemia and hypercapnia. Interpretation and therapy with help of the Stewart concept].

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Chappell, D; Hofmann-Kiefer, K; Jacob, M; Conzen, P; Rehm, M

2008-02-01

Acid-base disturbances are commonly found in critically ill patients and are often associated with fatal complications. The basis of a successful treatment is a thorough understanding of the causes of these disorders. The "classical methods" to explain acid-base disorders--pH, base excess and bicarbonate concentration--mostly do not provide a causal correlation to the underlying pathology. An unusual case of a combined respiratory-metabolic disorder with hyperlactatemia and hypercapnia is presented. An acidosis masked by hypochloremic and hypoalbuminemic alkalosis was identified with the help of Stewart's concept and finally permitted a successful therapy. The modern Stewart concept provides enhanced information, enabling an exact diagnosis and causal therapy even in complex cases.

Inherited renal tubulopathies associated with metabolic alkalosis: effects on blood pressure.

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Ariceta, Gema; Rodríguez-Soriano, Juan

2006-11-01

Inherited tubular disorders associated with metabolic alkalosis are caused by several gene mutations encoding different tubular transporters responsible for NaCl renal handling. Body volume and renin-angiotensin-aldosterone system status are determined by NaCl reabsorption in the distal nephron. Two common hallmarks in affected individuals: hypokalemia and normal / high blood pressure, support the differential diagnosis. Bartter's syndrome, characterized by hypokalemia and normal blood pressure, is a heterogenic disease caused by the loss of function of SLC12A1 (type 1), KCNJ1 (type 2), CLCNKB (type 3), or BSND genes (type 4). As a result, patients present with renal salt wasting and hypercalciuria. Gitelman's syndrome is caused by the loss of funcion of the SLC12A3 gene and may resemble Bartter's syndrome, though is associated with the very low urinary calcium. Liddle's syndrome, also with similar phenotype but with hypertension, is produced by the gain of function of the SNCC1B or SNCC1G genes, and must be distinguished from other entities of inherited hypertension such as Apparently Mineralocorticoid Excess, of glucocorticoid remediable hypertension.

Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease.

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Kazmaier, S; Weyland, A; Buhre, W; Stephan, H; Rieke, H; Filoda, K; Sonntag, H

1998-10-01

Variation of the arterial carbon dioxide partial pressure (PaCO2) is not uncommon in anesthetic practice. However, little is known about the myocardial consequences of respiratory alkalosis and acidosis, particularly in patients with coronary artery disease. The aim of the current study was to investigate the effects of variation in PaCO2 on myocardial blood flow (MBF), metabolism, and systemic hemodynamics in patients before elective coronary artery bypass graft surgery. In 10 male anesthetized patients, measurements of MBF, myocardial contractility, metabolism, and systemic hemodynamics were made in a randomized sequence at PaCO2 levels of 30, 40, and 50 mmHg, respectively. The MBF was measured using the Kety-Schmidt technique with argon as a tracer. End-diastolic left ventricular pressure and the maximal increase of left ventricular pressure were assessed using a manometer-tipped catheter. The cardiac index significantly changed with varying PaCO2 levels (hypocapnia, - 9%; hypercapnia, 13%). This reaction was associated with inverse changes in systemic vascular resistance index levels. The MBF significantly increased by 15% during hypercapnia, whereas no change was found during hypocapnia. Myocardial oxygen and glucose uptake and the maximal increase of left ventricular pressure were not affected by varying PaCO2 levels. In anesthetized patients with coronary artery disease, short-term variations in PaCO2 have significant effects on MBF but do not influence global myocardial oxygen and glucose uptake. Changes in systemic hemodynamics associated with respiratory alkalosis and acidosis are caused by changes in systemic vascular resistance rather than by alterations in myocardial contractility.

Pulmonary O2 uptake and leg blood flow kinetics during moderate exercise are slowed by hyperventilation-induced hypocapnic alkalosis

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Chin, Lisa M. K.; Heigenhauser, George J. F.; Paterson, Donald H.

2010-01-01

The effect of hyperventilation-induced hypocapnic alkalosis (Hypo) on the adjustment of pulmonary O2 uptake (V̇o2p) and leg femoral conduit artery (“bulk”) blood flow (LBF) during moderate-intensity exercise (Mod) was examined in eight young male adults. Subjects completed four to six repetitions of alternate-leg knee-extension exercise during normal breathing [Con; end-tidal partial pressure of CO2 (PetCO2) ∼40 mmHg] and sustained hyperventilation (Hypo; PetCO2 ∼20 mmHg). Increases in work rate were made instantaneously from baseline (3 W) to Mod (80% estimated lactate threshold). V̇o2p was measured breath by breath by mass spectrometry and volume turbine, and LBF (calculated from mean femoral artery blood velocity and femoral artery diameter) was measured simultaneously by Doppler ultrasound. Concentration changes of deoxy (Δ[HHb])-, oxy (Δ[O2Hb])-, and total hemoglobin-myoglobin (Δ[HbTot]) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). The kinetics of V̇o2p, LBF, and Δ[HHb] were modeled using a monoexponential equation by nonlinear regression. The time constants for the phase 2 V̇o2p (Hypo, 49 ± 26 s; Con, 28 ± 8 s) and LBF (Hypo, 46 ± 16 s; Con, 23 ± 6 s) were greater (P alkalosis is associated with slower convective (i.e., slowed femoral artery and microvascular blood flow) and diffusive (i.e., greater fractional O2 extraction for a given ΔV̇o2p) O2 delivery, which may contribute to the hyperventilation-induced slowing of V̇o2p (and muscle O2 utilization) kinetics. PMID:20339012

Gymnocypris przewalskii decreases cytosolic carbonic anhydrase expression to compensate for respiratory alkalosis and osmoregulation in the saline-alkaline lake Qinghai.

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Yao, Zongli; Guo, Wenfei; Lai, Qifang; Shi, Jianquan; Zhou, Kai; Qi, Hongfang; Lin, Tingting; Li, Ziniu; Wang, Hui

2016-01-01

Naked carp (Gymnocypris przewalskii), endemic to the saline-alkaline Lake Qinghai, have the capacity to tolerate combined high salinity and alkalinity, but migrate to spawn in freshwater rivers each year. In this study, the full-length cDNA of the cytosolic carbonic anhydrase c isoform of G. przewalskii (GpCAc) was amplified and sequenced; mRNA levels and enzyme activity of GpCAc and blood chemistry were evaluated to understand the compensatory responses as the naked carp returned to the saline-alkaline lake after spawning. We found that GpCAc had a total length of 1400 bp and encodes a peptide of 260 amino acids. Comparison of the deduced amino acid sequences and phylogenetic analysis showed that GpCAc was a member of the cytosolic carbonic anhydrase II-like c family. Cytosolic-carbonic-anhydrase-c-specific primers were used to analyze the tissue distribution of GpCAc mRNA expression. Expression of GpCAc mRNA was found in brain, gill, liver, kidney, gut, and muscle tissues, but primarily in the gill and posterior kidney; however, none was evident in red blood cells. Transferring fish from river water to lake water resulted in a respiratory alkalosis, osmolality, and ion rise in the blood, as well as significant decreases in the expression and enzyme activity of GpCAc in both the gill and kidney within 96 h. These results indicate that GpCAc may play an important role in the acclimation to both high salinity and carbonate alkalinity. Specifically, G. przewalskii decreases cytosolic carbonic anhydrase c expression to compensate for a respiratory alkalosis and to aid in osmoregulation during the transition from river to saline-alkaline lake.

Metabolic Alkalosis, Acute Renal Failure and Epileptic Seizures as Unusual Manifestations of an Upside-Down Stomach

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Johannes Stephani

2012-07-01

Full Text Available Upside-down stomach represents a critical and rare manifestation of hiatal hernias. Here we report on a 60-year-old male patient who was admitted to our hospital with epileptic seizures and dehydration. Laboratory tests revealed severe metabolic alkalosis (pH 7.56 with low potassium (2.7 mmol/l, hypochloremia (<60 mmol/l, increased hematocrit (53% and high levels of serum creatinine (651 µmol/l. Based on a history of recurrent vomiting, gastroscopy and computed tomography were performed. Both diagnostics showed an upside-down stomach with signs of incarceration. Upon infusion of sodium chloride 0.9%, acid-base state, electrolyte balance and renal function became improved. Subsequently, the patient was referred to the department of surgery for hiatoplasty with fundoplication. This case report highlights severe metabolic and neurological disorders as unusual and life-threatening complications of an upside-down stomach.

Severe metabolic alkalosis, hypokalemia, and respiratory acidosis induced by the Chinese herbal medicine yokukansan in an elderly patient with muscle weakness and drowsiness.

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Yamada, Shunsuke; Tokumoto, Masanori; Kansui, Yasuo; Wakisaka, Yoshinobu; Uchizono, Yuji; Tsuruya, Kazuhiko; Ooboshi, Hiroaki

2013-05-01

Yokukansan is a Chinese herbal medicine containing licorice that has been shown to alleviate the behavioral and psychological symptoms of Alzheimer's disease, with few adverse effects. Increasing numbers of patients with Alzheimer's disease in Japan are now being treated with this drug. However, yokukansan should be used with caution because of its potential to induce pseudoaldosteronism through the inhibition of 11-beta-hydroxysteroid dehydrogenase type 2, which metabolizes cortisol into cortisone. We present the case of an 88-year-old woman with a history of Alzheimer's disease who was transferred to our emergency department because of drowsiness, anorexia, and muscle weakness. Her blood pressure was 168/90 mmHg. Laboratory data showed serum potassium of 1.9 mmol/l, metabolic alkalosis (pH 7.54; HCO 3 - , 50.5 mmol/l; chloride, 81 mmol/l; sodium, 140 mmol/l), and respiratory disorders (pCO 2 , 60.5 mmHg; pO 2 , 63.8 mmHg). Plasma renin activity and aldosterone concentration were suppressed, and urinary potassium excretion was 22 mmol/l (calculated transtubular potassium gradient 12.9). An electrocardiogram showed flat T-waves and U-waves with ventricular premature contractions. Echocardiography denied volume depletion. Medical interview disclosed that she had been treated with a Chinese herbal medicine (yokukansan) containing licorice. The final diagnosis was pseudoaldosteronism and respiratory acidosis induced by licorice. Hypokalemia, metabolic alkalosis, and respiratory acidosis all subsided shortly after the discontinuation of yokukansan and initiation of intravenous potassium replacement. This case highlights the need for nephrologists to consider the possible involvement of Chinese herbal medicines, including yokukansan, when they encounter hypokalemia in elderly patients.

Post-hypercapnic alkalosis is associated with ventilator dependence and increased ICU stay.

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Banga, Amit; Khilnani, G C

2009-12-01

Posthypercapnic alkalosis (PHA) is frequently overlooked as a complication of mechanical ventilation in patients with exacerbation of chronic obstructive pulmonary disease (COPD). The current study was conducted to determine the incidence, risk factors for development and effect on outcome of PHA. Eighty-four patients (62 +/- 11 years, range 42-78 years, M:F 58: 26) with exacerbation of COPD with underlying chronic hypercapnic respiratory failure requiring mechanical ventilation were included in a retrospective fashion. PHA was defined as static or rising serum bicarbonate levels, 72 hours or more after return of PaCO2 to baseline, with concurrent pH > 7.44. Development of PHA was noted in 17 patients (20.2%). Corticosteroid use >or=10 days during the hospital stay was an independent risk factor for development of PHA (Adjusted OR, 95% CI: 9.4, 1.6-55.3; P = 0.013). Development of PHA was associated with an increased incidence of ventilator dependence (64.7% vs. 37.3%, OR, 95% CI: 3.1, 1.1-9.4, P = 0.04) and duration of ICU stay (14.7 +/- 6.7 vs. 9.5 +/- 5.9, P = 0.01) but no increase in hospital mortality (43.3% vs. 41.2%, P = NS). It is concluded that PHA is a common complication in patients with exacerbation of COPD requiring mechanical ventilation and is associated with increased incidence of ventilator dependence and ICU stay.

Respiratory alkalosis may impair the production of vitamin D and lead to significant morbidity, including the fibromyalgia syndrome.

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Lewis, John M; Fontrier, Toinette H; Coley, J Lynn

2017-05-01

Hyperventilation caused by physical and/or psychological stress may lead to significant respiratory alkalosis and an elevated systemic pH. The alkalotic pH may in turn suppress the normal renal release of phosphate into the urine, thereby interrupting the endogenous production of 1,25-dihydroxyvitamin D (calcitriol). This could cause a shortfall in its normal production, leading to a variety of adverse consequences. It might partially explain the pathogenesis of acute mountain sickness, a treatable disease characterized by severe hyperventilation secondary to the hypoxia of high altitude exposure. Milder degrees of hyperventilation due to different forms of stress may produce other conditions which share characteristics with acute mountain sickness. One of these may be the fibromyalgia syndrome, a chronic painful disorder for which no satisfactory treatment exists. Should fibromyalgia and acute mountain sickness have a common etiology, may they also share a common form of treatment? Evidence is presented to support this hypothesis. Copyright © 2017 Elsevier Ltd. All rights reserved.

Preexercise metabolic alkalosis induced via bicarbonate ingestion accelerates Vo2 kinetics at the onset of a high-power-output exercise in humans.

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Zoladz, Jerzy A; Szkutnik, Zbigniew; Duda, Krzysztof; Majerczak, Joanna; Korzeniewski, Bernard

2005-03-01

The present study investigated the effect of preexercise metabolic alkalosis on the primary component of oxygen uptake (Vo(2)) kinetics, characterized by tau(1). Seven healthy physically active nonsmoking men, aged 22.4 +/- 1.8 (mean +/- SD) yr, maximum Vo(2) (Vo(2 max)) 50.4 +/- 4 ml.min(-1).kg(-1), performed two bouts of cycling, corresponding to 40 and 87% of Vo(2 max), lasting 6 min each, separated by a 20-min pause, once as a control study and a few days later at approximately 90 min after ingestion of 3 mmol/kg body wt of NaHCO(3). Blood samples for measurements of bicarbonate concentration and hydrogen ion concentration were taken from antecubital vein via catheter. Pulmonary Vo(2) was measured continuously breath by breath. The values of tau(1) were calculated by using six various approaches published in the literature. Preexercise level of bicarbonate concentration after ingestion of NaHCO(3) was significantly elevated (P < 0.01) compared with the control study (28.96 +/- 2.11 vs. 24.84 +/- 1.18 mmol/l; P < 0.01), and [H(+)] was significantly (P < 0.01) reduced (42.79 +/- 3.38 nmol/l vs. 46.44 +/- 3.51 nmol/l). This shift (P < 0.01) was also present during both bouts of exercise. During cycling at 40% of Vo(2 max), no significant effect of the preexercise alkalosis on the magnitude of tau(1) was found. However, during cycling at 87% of Vo(2 max), the tau(1) calculated by all six approaches was significantly (P < 0.05) reduced, compared with the control study. The tau(1) calculated as in Borrani et al. (Borrani F, Candau R, Millet GY, Perrey S, Fuchsloscher J, and Rouillon JD. J Appl Physiol 90: 2212-2220, 2001) was reduced on average by 7.9 +/- 2.6 s, which was significantly different from zero with both the Student's t-test (P = 0.011) and the Wilcoxon's signed-ranks test (P = 0.014).

Effect of acetazolamide on post-NIV metabolic alkalosis in acute exacerbated COPD patients.

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Fontana, V; Santinelli, S; Internullo, M; Marinelli, P; Sardo, L; Alessandrini, G; Borgognoni, L; Ferrazza, A M; Bonini, M; Palange, P

2016-01-01

Non-invasive ventilation (NIV) is an effective treatment in patients with acute exacerbation of COPD (AECOPD). However, it may induce post-hypercapnic metabolic alkalosis (MA). This study aims to evaluate the effect of acetazolamide (ACET) in AECOPD patients treated with NIV. Eleven AECOPD patients, with hypercapnic respiratory failure and MA following NIV, were treated with ACET 500 mg for two consecutive days and compared to a matched control group. Patients and controls were non invasively ventilated in a bilevel positive airway pressure (BiPAP) mode to a standard maximal pressure target of 15-20 cmH2O. ACET intra-group analysis showed a significant improvement for PaCO2 (63.9 ± 9.8 vs. 54.9 ± 8.3 mmHg), HCO3- (43.5 ± 5.9 vs. 36.1 ± 5.4 mmol/L) and both arterial pH (7.46 ± 0.06 vs. 7.41 ± 0.06) and urinary pH (6.94 ± 0.77 vs 5.80 ± 0.82), already at day 1. No significant changes in endpoints considered were observed in the control group at any time-point. Inter-group analysis showed significant differences between changes in PaCO2 and HCO3- (delta), both at day 1 and 2. Furthermore, the length of NIV treatment was significantly reduced in the ACET group compared to controls (6 ± 8 vs. 19 ± 19 days). No adverse events were recorded in the ACET and control groups. ACET appears to be effective and safe in AECOPD patients with post-NIV MA.

Respiratory alkalosis and associated electrolytes in long-term ventilator dependent persons with tetraplegia.

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Watt, J W; Silva, P

2001-11-01

A pilot case control study of the acid-base and electrolyte status in 30 long-term ventilator-dependent (LTVD) and 30 self ventilating persons with tetraplegia. To assess the extent of respiratory alkalosis and screen for associated hypokalaemia, hypomagnesaemia and/or hypophosphataemia. Medically stable persons with tetraplegia under the long-term care of the Southport Spinal Injuries Centre, England. Blood gases and electrolytes were sampled from 30 control patients with tetraplegia and from 30 patients having been LTVD for more than 12 months. All the blood gas measurements in the LTVD group lay outside both the reference range and the 95% confidence intervals (CI) of the control group: pH 7.46 (0.06); PCO(2) 3.46 (1.1) kPa; bicarbonate 18.3 (3.8) and base excess -3.2 (2.8) mmol/l; PO(2) 13.8 (2.8) kPa (means and standard deviations). The serum potassium, magnesium, phosphate, and sodium means lay within the reference ranges but the potassium, phosphate and calcium were at or below the 95% CI of the control values. One patient on part-time ventilatory support having less bicarbonate compensation had low serum electrolytes during ventilation. There was no evidence of biochemical jeopardy from long-term mechanical hyperventilation although acutely administered hyperventilation has the potential to cause falls in serum potassium, magnesium and phosphate and so caution should be exercised in part-time ventilated persons. The full range of electrolytes should be assayed during stabilisation in LTVD and periodically thereafter. Hyperventilation helps to maintain good oxygenation in LTVD persons with paralysis and normal lungs. None.

Association of Smoking, Sleep Apnea, and Plasma Alkalosis With Nocturnal Ventricular Arrhythmias in Men With Systolic Heart Failure

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Shukla, Rakesh; Wexler, Laura

2012-01-01

Background: Excess sudden death due to ventricular tachyarrhythmias remains a major mode of mortality in patients with systolic heart failure. The aim of this study was to determine the association of nocturnal ventricular arrhythmias in patients with low ejection fraction heart failure. We incorporated a large number of known pathophysiologic triggers to identify potential targets for therapy to reduce the persistently high incidence of sudden death in this population despite contemporary treatment. Methods: Eighty-six ambulatory male patients with stable low (≤ 45%) ejection fraction heart failure underwent full-night attendant polysomnography and simultaneous Holter recordings. Patients were divided into groups according to the presence or absence of couplets (paired premature ventricular excitations) and ventricular tachycardia (VT) (at least three consecutive premature ventricular excitations) during sleep. Results: In multiple regression analysis, four variables (current smoking status, increased number of arousals, plasma alkalinity, and old age) were associated with VT and two variables (apnea-hypopnea index and low right ventricular ejection fraction) were associated with couplets during sleep. Conclusions: We speculate that cessation of smoking, effective treatment of sleep apnea, and plasma alkalosis could collectively decrease the incidence of nocturnal ventricular tachyarrhythmias and the consequent risk of sudden death, which remains high despite the use of β blockades. PMID:22172636

Fires. A Joint Publication for U.S. Artillery Professionals. November - December 2009

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2009-11-01

called respiratory alkalosis . If the pH is low, the blood is more acidic. Respiratory alkalosis . Respiratory alkalosis helps offset hypo- baric... Respiratory alkalosis allows more oxygen to be carried to working tissue such as muscle to fuel work. However, respiratory alkalosis also makes unload...ing oxygen to working muscle more difficult. Eventually, the hypoxic drive (the need for oxygen) overrides respiratory alkalosis due to the

Post-prandial metabolic alkalosis in the seawater-acclimated trout: the alkaline tide comes in.

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Bucking, Carol; Fitzpatrick, John L; Nadella, Sunita R; Wood, Chris M

2009-07-01

The consequences of feeding and digestion on acid-base balance and regulation in a marine teleost (seawater-acclimated steelhead trout; Oncorhynchus mykiss) were investigated by tracking changes in blood pH and [HCO3-], as well as alterations in net acid or base excretion to the water following feeding. Additionally the role of the intestine in the regulation of acid-base balance during feeding was investigated with an in vitro gut sac technique. Feeding did not affect plasma glucose or urea concentrations, however, total plasma ammonia rose during feeding, peaking between 3 and 24 h following the ingestion of a meal, three-fold above resting control values (approximately 300 micromol ml(-1)). This increase in plasma ammonia was accompanied by an increase in net ammonia flux to the water (approximately twofold higher in fed fish versus unfed fish). The arterial blood also became alkaline with increases in pH and plasma [HCO3-] between 3 and 12 h following feeding, representing the first measurement of an alkaline tide in a marine teleost. There was no evidence of respiratory compensation for the measured metabolic alkalosis, as Pa CO2 remained unchanged throughout the post-feeding period. However, in contrast to an earlier study on freshwater-acclimated trout, fed fish did not exhibit a compensating increase in net base excretion, but rather took in additional base from the external seawater, amounting to approximately 8490 micromol kg(-1) over 48 h. In vitro experiments suggest that at least a portion of the alkaline tide was eliminated through increased HCO3- secretion coupled to Cl- absorption in the intestinal tract. This did not occur in the intestine of freshwater-acclimated trout. The marked effects of the external salinity (seawater versus freshwater) on different post-feeding patterns of acid-base balance are discussed.

Acute Metabolic Alkalosis Enhances Response of C3H Mouse Mammary Tumors to the Weak Base Mitoxantrone

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Natarajan Raghunand

2001-01-01

Full Text Available Uptake of weak acid and weak base chemotherapeutic drugs by tumors is greatly influenced by the tumor extracellular/interstitial pH (pHe, the intracellular pH (pHi maintained by the tumor cells, and by the ionization properties of the drug itself. The acid-outside plasmalemmal pH gradient in tumors acts to exclude weak base drugs like the anthracyclines, anthraquinones, and vinca alkaloids from the cells, leading to a substantial degree of “physiological drug resistance” in tumors. We have induced acute metabolic alkalosis in C3H tumor-bearing C3H/hen mice, by gavage and by intraperitoneal (i.p. administration of NaHCO3. 31P magnetic resonance spectroscopic measurements of 3-aminopropylphosphonate show increases of up to 0.6 pH units in tumor pHe, and 0.2 to 0.3 pH units in hind leg tissue pHe, within 2 hours of i.p. administration of NaHCO3. Theoretical calculations of mitoxantrone uptake into tumor and normal (hind leg tissue at the measured pH, and pHI values indicate that a gain in therapeutic index of up to 3.3-fold is possible with NaHCO3 pretreatment. Treatment of C3H tumor-bearing mice with 12 mg/kg mitoxantrone resulted in a tumor growth delay of 9 days, whereas combined NaHCO3mitoxantrone therapy resulted in an enhancement of the TGD to 16 days.

The venous-arterial difference in CO2 should be interpreted with caution in case of respiratory alkalosis in healthy volunteers.

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Morel, Jerome; Gergelé, Laurent; Dominé, Alexandre; Molliex, Serge; Perrot, Jean-Luc; Labeille, Bruno; Costes, Frederic

2017-08-01

The venous-arterial difference in CO 2 (ΔCO 2 ) has been proposed as an index of the adequacy of tissue perfusion in shock states. We hypothesized that the variation in PaCO 2 (hyper- or hypocapnia) could impact ΔCO 2 , partly through microcirculation adaptations. Fifteen healthy males volunteered to participate. For hypocapnia condition (hCO 2 ), the subjects were asked to hyperventilate, while they were asked to breathe a gas mixture containing 8 % CO 2 for hypercapnia condition (HCO 2 ). The 2 conditions were randomly assigned. Blood gases were measured at baseline before each condition, and after 5-7 min of either hCO 2 or HCO 2 condition. Microcirculation was assessed by the muscle reoxygenation slope measured with near infrared spectroscopy following a vascular occlusion test and by skin circulation with in vivo reflectance confocal microscopy. ΔCO 2 was significantly increased with hCO 2 while it tended to decrease with HCO 2 (non-significant). HCO 2 induced a moderate increase of the resaturation slope of NIRS oxygenation. Skin microcirculatory blood flow significantly dropped with hCO 2 , while it remained unchanged with hypercapnia. Our results warrant cautious interpretation of ΔCO 2 as an indicator of tissue perfusion during respiratory alkalosis.

Effects of respiratory acidosis and alkalosis on the distribution of cyanide into the rat brain.

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Djerad, A; Monier, C; Houzé, P; Borron, S W; Lefauconnier, J M; Baud, F J

2001-06-01

The aim of this study was to determine whether respiratory acidosis favors the cerebral distribution of cyanide, and conversely, if respiratory alkalosis limits its distribution. The pharmacokinetics of a nontoxic dose of cyanide were first studied in a group of 7 rats in order to determine the distribution phase. The pharmacokinetics were found to best fit a 3-compartment model with very rapid distribution (whole blood T(1/2)alpha = 21.6 +/- 3.3 s). Then the effects of the modulation of arterial pH on the distribution of a nontoxic dose of intravenously administered cyanide into the brains of rats were studied by means of the determination of the permeability-area product (PA). The modulation of arterial blood pH was performed by variation of arterial carbon dioxide tension (PaCO2) in 3 groups of 8 anesthetized mechanically ventilated rats. The mean arterial pH measured 20 min after the start of mechanical ventilation in the acidotic, physiologic, and alkalotic groups were 7.07 +/- 0.03, 7.41 +/- 0.01, and 7.58 +/- 0.01, respectively. The mean PAs in the acidotic, physiologic, and alkalotic groups, determined 30 s after the intravenous administration of cyanide, were 0.015 +/- 0.002, 0.011 +/- 0.001, and 0.008 +/- 0.001 s(-1), respectively (one-way ANOVA; p < 0.0087). At alkalotic pH the mean permeability-area product was 43% of that measured at acidotic pH. This effect of pH on the rapidity of cyanide distribution does not appear to be limited to specific areas of the brain. We conclude that modulation of arterial pH by altering PaCO2 may induce significant effects on the brain uptake of cyanide.

Effect of airway acidosis and alkalosis on airway vascular smooth muscle responsiveness to albuterol.

Science.gov (United States)

Cancado, Jose E; Mendes, Eliana S; Arana, Johana; Horvath, Gabor; Monzon, Maria E; Salathe, Matthias; Wanner, Adam

2015-04-02

In vitro and animal experiments have shown that the transport and signaling of β2-adrenergic agonists are pH-sensitive. Inhaled albuterol, a hydrophilic β2-adrenergic agonist, is widely used for the treatment of obstructive airway diseases. Acute exacerbations of obstructive airway diseases can be associated with changes in ventilation leading to either respiratory acidosis or alkalosis thereby affecting albuterol responsiveness in the airway. The purpose of this study was to determine if airway pH has an effect on albuterol-induced vasodilation in the airway. Ten healthy volunteers performed the following respiratory maneuvers: quiet breathing, hypocapnic hyperventilation, hypercapnic hyperventilation, and eucapnic hyperventilation (to dissociate the effect of pH from the effect of ventilation). During these breathing maneuvers, exhaled breath condensate (EBC) pH and airway blood flow response to inhaled albuterol (ΔQ̇aw) were assessed. Mean ± SE EBC pH (units) and ΔQ̇aw (μl.min(-1).mL(-1)) were 6.4 ± 0.1 and 16.8 ± 1.9 during quiet breathing, 6.3 ± 0.1 and 14.5 ± 2.4 during eucapnic hyperventilation, 6.6 ± 0.2 and -0.2 ± 1.8 during hypocapnic hyperventilation (p = 0.02 and <0.01 vs. quiet breathing), and 5.9 ± 0.1 and 2.0 ± 1.5 during hypercapnic hyperventilation (p = 0.02 and <0.02 vs quiet breathing). Albuterol responsiveness in the airway as assessed by ΔQ̇aw is pH sensitive. The breathing maneuver associated with decreased and increased EBC pH both resulted in a decreased responsiveness independent of the level of ventilation. These findings suggest an attenuated response to hydrophilic β2-adrenergic agonists during airway disease exacerbations associated with changes in pH. Registered at clinicaltrials.gov: NCT01216748 .

Shakuyaku-kanzo-to induces pseudoaldosteronism characterized by hypokalemia, rhabdomyolysis, metabolic alkalosis with respiratory compensation, and increased urinary cortisol levels.

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Kinoshita, Hiroyuki; Okabayashi, Misako; Kaneko, Masakazu; Yasuda, Mutsuko; Abe, Keisuke; Machida, Akira; Ohkubo, Takuya; Kamata, Tomoyuki; Yakushiji, Fumiatsu

2009-04-01

Licorice, the primary ingredient of the Japanese herbal medicine shakuyaku-kanzo-to, can cause pseudoaldosteronism. Thus, shakuyaku-kanzo-to can cause this condition. A 79-year-old woman was brought to the emergency room. She had been experiencing general fatigue, numbness in the hands, and weakness in the lower limbs and could not stand up without assistance. She presented with hypokalemia (potassium level, 1.7 mEq/L), increased urinary excretion of potassium (fractional excretion of K, 21.2%), abnormalities on an electrocardiogram (flat T waves in II, III, AVF, and V1-6), rhabdomyolysis (creatine kinase level, 28,376 U/L), myopathy, metabolic alkalosis with respiratory compensation (O(2) flow rate, 2 L/min; pH, 7.473; pco(2), 61.0 mm Hg; po(2), 78.0 mm Hg; HCO(3), 44.1 mmol/L), hypertension (174/93 mm Hg), hyperglycemia (blood glucose level, 200-300 mg/dL), frequent urination, suppressed plasma renin activity (0.1 ng/mL/hour), decreased aldosterone levels (2.6 ng/dL), and increased urinary cortisol levels (600.6 microg/day; reference range, 26.0-187.0 microg/day). In this case, the observed reduction in the urinary cortisol levels, from 600.6 to 37.8 microg/day, led to a definitive diagnosis of pseudoaldosteronism instead of the apparent mineralocorticoid excess syndrome. Discontinuing shakuyaku-kanzo-to treatment and administering spironolactone and potassium proved effective in improving the patient's condition. Medical practitioners prescribing shakuyaku-kanzo-to should take into account the association between licorice, which is its main ingredient, and pseudoaldosteronism.

Sodium acetate induces a metabolic alkalosis but not the increase in fatty acid oxidation observed following bicarbonate ingestion in humans.

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Smith, Gordon I; Jeukendrup, Asker E; Ball, Derek

2007-07-01

We conducted this study to quantify the oxidation of exogenous acetate and to determine the effect of increased acetate availability upon fat and carbohydrate utilization in humans at rest. Eight healthy volunteers (6 males and 2 females) completed 2 separate trials, 7 d apart in a single-blind, randomized, crossover design. On each occasion, respiratory gas and arterialized venous blood samples were taken before and during 180 min following consumption of a drink containing either sodium acetate (NaAc) or NaHCO3 at a dose of 2 mmol/kg body mass. Labeled [1,2 -13C] NaAc was added to the NaAc drink to quantify acetate oxidation. Both sodium salts induced a mild metabolic alkalosis and increased energy expenditure (P < 0.05) to a similar magnitude. NaHCO3 ingestion increased fat utilization from 587 +/- 83 kJ/180 min to 693 +/- 101 kJ/180 min (P = 0.01) with no change in carbohydrate utilization. Following ingestion of NaAc, the amount of fat and carbohydrate utilized did not differ from the preingestion values. However, oxidation of the exogenous acetate almost entirely (90%) replaced the additional fat that had been oxidized during the bicarbonate trial. We determined that 80.1 +/- 2.3% of an exogenous source of acetate is oxidized in humans at rest. Whereas NaHCO3 ingestion increased fat oxidation, a similar response did not occur following NaAc ingestion despite the fact both sodium salts induced a similar increase in energy expenditure and shift in acid-base balance.

Interaction of Stress and Anxiogenic Drugs on Behaviors of Rats and Antagonism with Indomethacin

Science.gov (United States)

2001-10-19

also produces panic attacks. Hyperventilation produces respi ratory alkalosis and hypocapnea 22 (reduced CO2 tension in arterial blood) . and...minute stressor hyperventilated, a result would be hypocapnia and alkalosis (Guyton & Hall, 1996). Alkalosis is known to increase the binding of...neuroanatomical hypothesis for panic disorder. American Journal of Psychology, 146, 148-161 . Gorman, J.M., & Papp, LA (1990). Respiratory

Microaggregates: Experimental and Clinical Aspects - Symposium on Microaggregates, Held at Letterman Army Institute of Research on 20-21 June 1977,

Science.gov (United States)

1980-06-01

clearing of lactic acidosis within 24 hr. By permission, Journal of Trauma, 1975. Respiratory alkalosis occurs secondary to hyperventillation...citrate moiety of liquid-preserved blood produces a metabolic alkalosis . The combination of respiratory and metabolic alkalosis , hypothermia, and...fThe Role of Microaggregates in the Respiratory 233 Distress Syndrome. Frank R. Lewis, M.D. Summary 247 Distribution List j 251 SESSION I June 20, 1977

Acute Infectious Disease,

Science.gov (United States)

1984-03-23

accelerated respiration. This tachypnia causes an exaggerated loss of carbon dioxide.3 The respiratory alkalosis that ensues is typically seen during all...with respiratory alkalosis . During periods of heat-induced tachypnia, U’. inorganic phosphates may virtually disappear for a time from urine and sweat...urine and sweat during the period when respiratory alkalosis and hyperventilation are taking place. On the other hand, losses of phosphate may be

Profile of acid-base disturbances in an intensive care unit of Fortaleza, Ceará, Brazil.

Directory of Open Access Journals (Sweden)

Renan Barbosa Rodrigues

2014-09-01

Full Text Available Introduction: Acid – base disturbances are entities caused by the deregulation of the concentration of bicarbonate ions, the concentration of hydrogen ions and the partial pressure of carbon dioxide in the blood. These disturbances modify most cell fuctions when present, jeopardizing the proper functioning of organs.Methods: Cross-sectional analytical study based upon data collected from medical files of patients in ICU as seen from August 1 to December 31, 2013 at the Dr. José Frota Institute in Fortaleza, Ceará. The variables studied were: age, sex, cause of ICU admission, pH, HCO3-, pO2, pCO2 , glomerular filtration rate ( GFR , serum potassium concentrarion, serum magnesium concentration, serum creatinine and hemoglobin levels.Results: The most frequent disorders were primary respiratory alkalosis with               33 ( 38,4 % cases, 30 ( 34,9 % of metabolic alkalosis, 13 ( 15.1% of metabolic acidosis,    7 ( 8,2% did not present acid-base disorders and respiratory acidosis           3 ( 3,5%. Patients admitted with TBI had respiratory alkalosis as the most common primary disorder, followed by metabolic alkalosis, 16 ( 47,0 % and 13 ( 38,2 % , respectively. The main disturbances were mixed respiratory alkalosis with metabolic alkalosis and respiratory alkalosis with metabolic alkalosis found in 15.12% of patients in each of these combinations. Conclusion:The importance  of a detailed evaluation of acid-base disturbances is necessary since these disorders lead to higher mortality rates, so it is necessary to establish the main types of disorders that are associated with a particular cause of hospitalization .

Blood Gases Test

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... pulmonary disease (COPD) , and over-sedation from narcotics. Respiratory alkalosis, characterized by a raised pH and a decreased ... myasthenia gravis Greater than 7.45 Low Low Respiratory alkalosis Hyperventilation, pain, anxiety, brain trauma, pneumonia, certain drugs ( ...

Chloride Test

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... metabolic acidosis ) or when a person hyperventilates (causing respiratory alkalosis ). A decreased level of blood chloride (called hypochloremia) ... disease , emphysema or other chronic lung diseases (causing respiratory ... metabolic alkalosis). An increased level of urine chloride can indicate ...

Bicarbonate Concentration, Acid-Base Status, and Mortality in the Health, Aging, and Body Composition Study.

Science.gov (United States)

Raphael, Kalani L; Murphy, Rachel A; Shlipak, Michael G; Satterfield, Suzanne; Huston, Hunter K; Sebastian, Anthony; Sellmeyer, Deborah E; Patel, Kushang V; Newman, Anne B; Sarnak, Mark J; Ix, Joachim H; Fried, Linda F

2016-02-05

Low serum bicarbonate associates with mortality in CKD. This study investigated the associations of bicarbonate and acid-base status with mortality in healthy older individuals. We analyzed data from the Health, Aging, and Body Composition Study, a prospective study of well functioning black and white adults ages 70-79 years old from 1997. Participants with arterialized venous blood gas measurements (n=2287) were grouped into respiratory alkalosis, and 1.35 (95% CI, 1.08 to 1.69) for metabolic alkalosis categories. Respiratory acidosis did not associate with mortality. In generally healthy older individuals, low serum bicarbonate associated with higher mortality independent of systemic pH and potential confounders. This association seemed to be present regardless of whether the cause of low bicarbonate was metabolic acidosis or respiratory alkalosis. Metabolic alkalosis also associated with higher mortality. Copyright © 2016 by the American Society of Nephrology.

Acid-base disturbances in nephrotic syndrome: analysis using the CO2/HCO3 method (traditional Boston model) and the physicochemical method (Stewart model).

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Kasagi, Tomomichi; Imai, Hirokazu; Miura, Naoto; Suzuki, Keisuke; Yoshino, Masabumi; Nobata, Hironobu; Nagai, Takuhito; Banno, Shogo

2017-10-01

The Stewart model for analyzing acid-base disturbances emphasizes serum albumin levels, which are ignored in the traditional Boston model. We compared data derived using the Stewart model to those using the Boston model in patients with nephrotic syndrome. Twenty-nine patients with nephrotic syndrome and six patients without urinary protein or acid-base disturbances provided blood and urine samples for analysis that included routine biochemical and arterial blood gas tests, plasma renin activity, and aldosterone. The total concentration of non-volatile weak acids (A TOT ), apparent strong ion difference (SIDa), effective strong ion difference (SIDe), and strong ion gap (SIG) were calculated according to the formulas of Agrafiotis in the Stewart model. According to the Boston model, 25 of 29 patients (90%) had alkalemia. Eighteen patients had respiratory alkalosis, 11 had metabolic alkalosis, and 4 had both conditions. Only three patients had hyperreninemic hyperaldosteronism. The Stewart model demonstrated respiratory alkalosis based on decreased PaCO 2 , metabolic alkalosis based on decreased A TOT , and metabolic acidosis based on decreased SIDa. We could diagnose metabolic alkalosis or acidosis with a normal anion gap after comparing delta A TOT [(14.09 - measured A TOT ) or (11.77 - 2.64 × Alb (g/dL))] and delta SIDa [(42.7 - measured SIDa) or (42.7 - (Na + K - Cl)]). We could also identify metabolic acidosis with an increased anion gap using SIG > 7.0 (SIG = 0.9463 × corrected anion gap-8.1956). Patients with nephrotic syndrome had primary respiratory alkalosis, decreased A TOT due to hypoalbuminemia (power to metabolic alkalosis), and decreased levels of SIDa (power to metabolic acidosis). We could detect metabolic acidosis with an increased anion gap by calculating SIG. The Stewart model in combination with the Boston model facilitates the analysis of complex acid-base disturbances in nephrotic syndrome.

Een geval van hypochloremische alkalose bij een pasgeborene

NARCIS (Netherlands)

van de Bor, M.; Ruys, J. H.; Kenter, G.; Zoethout, H. E.

1984-01-01

A full term neonate in which by accident a metabolic alkalosis was found, is described. The origin of the metabolic alkalosis was excessive vomiting by the mother during the days prior to delivery. The simplified form of the Henderson Hasselbalch equation is used to describe the factors responsible

Teaching acid/base physiology in the laboratory

DEFF Research Database (Denmark)

Friis, Ulla G; Plovsing, Ronni; Hansen, Klaus

2010-01-01

exercise in acid/base physiology that would provide students with unambiguous and reproducible data that clearly would illustrate the theory in practice. The laboratory exercise was developed to include both metabolic acidosis and respiratory alkalosis. Data were collected from 56 groups of medical...... students that had participated in this laboratory exercise. The acquired data showed very consistent and solid findings after the development of both metabolic acidosis and respiratory alkalosis. All results were consistent with the appropriate diagnosis of the acid/base disorder. Not one single group...... failed to obtain data that were compatible with the diagnosis; it was only the degree of acidosis/alkalosis and compensation that varied....

[Pseudo-Bartter syndrome--2 cases].

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Jóźwiak, Lucyna; Jaroszyński, Andrzej; Baranowicz-Gaszczyk, Iwona; Borowicz, Ewa; Ksiazek, Andrzej

2010-01-01

Bartter syndrome represents the group of renal disturbances characterized by hypokaliemia and metabolic alkalosis. Some diseases could display hypokalemic metabolic alkalosis without primary tubular dysfunction. These disorders are called pseudo-Bartter syndrome. In this paper we present 2 cases of pseudo-Bartter syndrome related among to other things to overuse of diuretic drugs.

Incidence of hypochloremic metabolic alkalosis in dogs and cats with and without nasogastric tubes over a period of up to 36 hours in the intensive care unit.

Science.gov (United States)

Chih, Annie; Rudloff, Elke; Waldner, Cheryl; Linklater, Andrew K J

2018-05-01

To evaluate the incidence of hypochloremic metabolic alkalosis (HCMA) in dogs and cats in the ICU that had intermittent nasogastric tube (NGT) aspiration for up to 36 hours. Prospective cohort study (December 2013 to October 2014). Privately owned emergency and referral teaching hospital. Forty-nine client-owned dogs and 16 client-owned cats. Patients wherein NGT placement was recommended and client consent was obtained were included in the interventional group. Those with an NGT placed (NGT group) had the NGT aspirated every 4 hours. Patients for whom placement of a NGT was declined by the owner served as a reference group (NoNGT). Venous blood gas and electrolyte values were obtained every 12 hours. Thirty-five dogs and cats had an NGT placed. Thirty dogs and cats did not have an NGT placed. The serum venous blood gas and electrolyte changes were compared over time within the NGT group and between the NGT and NoNGT groups. No cases developed HCMA. In the NGT group, blood pH increased over time. There was no significant difference between the NGT and the NoNGT group in the average value of pH, HCO 3 - , base excess, chloride, or corrected chloride. Serum venous blood gas, chloride, and corrected chloride changes were not associated with the volumes of gastric fluid aspirated over time. In this small population of dogs and cats, intermittent NGT aspiration was not associated with the development of HCMA over a period of up to 36 hours after NGT placement. © Veterinary Emergency and Critical Care Society 2018.

A patient with cystinosis presenting like bartter syndrome and review of literature.

Science.gov (United States)

Ertan, Pelin; Evrengul, Havva; Ozen, Serkan; Emre, Sinan

2012-12-01

Nephropathic cystinosis is an autosomal recessively inherited metabolic disorder presenting with metabolic acidosis, Fanconi syndrome and renal failure. We present a 6-year-old girl with severe growth failure, hyponatremia and hypokalemia. Her parents were 4(th) degree relatives. Two relatives were diagnosed as end stage renal failure. She also had persistant hypokalemic hypochloremic metabolic alkalosis. Her renal function was normal at presentation. She was thought to have Bartter syndrome with supporting findings of elevated levels of renin and aldosterone with normal blood pressure, and hyperplasia of juxtaglomerular apparatus. Her metabolic alkalosis did not resolve despite supportive treatment. At 6(th) month of follow-up proteinuria, glucosuria and deterioration of renal function developed. Diagnosis of cystinosis was made with slit lamp examination and leukocyte cystine levels. At 12(th) month of follow-up her metabolic alkalosis has converted to metabolic acidosis. In children presenting with persistant metabolic alkalosis, with family history of renal failure, and parental consanguinity, cystinosis should always be kept in mind as this disease is an important cause of end stage renal failure which may have features mimmicking Bartter syndrome.

[Pseudo-Bartter syndrome as manifestation of cystic fibrosis with DF508 mutation].

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Galaviz-Ballesteros, María de Jesús; Acosta-Rodríguez-Bueno, Carlos Patricio; Consuelo-Sánchez, Alejandra; Franco-Álvarez, Isidro; Olalla-Mora, Odilo Iván; Vázquez-Frias, Rodrigo

Pseudo Bartter syndrome (PBS) is defined as hypokalaemic hypochloraemic metabolic alkalosis in the absence of renal tubular pathology. Children with cystic fibrosis (CF) are at risk of developing electrolyte abnormalities and even PBS may occur. 5 months old female infant with a history of two events of dehydration with vomit, refusal to eat, chronic cough, polyuria, malnutrition, metabolic alkalosis, hypokalemia, hyponatremia, hypochloremia and acute renal failure. Chronic cough study was performed, discarding pulmonary tuberculosis, gastroesophageal reflux disease and impaired swallowing. PBS was diagnosed due to hypokalaemic hypochloraemic metabolic alkalosis in the absence of renal tubular pathology. CF was corroborated by electrolytes in sweat and through molecular analysis of the delta F508 mutation. This is one of the few reported cases linking PBS and this mutation. In patients with hyponatremic dehydration episodes with hypokalaemic hypochloraemic metabolic alkalosis, PBS should be considered as differential diagnosis. CF could be presented as PBS, mainly in patients younger than 2 years. Copyright © 2016 Hospital Infantil de México Federico Gómez. Publicado por Masson Doyma México S.A. All rights reserved.

[A man with a classic serious milk-alkali syndrome and a carcinoma of the stomach].

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Verburg, F A J; van Zanten, R A A; Brouwer, R M L; Woittiez, A J J; Veneman, Th F

2006-07-22

A 42-year-old man was transferred to the Emergency Department after his friends had found him unresponsive and confused in his room. He had been experiencing upper abdominal complaints for a period of several months. He had taken large amounts of a calcium carbonate/magnesium subcarbonate preparation (Rennie) and had consumed at least 3 litres of dairy products per day. His behaviour was reported as being more and more abnormal during the previous few weeks. On admission he was confused and agitated and had involuntary movements of his limbs. Laboratory investigation indicated a triple acid base disorder, i.e. metabolic alkalosis, respiratory alkalosis and high anion gap metabolic acidosis, with severe dehydration. The metabolic alkalosis was caused by the intake of large amounts of dairy and antacids: milk-alkali syndrome. The metabolic acidosis was the result of hypovolaemia and pre-renal renal failure and the respiratory alkalosis was caused by hyperventilation due to the organic psychosyndrome. The patient was treated with volume expansion by isotonic saline and the administration of potassium and he was sedated with low-dose midazolam, which led to a full respiratory compensation of the metabolic alkalosis. A few days following admission, both the plasma calcium concentration and renal function returned to normal; the acid-base disorder completely normalized and the organic psychosyndrome disappeared. On gastroduodenoscopy a gastric ulcer was found; biopsies revealed a signet ring cell adenocarcinoma of the stomach.

The influence of respiratory acid-base changes on muscle performance and excitability of the sarcolemma during strenuous intermittent hand grip exercise.

Science.gov (United States)

Hilbert, M; Shushakov, V; Maassen, N

2012-02-01

Acidification has been reported to provide protective effects on force production in vitro. Thus, in this study, we tested if respiratory acid-base changes influence muscle function and excitability in vivo. Nine subjects performed strenuous, intermittent hand grip exercises (10 cycles of 15 s of work/45 s of rest) under respiratory acidosis by CO(2) rebreathing, alkalosis by hyperventilation, or control. The Pco(2), pH, K(+) concentration ([K(+)]), and Na(+) concentration were measured in venous and arterialized blood. Compound action potentials (M-wave) were elicited to examine the excitability of the sarcolemma. The surface electromyogram (EMG) was recorded to estimate the central drive to the muscle. The lowest venous pH during the exercise period was 7.24 ± 0.03 in controls, 7.31 ± 0.05 with alkalosis, and 7.17 ± 0.04 with acidosis (P alkalosis, and, after the second cycle, it was smaller with acidosis than with the control condition (P Respiratory alkalosis stabilized the M-wave area without influencing performance. Thus, we did not find a direct link between performance and alteration of excitability of the sarcolemma due to changes in pH in vivo.

Warfighter Physiological and Environmental Monitoring: A Study for the U.S. Army Research Institute in Environmental Medicine and the Soldier Systems Center

Science.gov (United States)

2004-11-01

should scale accordingly. Any deviation from this ratio would result in either respiratory alkalosis (minute rate too high) or acidosis (minute rate too...low). In combat situations, hyperventilation may occur, and thus some degree of respiratory alkalosis is expected. If the minute rate were to fall...Derived information including a. Blood volume b. Blunt trauma events and localization c. Burn trauma events and localization d. Respiratory distress

Journal of Special Operation Medicine: A Peer Reviewed Journal for SOF Medical Professionals. Training Supplement, Winter 10

Science.gov (United States)

2010-01-01

respiratory alkalosis o Hypocalcemia o Hypokalemia o Hypernatremia Pregnancy Category C Side-effects/precautions: o Metabolic alkalosis may occur...altitude, HAPE is the most common cause of death from altitude illness. 2. Usually occurs above 8,000ft. Respiratory distress at high altitude is HAPE...they may depress respiratory drive and worsen high altitude illness. 6. Treat per Nausea and Vomiting Protocol 7. For signs or symptoms of either

Annual Progress Report, Fiscal Year 1982.

Science.gov (United States)

1982-10-01

incompletely compensated respiratory alkalosis . This condition is accompanied ’ an increase in the excretion of urinary bicarbonate and an elevation of urinary...interfering with the respiratory alkalosis which develops at altitude or by altering the chemical environment of the working muscles. In one study...Orthopedic (32.9%); Respiratory Infection (17.19%); Dermatological (9.4%); Ear, Eye, Nose and Throat (9.4%); Gastrointestinal (7.5); and Adverse Weather Injry

Acetazolamide: a second wind for a respiratory stimulant in the intensive care unit?

Science.gov (United States)

Heming, Nicholas; Urien, Saïk; Faisy, Christophe

2012-08-07

Patients with chronic obstructive pulmonary disease (COPD) are affected by episodes of respiratory exacerbations, some of which can be severe and may necessitate respiratory support. Prolonged invasive mechanical ventilation is associated with increased mortality rates. Persistent failure to discontinue invasive mechanical ventilation is a major issue in patients with COPD. Pure or mixed metabolic alkalosis is a common finding in the intensive care unit (ICU) and is associated with a worse outcome. In patients with COPD, the condition is called post-hypercapnic alkalosis and is a complication of mechanical ventilation. Reversal of metabolic alkalosis may facilitate weaning from mechanical ventilation of patients with COPD. Acetazolamide, a non-specific carbonic anhydrase inhibitor, is one of the drugs employed in the ICU to reverse metabolic alkalosis. The drug is relatively safe, undesirable effects being rare. The compartmentalization of the different isoforms of the carbonic anhydrase enzyme may, in part, explain the lack of evidence of the efficacy of acetazolamide as a respiratory stimulant. Recent findings suggest that the usually employed doses of acetazolamide in the ICU may be insufficient to significantly improve respiratory parameters in mechanically ventilated patients with COPD. Randomized controlled trials using adequate doses of acetazolamide are required to address this issue.

Journal of Special Operations Medicine. Volume 9, Edition 4, Fall 2009

Science.gov (United States)

2009-01-01

place in the evaluation, without full blood gas analysis, the body’s compensation mechanisms such as a respiratory alkalosis may maintain a normal or...sam- pling and relatively simple handheld diagnostic tools. Arterial pH has long been used to assess pa- tients for presence of respiratory /metabolic...acido- sis/ alkalosis . There is only a narrow physiologic range of intracellular pH which allows for normal function, typically 7.35-7.45. Acidosis

Homespun remedy, homespun toxicity: baking soda ingestion for dyspepsia.

Science.gov (United States)

Ajbani, Keyur; Chansky, Michael E; Baumann, Brigitte M

2011-04-01

A 68-year-old man presented to the Emergency Department with a severe metabolic alkalosis after ingesting large quantities of baking soda to treat his dyspepsia. His underlying pulmonary disease and a progressively worsening mental status necessitated intubation for respiratory failure. Laboratory studies revealed a hyponatremic, hypochloremic, hypokalemic metabolic alkalosis. The patient was successfully treated after cessation of the oral bicarbonate, initiation of intravenous hydration, and correction of electrolyte abnormalities. Copyright © 2011 Elsevier Inc. All rights reserved.

Bartter Syndrome with Normal Aldosterone Level: An Unusual Presentation.

Science.gov (United States)

Huque, S S; Rahman, M H; Khatun, S

2016-04-01

Bartter syndrome (BS) is a hereditary disease, with an autosomal recessive or autosomal dominant mode of transmission. It is characterized by salt wasting hypochloraemic, hypokalaemic metabolic alkalosis and hyperreninaemia with normal blood pressure. The primary defect is in the thick ascending limb of loop of Henle (TAL). Herein, we report a case that had typical features of BS like severe dehydration, severe hypokalaemia, metabolic alkalosis and failure to thrive but had normal aldosterone level which is very uncommon.

Soluble adenylyl cyclase is an acid-base sensor in epithelial base-secreting cells.

Science.gov (United States)

Roa, Jinae N; Tresguerres, Martin

2016-08-01

Blood acid-base regulation by specialized epithelia, such as gills and kidney, requires the ability to sense blood acid-base status. Here, we developed primary cultures of ray (Urolophus halleri) gill cells to study mechanisms for acid-base sensing without the interference of whole animal hormonal regulation. Ray gills have abundant base-secreting cells, identified by their noticeable expression of vacuolar-type H(+)-ATPase (VHA), and also express the evolutionarily conserved acid-base sensor soluble adenylyl cyclase (sAC). Exposure of cultured cells to extracellular alkalosis (pH 8.0, 40 mM HCO3 (-)) triggered VHA translocation to the cell membrane, similar to previous reports in live animals experiencing blood alkalosis. VHA translocation was dependent on sAC, as it was blocked by the sAC-specific inhibitor KH7. Ray gill base-secreting cells also express transmembrane adenylyl cyclases (tmACs); however, tmAC inhibition by 2',5'-dideoxyadenosine did not prevent alkalosis-dependent VHA translocation, and tmAC activation by forskolin reduced the abundance of VHA at the cell membrane. This study demonstrates that sAC is a necessary and sufficient sensor of extracellular alkalosis in ray gill base-secreting cells. In addition, this study indicates that different sources of cAMP differentially modulate cell biology. Copyright © 2016 the American Physiological Society.

Maternal Pseudo-Bartter Syndrome Associated with Severe Perinatal Brain Injury.

Science.gov (United States)

Vora, Shrenik; Ibrahim, Thowfique; Rajadurai, Victor Samuel

2017-09-15

Maternal electrolyte imbalance is rarely reported as causative factor of severe perinatal brain injury. This case outlines a unique maternal and neonatal pseudo-Bartter syndrome presented with metabolic alkalosis and hypochloremia due to maternal severe vomiting. Neonatal MRI brain revealed extensive brain hemorrhages with porencephalic cysts. Subsequent investigation workup points towards maternal severe metabolic alkalosis as its cause. Careful medical attention should be paid to pregnant women with excessive vomiting to ensure a healthy outcome for both the mother and the baby.

Effects of early administration of acetazolamide on the duration of mechanical ventilation in patients with chronic obstructive pulmonary disease or obesity-hypoventilation syndrome with metabolic alkalosis. A randomized trial.

Science.gov (United States)

Rialp Cervera, G; Raurich Puigdevall, J M; Morán Chorro, I; Martín Delgado, M C; Heras la Calle, G; Mas Serra, A; Vallverdú Perapoch, I

2017-06-01

Metabolic alkalosis (MA) inhibits respiratory drive and may delay weaning from mechanical ventilation (MV). MA is common in CO 2 -retainer patients that need MV. Acetazolamide (ACTZ) decreases serum bicarbonate concentration and stimulates respiratory drive. This study evaluated the effects of ACTZ on the duration of MV in patients with MA and COPD or obesity hypoventilation syndrome (OHS) intubated with acute respiratory failure. Multicenter, randomized, controlled, double-blind study, with COPD or OHS patients with MV 28 mmol/L and pH > 7.35. Test-treatment, ACTZ 500 mg or placebo, was daily administered if pH > 7.35 and bicarbonate >26 mmol/L. Clinical, respiratory and laboratory parameters were recorded. 47 patients (36 men) were randomized. There were no significant differences between groups in comorbidities, baseline characteristics or arterial blood gases at inclusion. The mean difference in the duration of MV between placebo and ACTZ group was 1.3 days (95%CI, -2.1-4.8; p = 0.44). Kaplan-Meier curves showed no differences in the duration of MV (Log-Rank p = 0.41). Between-group comparison of estimated marginal means (CI 95%) during MV were, respectively: PaCO 2 55 (51-59) vs 48 (47-50) mm Hg, p = 0.002; bicarbonate concentration 34 (32-35) vs 29 (28-30) mmol/L, p < 0.0001; and minute volume 9.7 (8.9-10.4) vs 10.6 (9.2-12.0) L/min, p = 0.26. There were no severe adverse effects with ACTZ administration. Among patients with MA and COPD or OHS, early treatment with ACTZ did not shorten significantly the duration of MV compared with placebo. clinical.trials.gov; NCT01499485; URL:.www.clinicaltrials.gov. Copyright © 2017 Elsevier Ltd. All rights reserved.

Enhancement on Wingate Anaerobic Test Performance With Hyperventilation.

Science.gov (United States)

Leithäuser, Renate M; Böning, Dieter; Hütler, Matthias; Beneke, Ralph

2016-07-01

Relatively long-lasting metabolic alkalizing procedures such as bicarbonate ingestion have potential for improving performance in long-sprint to middle-distance events. Within a few minutes, hyperventilation can induce respiratory alkalosis. However, corresponding performance effects are missing or equivocal at best. To test a potential performance-enhancing effect of respiratory alkalosis in a 30-s Wingate Anaerobic Test (WAnT). 10 men (mean ± SD age 26.6 ± 4.9 y, height 184.4 ± 6.1 cm, body-mass test 1 80.7 ± 7.7 kg, body-mass test 2 80.4 ± 7.2 kg, peak oxygen uptake 3.95 ± 0.43 L/min) performed 2 WAnTs, 1 with and 1 without a standardized 15-min hyperventilation program pre-WAnT in randomized order separated by 1 wk. Compared with the control condition, hyperventilation reduced (all P respiratory alkalosis can enhance WAnT cycling sprint performance well in the magnitude of what is seen after successful bicarbonate ingestion.

Hypothermia and hypokalemia in a patient with diabetic ketoacidosis

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Osamu Saito

2015-01-01

Full Text Available We present the case of a 36-year-old man with type-1 diabetes who was hospitalized with diabetic ketoacidosis (DKA. On admission, he had hypothermia, hypokalemia and combined metabolic and respiratory alkalosis, in addition to hyperglycemia. Hypothermia, hypokalemia and metabolic alkalosis, with a concurrent respiratory alkalosis, are not commonly seen in DKA. After admission, intravenous infusion of 0.45% saline was administered, which resulted in the development of pure metabolic acidosis. After starting insulin infusion, hypokalemia and hypophosphatemia became evident and finally resulted in massive rhabdomyolysis. Hyperkalemia accompanying oliguric acute kidney injury (AKI warranted initiation of hemodialysis (HD on Day-five. On the 45th hospital day, his urine output started to increase and a total of 22 HD sessions were required. We believe that in this case severe dehydration, hypothermia and hypokalemia might have contributed to the initial symptoms of DKA as well as the prolongation of AKI.

Milk alkali syndrome induced by calcitriol and calcium bicarbonate in a patient with hypoparathyroidism

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Eda Altun

2013-01-01

Full Text Available The milk-alkali syndrome (MAS was a common cause of hypercalcemia, metabolic alkalosis, and renal failure in the early 20 th century. This syndrome was first recognized secondary to treatment of peptic ulcer disease with milk and absorbable alkali. Its incidence fell after the introduction of H2-blocker and proton pump inhibitor. Persistent ingestion of calcium carbonate and vitamin D caused MAS. We report a patient presenting with a triad of hypercalcemia, metabolic alkalosis and renal failure secondary to treatment of idiopathic hypoparathyroidism.

Acid-base status after whole-body irradiation in dairy cows

International Nuclear Information System (INIS)

Schaefer, M.; Koch, F.; Dyrba, W.; Kirbach, M.

1989-01-01

Whole-body irradiation using 9 MeV X-rays of a linear accelerator of 10 clinically healthy lactating cows aged between 3.5 and 8 years produced an acute radiation syndrome in the LD 100/30 range. Blood analysis 1 day after irradiation showed a compensated metabolic acidosis with a low renal net acid-base excretion and hyerphosphaturia. Later the acid-base status indicated a differently marked metabolic alkalosis. In the main reaction period acidotic disturbances occurred, which partially were camouflaged by respiratory alkalosis. (author)

Furosemide Induced Electrolyte Imbalance: A Real Danger of Overdiuresis in Patients with Heart Failure

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Yaseen Ali

2014-12-01

Full Text Available Background: Chronic heart failure is one of the most common reasons for hospital admissions in the United States. There have been several approaches for treating heart failure but loop diuretics has been at the forefront to alleviate the symptoms. Loop diuretics have their own side effects as with any medication use, and a lesser known and monitored one is metabolic alkalosis. Case report: The patient was a 76 years old female with past medical history of diabetes, hypertension, chronic kidney disease, dyslipidemia and chronic heart failure who came to the hospital with progressive shortness of breath for the past few days and was started on aggressive diuresis with intravenous loop diuretics and well responded. On the morning of d 6 of her admission, she was kept on the floor and started on BIPAP to correct hypercarbia and respiratory acidosis due to metabolic alkalosis and back to baseline with normal mentation by the middle of the day. Conclusion: Hypokalemia due to the diuretic effect can cause alkalosis by resulting in the shift of hydrogen ions intracellularly, stimulating the apical H+/K+ ATPase in the collecting duct, stimulating renal ammonia genesis, reabsorption, and secretion, leading to impaired chloride ion reabsorption in the distal nephron and reducing the glomerular filtration rate (GFR. The patient improved after being started on oxygen therapy and switched to acetazolamide as an alternative diuretic, indicating that acetazolamide corrected the effect of metabolic alkalosis by causing metabolic acidosis due to decrease reclamation of bicarbonate at the level of proximal convoluted tubule.

Gitelman′s syndrome with panhypopituitarism: Reno-endocrine interplay

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Vimal Upreti

2012-01-01

Full Text Available Gitelman′s syndrome is an inherited tubulopathy affecting thiazide-sensitive sodium chloride cotransporter, which manifests with hypokalemic alkalosis, hypomagnesemia, and hypocalciuria. Recently few cases have been described having an association of Gitelman′s syndrome with pituitary abnormalities on imaging, though with normal hormonal status. We describe the first case of an adult patient having Gitelman′s syndrome and hypopituitarism with abnormal pituitary imaging. She presented to us with hypotension, hypokalemia, hypomagnesemia with alkalosis, hypothyroidism, hypocortisolism, and hypogonadism. She was treated with replacement of electrolytes and hormones, to which she showed an excellent response.

Is the alkaline tide a signal to activate metabolic or ionoregulatory enzymes in the dogfish shark (Squalus acanthias)?

Science.gov (United States)

Wood, Chris M; Kajimura, Makiko; Mommsen, Thomas P; Walsh, Patrick J

2008-01-01

Experimental metabolic alkalosis is known to stimulate whole-animal urea production and active ion secretion by the rectal gland in the dogfish shark. Furthermore, recent evidence indicates that a marked alkaline tide (systemic metabolic alkalosis) follows feeding in this species and that the activities of the enzymes of the ornithine-urea cycle (OUC) for urea synthesis in skeletal muscle and liver and of energy metabolism and ion transport in the rectal gland are increased at this time. We therefore evaluated whether alkalosis and/or NaCl/volume loading (which also occurs with feeding) could serve as a signal for activation of these enzymes independent of nutrient loading. Fasted dogfish were infused for 20 h with either 500 mmol L(-1) NaHCO3 (alkalosis + volume expansion) or 500 mmol L(-1) NaCl (volume expansion alone), both isosmotic to dogfish plasma, at a rate of 3 mL kg(-1) h(-1). NaHCO3 infusion progressively raised arterial pH to 8.28 (control = 7.85) and plasma [HCO3-] to 20.8 mmol L(-1) (control = 4.5 mmol L(-1)) at 20 h, with unchanged arterial P(CO2), whereas NaCl/volume loading had no effect on blood acid-base status. Rectal gland Na+,K+-ATPase activity was increased 50% by NaCl loading and more than 100% by NaHCO3 loading, indicating stimulatory effects of both volume expansion and alkalosis. Rectal gland lactate dehydrogenase activity was elevated 25% by both treatments, indicating volume expansion effects only, whereas neither treatment increased the activities of the aerobic enzymes citrate synthase, NADP-isocitrate dehydrogenase, or the ketone body-utilizing enzyme beta-hydroxybutyrate dehydrogenase in the rectal gland or liver. The activity of ornithine-citrulline transcarbamoylase in skeletal muscle was doubled by NaHCO3 infusion, but neither treatment altered the activities of other OUC-related enzymes (glutamine synthetase, carbamoylphosphate synthetase III). We conclude that both the alkaline tide and salt loading/volume expansion act as

Pathophysiological aspect of metabolic acid-base disorders

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Nešović-Ostojić Jelena

2016-01-01

Full Text Available Maintaing the arterial pH values (in normal range of 7,35-7,45 is one of the main principles of homeostasis. Regulatory responses, including chemical buffering (extracellular, intracellular, sceletal, the regulation of pCO2 by the respiratory system, and the regulation of [HCO3-] by the kidneys, act in concert to maintain normal arterial pH value. The main extracellular chemical buffer is bicarbonate-carbonic acid buffer system. The kidneys contribute to the regulation of hydrogen (and bicarbonate in body fluids in two ways. Proximal tubules are important in bicarbonate reabsorption and distal tubules excrete hydrogen ion (as ammonium ion or titratable acid. There are four simple acid-base disorders: metabolic acidosis and metabolic alkalosis; respiratory acidosis and respiratory alkalosis. Metabolic acidosis can occur because of an increase in endogenous acid production (such as lactate and ketoacids, loss of bicarbonate (as in diarrhea, or accumulation of endogenous acids (as in renal failure. Metabolic acidosis can also be with high and normal (hyperchloremic metabolic acidosis anion gap. Renal tubular acidosis (RTA is a form of hyperchloremic metabolic acidosis which occurs when the renal damage primarily affects tubular function. The main problem in distal RTA is reduced H+ excretion in distal tubule. Type 2 RTA is also called proximal RTA because the main problem is greatly impaired reabsorption of bicarbonate in proximal tubule. Impaired cation exchange in distal tubule is the main problem in RTA type 4. Metabolic alkalosis occurs as a result of net gain of [HCO3-] or loss of nonvolatile acid from extracellular fluids. Metabolic alkalosis can be associated with reduced or increased extracellular volume.

Effect of systemic pH on pHi and lactic acid generation in exhaustive forearm exercise

International Nuclear Information System (INIS)

Hood, V.L.; Schubert, C.; Keller, U.; Mueller, S.

1988-01-01

To investigate whether changes in systemic pH affect intracellular pH (pH i ), energy-rich phosphates, and lactic acid generation in muscle, eight normal volunteers performed exhaustive forearm exercise with arterial blood flow occluded for 2 min on three occasions. Subjects ingested 4 mmol/kg NH 4 Cl (acidosis; A) or NaHCO 3 (alkalosis; B) or nothing (control; C) 3 h before the exercise. Muscle pH i and phosphocreatine (PCr) content were measured with 31 P-nuclear magnetic resonance ( 31 P-NMR) spectroscopy during exercise and recovery. Lactate output during 0.5-7 min of recovery was calculated as deep venous-arterial concentration differences times forearm blood flow. Before exercise, blood pH and bicarbonate were lower in acidosis than alkalosis and intermediate in control. Lactic acid output during recovery was less with A than B and intermediate in C. PCr utilization and resynthesis were not affected by extracellular pH changes. pH i did not differ before exercise or at its end. Hence systemic acidosis inhibited and alkalosis stimulated lactic acid output. These findings suggest that systemic pH regulates cellular acid production, protecting muscle pH, at the expense of energy availability

A patient with Dent disease and features of Bartter syndrome caused by a novel mutation of CLCN5.

Science.gov (United States)

Okamoto, Takayuki; Tajima, Toshihiro; Hirayama, Tomoya; Sasaki, Satoshi

2012-02-01

Dent disease is an X-linked tubulopathy mainly caused by inactivating mutations of CLCN5. Features of Bartter syndrome such as hypokalemic metabolic alkalosis are rarely observed in patients with Dent disease. We report a Japanese male patient with Dent disease who also manifested features of Bartter syndrome. At the age of 3 years, he was diagnosed with Dent disease based on low molecular weight proteinuria and hypercalciuria. One year later, he was found to have features of Bartter syndrome, i.e., hypokalemia and metabolic alkalosis, and high levels of plasma renin activity and aldosterone with a normal blood pressure. Despite medical interventions, he developed chronic kidney disease stage 3 at the age of 21 years. To investigate the molecular basis of his disease, CLCN5, KCNJ1, SLC12A1, and CLCkb were analyzed and a novel mutation (Y567X) in CLCN5 was identified. Hypokalemic metabolic alkalosis is a rare manifestation in Dent disease. It is speculated that Dent patients with features of Bartter syndrome are susceptible to progression to renal failure. To study this hypothesis, additional observations and long-term follow-up of such patients are necessary.

[Dynamics of bioelectric activity of the brain and erythrocyte ultrastructure after intravenous infusion of sodium bicarbonate to oncologic patients].

Science.gov (United States)

Davydova, I G; Kassil', V L; Raĭkhlin, N T; Filippova, N A

1992-04-01

23 patients with malignant tumors of different location and histogenesis were investigated. There were no metastases in 9 cases. 10 patients had metastases in regional areas and 4--distant. The results were compared with those obtained in 4 patients with nonmalignant diseases. EEG, blood gases, plasma acid--base balance and ultrastructure of erythrocytes were explored before and after intravenous infusion of 4.2% sodium bicarbonate solution. The metabolic alkalosis induced amelioration of EEG, which was changed basically, the condense of pre-membrane layer disappeared or decreased in erythrocytes, and disaggregation of erythrocytes took place in cancer patients vs those with nonmalignant tumors. The results confirm the suggestion of generalized intracellular acidosis in malignant tumor patients. This acidosis can be temporarily avoided or diminished artificially by blood alkalosis.

Lazarusfænomen

DEFF Research Database (Denmark)

Schierbeck, Louise; Lenz, Katja Charlotte

2014-01-01

The pathophysiological mechanisms of auto resuscitation - also called the Lazarus phenomenon - are unknown, but they are thought to be related to matters such as hyperkalaemia, hyperventilation and alkalosis or increased end-expiratory pressure during assisted ventilation. The phenomenon is proba......The pathophysiological mechanisms of auto resuscitation - also called the Lazarus phenomenon - are unknown, but they are thought to be related to matters such as hyperkalaemia, hyperventilation and alkalosis or increased end-expiratory pressure during assisted ventilation. The phenomenon...... is probably underreported and this case report of the Lazarus phenomenon in a patient with severe hyperkalaemia demonstrates the necessity of following recommendations regarding resuscitation such as allowing pauses in assisted ventilation as well as ten minutes post resuscitation monitoring before declaring...

Primary Molecular Disorders and Secondary Biological Adaptations in Bartter Syndrome

Science.gov (United States)

Deschênes, Georges; Fila, Marc

2011-01-01

Bartter syndrome is a hereditary disorder that has been characterized by the association of hypokalemia, alkalosis, and the hypertrophy of the juxtaglomerular complex with secondary hyperaldosteronism and normal blood pressure. By contrast, the genetic causes of Bartter syndrome primarily affect molecular structures directly involved in the sodium reabsorption at the level of the Henle loop. The ensuing urinary sodium wasting and chronic sodium depletion are responsible for the contraction of the extracellular volume, the activation of the renin-aldosterone axis, the secretion of prostaglandins, and the biological adaptations of downstream tubular segments, meaning the distal convoluted tubule and the collecting duct. These secondary biological adaptations lead to hypokalemia and alkalosis, illustrating a close integration of the solutes regulation in the tubular structures. PMID:21941653

Primary Molecular Disorders and Secondary Biological Adaptations in Bartter Syndrome

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Georges Deschênes

2011-01-01

Full Text Available Bartter syndrome is a hereditary disorder that has been characterized by the association of hypokalemia, alkalosis, and the hypertrophy of the juxtaglomerular complex with secondary hyperaldosteronism and normal blood pressure. By contrast, the genetic causes of Bartter syndrome primarily affect molecular structures directly involved in the sodium reabsorption at the level of the Henle loop. The ensuing urinary sodium wasting and chronic sodium depletion are responsible for the contraction of the extracellular volume, the activation of the renin-aldosterone axis, the secretion of prostaglandins, and the biological adaptations of downstream tubular segments, meaning the distal convoluted tubule and the collecting duct. These secondary biological adaptations lead to hypokalemia and alkalosis, illustrating a close integration of the solutes regulation in the tubular structures.

Chloride test - blood

Science.gov (United States)

Serum chloride test ... A greater-than-normal level of chloride is called hyperchloremia. It may be due to: Carbonic anhydrase inhibitors (used to treat glaucoma) Diarrhea Metabolic acidosis Respiratory alkalosis (compensated) Renal ...

TRPV1 deletion exacerbates hyperthermic seizures in an age-dependent manner in mice.

Science.gov (United States)

Barrett, Karlene T; Wilson, Richard J A; Scantlebury, Morris H

2016-12-01

Febrile seizures (FS) are the most common seizure disorder to affect children. Although there is mounting evidence to support that FS occur when children have fever-induced hyperventilation leading to respiratory alkalosis, the underlying mechanisms of hyperthermia-induced hyperventilation and links to FS remain poorly understood. As transient receptor potential vanilloid-1 (TRPV1) receptors are heat-sensitive, play an important role in adult thermoregulation and modulate respiratory chemoreceptors, we hypothesize that TRPV1 activation is important for hyperthermia-induced hyperventilation leading to respiratory alkalosis and decreased FS thresholds, and consequently, TRPV1 KO mice will be relatively protected from hyperthermic seizures. To test our hypothesis we subjected postnatal (P) day 8-20 TRPV1 KO and C57BL/6 control mice to heated dry air. Seizure threshold temperature, latency and the rate of rise of body temperature during hyperthermia were assessed. At ages where differences in seizure thresholds were identified, head-out plethysmography was used to assess breathing and the rate of expired CO 2 in response to hyperthermia, to determine if the changes in seizure thresholds were related to respiratory alkalosis. Paradoxically, we observed a pro-convulsant effect of TRPV1 deletion (∼4min decrease in seizure latency), and increased ventilation in response to hyperthermia in TRPV1 KO compared to control mice at P20. This pro-convulsant effect of TRPV1 absence was not associated with an increased rate of expired CO 2 , however, these mice had a more rapid rise in body temperature following exposure to hyperthermia than controls, and the expected linear relationship between body weight and seizure latency was absent. Based on these findings, we conclude that deletion of the TRPV1 receptor prevents reduction in hyperthermic seizure susceptibility in older mouse pups, via a mechanism that is independent of hyperthermia-induced respiratory alkalosis, but

Ammonia Test

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... ammonia, but both can damage the eyes, skin, respiratory tract, and, if swallowed, the mouth, throat, and ...

First Trimester Down Syndrome Screen

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... and can be associated with congenital heart defects, respiratory and hearing problems, leukemia , and thyroid disorders . Many ...

Second Trimester Maternal Serum Screening

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... and can be associated with congenital heart defects, respiratory and hearing problems, leukemia , and thyroid disorders . Many ...

AFB (Acid-Fast Bacillus) Smear and Culture

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... to produce sputum, a health practitioner may collect respiratory samples using a procedure called a bronchoscopy. Bronchoscopy ...

Amniotic Fluid Analysis

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... surfactants, a newborn may develop life-threatening neonatal respiratory distress syndrome (RDS). Tests include: Lamellar body count ...

BMP (Basic Metabolic Panel)

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... as kidney failure, insulin shock or diabetic coma, respiratory distress, or heart rhythm changes. What does the ...

Pertussis Tests

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... tested? Pertussis, commonly called whooping cough, is a respiratory infection caused by the bacteria Bordetella pertussis . These ...

Alpha-1 Antitrypsin Test

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... deficiency. AAT levels may be decreased in neonatal respiratory distress syndrome and in conditions that cause a ...

Dengue Fever Testing

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... person-to-person contact or by exposure to respiratory secretions. The virus is spread when a mosquito ...

CSF Analysis

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... rivers. Infection occurs when the parasite enters the respiratory system through the nose of a person swimming ...

Parvovirus B19 Test

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... or "erythema infectiosum." The virus is found in respiratory droplets during an infection and is easily transmitted ...

Strep Throat Test

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... spreads from person-to-person through contact with respiratory secretions that contain the streptococcal bacteria. During influenza ...

Suicide by Fire Extinguisher Powder Ingestion: A Case Report

Directory of Open Access Journals (Sweden)

Hamid Mohammadi Kojidi

2017-07-01

Full Text Available A 51-year-old man committed suicide by swallowing the contents of a fire extinguisher. A few hours after his suicide attempt, he was referred to the medical center for poisoning. At the time of admission, the patient was conscious with stable vital signs. The patient complained of burning lips and mouth, mentioning diarrhea. Initial treatments included gastric lavage with activated charcoal, while paraclinical measures were requested. The patient had undergone hypernatremia (Na: 152 mEq/l and metabolic alkalosis. Treatment focused on the adjustment of sodium level and alkalosis. On the first day of hospitalization, the patient experienced recurrent episodes of tonic-clonic seizure along with the loss of consciousness. On the third day of hospitalization, the patient developed respiratory arrest followed by cardiac arrest and death.

hCG Test (Pregnancy Test)

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... Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer Disease Anemia Angina Ankylosing Spondylitis Anthrax ... Patient Resources For Health Professionals Subscribe Search hCG Pregnancy Send Us Your Feedback Choose Topic At a ...

Pleural Fluid Analysis Test

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... Less Related Images View More × Diagram of the Respiratory System, including the Lungs. Image credit: National Cancer ...

Pericardial Fluid Analysis

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... of Conditions Not Listed? Not Listed? Acidosis and Alkalosis Adrenal Insufficiency and Addison Disease Alcoholism Allergies Alzheimer ... the body. For example, pericarditis may follow a respiratory infection or a chest cold. Bleeding – bleeding disorders ...

Severe hypernatremia and hyperchloremia in an elderly patient with IgG-kappa type

Directory of Open Access Journals (Sweden)

Berend K

2013-12-01

Full Text Available Kenrick BerendSt Elisabeth Hospital, Willemstad, CuraçaoImashuku et al1 describe a 77-year-old male patient with multiple myeloma who was admitted to the hospital after suffering a pelvic bone fracture due to a road traffic accident. Several days after admission the arterial blood gas showed a pH of 7.481; arterial carbon dioxide tension (PaCO2 of 28.2 mmHg; arterial oxygen tension (PaO2 of 84.0 mmHg; HCO3- of 20.8 mmol/L (normal; 23–31 mmol/L; and an anion gap of 8.9 mmol/L (normal;12 mmol/L. These data, as the authors concluded, were suggestive of metabolic acidosis. First, this is not true because a high pH and low PaCO2 confirm a respiratory alkalosis. Since the test was conducted days later we may expect a chronic respiratory alkalosis to be present, perhaps because of pain or a secondary pulmonary problem, as may be expected with a relatively low PaO2. In chronic respiratory alkalosis one would expect the HCO3- to decrease about 4 mmol/L with every 10 mmHg decrease of PaCO2.2 If the initial HCO3- had been about 25 mmol/L, the expected PaCO2 would be about 20.28 mmol/L, almost identical with the patient’s HCO3-.View original paper by Imashuku and colleagues.

Newborn ventilatory response to maternal chronic hypercapnia.

Science.gov (United States)

DeLuca, L; Holzman, I; Gibbs, K

2012-10-01

This is a case of a neonate born with a respiratory acidosis with a compensatory metabolic alkalosis. This case demonstrates placental physiology of gas exchange as well as the blunted ventilatory response in the neonate from chronic hypercapnia.

Generaliserede kramper som debutsymptom ved Gitelmans syndrom

DEFF Research Database (Denmark)

Hvelplund, Carolina; Jeppesen, Eva Mosfeldt; Mortensen, Henrik B

2009-01-01

Gitelman's syndrome is a rare autosomal recessive syndrome presenting with hypocalciuria, hypomagnesiemia and hypokalemic metabolic alkalosis. This case reports a patient admitted with generalized seizures with the above-mentioned biochemical abnormalities, thus representing a rare onset of Gitel...

Gitelman's syndrome: a rare presentation mimicking cauda equina syndrome.

LENUS (Irish Health Repository)

Quinlan, C S

2012-02-01

We describe a case of bilateral weakness of the lower limbs, sensory disturbance and intermittent urinary incontinence, secondary to untreated Gitelman\\'s syndrome, in a 42-year-old female who was referred with presumed cauda equina syndrome. On examination, the power of both legs was uniformly reduced, and the perianal and lower-limb sensation was altered. However, MRI of the lumbar spine was normal. Measurements of serum and urinary potassium were low and blood gas analysis revealed metabolic alkalosis. Her symptoms resolved following potassium replacement. We emphasise the importance of measurement of the plasma and urinary levels of electrolytes in the investigation of patients with paralysis of the lower limbs and suggest that they, together with blood gas analysis, allow the exclusion of unusual causes of muscle weakness resulting from metabolic disorders such as metabolic alkalosis.

Hypokalemic Paralysis Complicated by Concurrent Hyperthyroidism and Hyperaldosternoism: A Case Report.

Science.gov (United States)

Hsiao, Yu-Hsin; Fang, Yu-Wei; Leu, Jyh-Gang; Tsai, Ming-Hsein

2017-01-04

BACKGROUND Thyrotoxic periodic paralysis (TPP) is commonly observed in patients with acute paralysis and hyperthyroidism. However, there is a possibility of secondary causes of hypokalemia in such a setting. CASE REPORT Herein, we present the case of a 38-year-old woman with untreated hypertension and hyperthyroidism. She presented with muscle weakness, nausea, vomiting, and diarrhea since one week. The initial diagnosis was TPP. However, biochemistry tests showed hypokalemia with metabolic alkalosis and renal potassium wasting. Moreover, a suppressed plasma renin level and a high plasma aldosterone level were noted, which was suggestive of primary aldosteronism. Abdominal computed tomography confirmed this diagnosis. CONCLUSIONS Therefore, it is imperative to consider other causes of hypokalemia (apart from TPP) in a patient with hyperthyroidism but with renal potassium wasting and metabolic alkalosis. This can help avoid delay in diagnosis of the underlying disease.

Cerebral vascular control and metabolism in heat stress

DEFF Research Database (Denmark)

Bain, Anthony R; Nybo, Lars; Ainslie, Philip N

2015-01-01

implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced...

Gitelman syndrome.

NARCIS (Netherlands)

Knoers, N.V.A.M.; Levtchenko, E.N.

2008-01-01

Gitelman syndrome (GS), also referred to as familial hypokalemia-hypomagnesemia, is characterized by hypokalemic metabolic alkalosis in combination with significant hypomagnesemia and low urinary calcium excretion. The prevalence is estimated at approximately 1:40,000 and accordingly, the prevalence

Gitelman syndrome : consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

NARCIS (Netherlands)

Blanchard, Anne; Bockenhauer, Detlef; Bolignano, Davide; Calò, Lorenzo A; Cosyns, Etienne; Devuyst, Olivier; Ellison, David H; Karet Frankl, Fiona E; Knoers, Nine V A M; Konrad, Martin; Lin, Shih-Hua; Vargas-Poussou, Rosa

Gitelman syndrome (GS) is a rare, salt-losing tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. The disease is recessively inherited, caused by inactivating mutations in the SLC12A3 gene that encodes the thiazide-sensitive sodium-chloride

Hjertestopbehandling. Nyere aspekter af kardiopulmonal genoplivning

DEFF Research Database (Denmark)

Herlevsen, Per Ove; Andersen, H H; Jepsen, S

1989-01-01

compression and increase survival. Cardiac arrest results in anaerobic metabolism and combined metabolic and respiratory acidosis. On account of relatively low minute volume during external cardiac compression decrease in end-tidal carbon dioxide concentration is observed together with arterial alkalosis...

Plasma Exchange for Refractory MDA5 Myositis and ILD

Science.gov (United States)

2017-04-26

plasma exchange, the patient had improvement of hypocarbic respiratory alkalosis and reversal of myositis with resolution of dysphagia/odynophagia and...symptoms with respiratory distress. A five day course of plasmapheresis was initiated on hospital day eight. Subsequently his respiratory acid-base

Effect of hypoxaemia on water and sodium homeostatic hormones and renal function

DEFF Research Database (Denmark)

Olsen, Niels Vidiendal

1995-01-01

, a hypoxic ventilatory response produces hypocapnia and respiratory alkalosis. Acute hypoxaemia depresses aldosterone secretion secondary to a direct effect on adrenal cells. Also plasma renin is decreased in resting hypoxaemic conditions, but the mechanism remains unknown. These hormonal changes may have...

Influence of bicarbonate on ventilatory drive in healthy subjects

NARCIS (Netherlands)

Mos-Oppersma, Eline; Doorduin, Jonne; van der Hoeven, J.G.; Veltink, Peter; Heunks, Leo M.A.

2016-01-01

Background Acute hypoventilation results in CO2 retention and respiratory acidosis. Bicarbonate retention aims to restore pH level. However, after institution of mechanical ventilation metabolic alkalosis may develop, which could impair respiratory drive. Aim To investigate whether increased plasma

Effects of acetazolamide and furosemide on ventilation and cerebral blood volume in normocapnic and hypercapnic patients with COPD.

NARCIS (Netherlands)

Ven, M.J.T. van de; Colier, W.N.J.M.; Sluijs, M.C. van der; Oeseburg, B.; Vis, P.; Folgering, H.T.M.

2002-01-01

STUDY OBJECTIVES: Effects of chronic metabolic alkalosis and acidosis and their relation to central chemoregulation may differ between normocapnic and chronic hypercapnic patients with COPD. The relationship between responses of inspired ventilation (VI), mouth occlusion pressure (P(0.1)), and

[Acid-base equilibrium and the brain].

Science.gov (United States)

Rabary, O; Boussofara, M; Grimaud, D

1994-01-01

In physiological conditions, the regulation of acid-base balance in brain maintains a noteworthy stability of cerebral pH. During systemic metabolic acid-base imbalances cerebral pH is well controlled as the blood/brain barrier is slowly and poorly permeable to electrolytes (HCO3- and H+). Cerebral pH is regulated by a modulation of the respiratory drive, triggered by the early alterations of interstitial fluid pH, close to medullary chemoreceptors. As blood/brain barrier is highly permeable to Co2, CSF pH is corrected in a few hours, even in case of severe metabolic acidosis and alkalosis. Conversely, during ventilatory acidosis and alkalosis the cerebral pH varies in the same direction and in the same range than blood pH. Therefore, the brain is better protected against metabolic than ventilatory acid-base imbalances. Ventilatory acidosis and alkalosis are able to impair cerebral blood flow and brain activity through interstitial pH alterations. During respiratory acidosis, [HCO3-] increases in extracellular fluids to control cerebral pH by two main ways: a carbonic anhydrase activation at the blood/brain and blood/CSF barriers level and an increase in chloride shift in glial cells (HCO3- exchanged for Cl-). During respiratory alkalosis, [HCO3-] decreases in extracellular fluids by the opposite changes in HCO3- transport and by an increase in lactic acid synthesis by cerebral cells. The treatment of metabolic acidosis with bicarbonates may induce a cerebral acidosis and worsen a cerebral oedema during ketoacidosis. Moderate hypocapnia carried out to treat intracranial hypertension is mainly effective when cerebral blood flow is high and vascular CO2 reactivity maintained. Hypocapnia may restore an altered cerebral blood flow autoregulation. Instrumental hypocapnia requires a control of cerebral perfusion pressure and cerebral arteriovenous difference for oxygen, to select patients for whom this kind of treatment may be of benefit, to choose the optimal level of

Bartter syndrome Type III and congenital anomalies of the kidney and urinary tract: an antenatal presentation

NARCIS (Netherlands)

Westland, R.; Hack, W.W.; van der Horst, H.J.; Uittenbogaard, L.B.; van Hagen, J.M.; van der Valk, P.; Kamsteeg, E.J.; Heuvel, L.P.W.J. van den; van Wijk, J.A.

2012-01-01

Bartter syndrome encompasses a variety of inheritable renal tubular transport disorders characterized by hypokalemia and hypochloremic metabolic alkalosis. Bartter syndrome Type III is caused by genetic alterations in the chloride channel kidney B (CLCNKB) gene and often presents in the first 2

Antenatal Bartter's syndrome with sensorineural deafness

OpenAIRE

Bhamkar, R. P.; Gajendragadkar, A.

2009-01-01

Bartter's syndrome is a group of inherited, salt-losing tubulopathies presenting as metabolic alkalosis with normotensive hyperreninemia and hyperaldosteronism. We report here the first case of a neonate with bilateral, sensorineural deafness, a variant of antenatal Bartter's syndrome from an Indian community.

Classic Bartter syndrome: a rare cause of failure to thrive in a child.

Science.gov (United States)

Vieira, Helena; Mendes, Leonor; Mendes, Patricia; da Silva, José Esteves

2012-06-28

Bartter syndrome is a group of rare autosomal-recessive disorders caused by a defect in distal tubule transport of sodium and chloride. Blood gases and plasma electrolytes raise suspicion of this diagnosis and the definitive diagnosis is made by genetic study. Early treatment improves prognosis. The authors present the case of an 11-month-old child with early failure to thrive and severe regurgitation. Blood gases revealed hypochloraemic metabolic alkalosis, hyponatraemia and hypokalaemia. Blood pressure was normal and polyuria was documented. She began therapy with potassium chloride supplementation and indomethacin. There was clinical improvement and plasma potassium and bicarbonate normalised. The molecular study confirmed it was the classic form of Bartter syndrome. Despite being rare in clinical practice, which may lead to unnecessary medical investigation and diagnosis delay, in a child with failure to thrive, hypochloraemic metabolic alkalosis and hypokalaemia, this diagnosis must be considered.

Bartter Syndrome Type 1 Presenting as Nephrogenic Diabetes Insipidus

Directory of Open Access Journals (Sweden)

Gianluca Vergine

2018-01-01

Full Text Available Bartter syndrome (BS type 1 (OMIM #601678 is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, polyuria, recurrent vomiting, and growth retardation. It is caused by loss-of-function mutations of the SLC12A1 gene, encoding the furosemide-sensitive Na-K-Cl cotransporter. Recently, a phenotypic variability has been observed in patients with genetically determined BS, including absence of nephrocalcinosis, hypokalemia, and/or metabolic alkalosis in the first year of life as well as persistent metabolic acidosis mimicking distal renal tubular acidosis. We report the case of a child with a genetically determined diagnosis of Bartter syndrome type 1 who presented with a phenotype of nephrogenic diabetes insipidus, with severe hypernatremia and urinary concentrating defect. In these atypical cases, molecular analysis is mandatory to define the diagnosis, in order to establish the correct clinical and therapeutic management.

Bartter Syndrome Type 1 Presenting as Nephrogenic Diabetes Insipidus.

Science.gov (United States)

Vergine, Gianluca; Fabbri, Elena; Pedini, Annalisa; Tedeschi, Silvana; Borsa, Niccolò

2018-01-01

Bartter syndrome (BS) type 1 (OMIM #601678) is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, polyuria, recurrent vomiting, and growth retardation. It is caused by loss-of-function mutations of the SLC12A1 gene, encoding the furosemide-sensitive Na-K-Cl cotransporter. Recently, a phenotypic variability has been observed in patients with genetically determined BS, including absence of nephrocalcinosis, hypokalemia, and/or metabolic alkalosis in the first year of life as well as persistent metabolic acidosis mimicking distal renal tubular acidosis. We report the case of a child with a genetically determined diagnosis of Bartter syndrome type 1 who presented with a phenotype of nephrogenic diabetes insipidus, with severe hypernatremia and urinary concentrating defect. In these atypical cases, molecular analysis is mandatory to define the diagnosis, in order to establish the correct clinical and therapeutic management.

Incidence of Postoperative Acid-Base Disturbances in Abdominal Surgery

Directory of Open Access Journals (Sweden)

Taghavi Gilani M

2014-04-01

Full Text Available Introduction: Respiratory and blood pressure changes as well as fluid administration alter the acid-base balance during the perioperative period which may cause consciousness disturbance and additional hemodynamic disorders. The aim of this study was to identify frequent postoperative acid-base disturbances in order to control postoperative complications. Materials and Methods:This prospective, observational study design was used on patients who underwent abdominal surgery during a six-month period. Gasometry was performed immediately after the patients’ admittion to ICU and six and 12 hours postoperatively. SPSS v13 software was used, and PResults: 213 patients (123 male and 90 female aged 14-85 years (51.7± 22.4 were evaluated. During admission, PH and PaCO2 were (7.29±0.13 and (38.3±11.9, respectively; however, although PH increased gradually (P=0.001, PaCO2 was reduced (P=0.03. Bicarbonate and base excess had opposite effects; bicarbonate initially decreased but increased after 12 hours (P=0.001, whereas base excess initially increased (-6.3±11.6 and then decreased gradually (P=0.003. The arterial oxygen pressure was reduced for 22.5% of the patients throughout the admission period, and this did not significantly change (P=0.57. Conclusion: According to the results, in admission, 65.7% had metabolic acidosis, but metabolic alkalosis was the least. Gradually, metabolic acidosis was modified, but metabolic alkalosis increased. Intraoperative hypotension and fluid infusion may be the main factors of early metabolic acidosis and control of hypotension, or correction of acidosis may increase metabolic alkalosis.

Acid base imbalances in ill neonatal foals and their association with survival.

Science.gov (United States)

Viu, J; Armengou, L; Ríos, J; Cesarini, C; Jose-Cunilleras, E

2017-01-01

Acid-base imbalances observed in human paediatric patients are associated with outcome. Likewise, neonatal foals may have different acid-base imbalances associated with diagnosis or prognosis. To determine acid-base imbalances by the quantitative method in ill neonatal foals and assess their association with diagnosis and prognosis. Observational prospective clinical study. This study included 65 ill neonatal foals (32 septic, 33 nonseptic) admitted to an equine referral hospital from 2005 to 2011with acid-base parameters determined on admission and a control group of 33 healthy neonatal foals. Blood pH, pCO 2 , sodium, potassium, chloride, L-lactate, albumin and phosphate concentrations were determined. Bicarbonate, globulin, measured strong ion difference (SID m ), nonvolatile weak buffer concentrations (A tot ), base excess and its components were calculated. Analysis of covariance (ANCOVA) and multiple linear regression statistical analyses were performed. Results are summarised as mean ± s.d. for normally distributed variables and median [25-75th percentiles] for non-normally distributed ones. A total of 63% of ill foals had respiratory alkalosis and 58.5% had SID m acidosis. The combination of both alterations was detected in 21 of 65 ill foals and abnormal pH was found in 24 of 65. Compared with healthy foals, ill foals had significantly lower SID m (nonseptic 31.6 ± 6.3 [Pacid-base imbalances observed in ill foals were respiratory alkalosis, SID m acidosis or mixed respiratory alkalosis with strong ion acidosis. Increased venous pCO 2 and blood L-lactate concentration were associated with poor outcome. © 2015 EVJ Ltd.

Point-of-care testing on admission to the intensive care unit: lactate and glucose independently predict mortality.

Science.gov (United States)

Martin, Jan; Blobner, Manfred; Busch, Raymonde; Moser, Norman; Kochs, Eberhard; Luppa, Peter B

2013-02-01

The aim of the study was to retrospectively investigate whether parameters of routine point-of-care testing (POCT) predict hospital mortality in critically ill surgical patients on admission to the intensive care unit (ICU). Arterial blood analyses of 1551 patients on admission to the adult surgical ICU of the Technical University Munich were reviewed. POCT was performed on a blood gas analyser. The association between acid-base status and mortality was evaluated. Metabolic acidosis was defined by base excess (BE) lactate >50% of BE, anion gap (AG)-acidosis by AG >16 mmol/L, hyperchloraemic acidosis by chloride >115 mmol/L. Metabolic alkalosis was defined by BE ≥3 mmol/L. Logistic regression analysis identified variables independently associated with mortality. Overall mortality was 8.8%. Mortality was greater in male patients (p=0.012). Mean age was greater in non-survivors (p55 mm Hg (mortality 23.1%). Three hundred and seventy-seven patients presented with acidosis (mortality 11.4%), thereof 163 patients with lactic acidosis (mortality 19%). Mortality for alkalosis (174 patients) was 12.1%. Mean blood glucose level for non-survivors was higher compared to survivors (plactate, glucose, age, male gender as independent predictors of mortality. Lactate and glucose on ICU admission independently predict mortality. BE and AG failed as prognostic markers. Lactic acidosis showed a high mortality rate implying that lactate levels should be obtained on ICU admission. Prevalence of hyperchloraemic acidosis was low. Metabolic alkalosis was associated with an increased mortality. Further studies on this disturbance and its attendant high mortality are warranted.

CO2 blood test

Science.gov (United States)

Bicarbonate test; HCO3-; Carbon dioxide test; TCO2; Total CO2; CO2 test - serum; Acidosis - CO2; Alkalosis - CO2 ... Many medicines can interfere with blood test results. Your health ... need to stop taking any medicines before you have this test. DO ...

Effect of carbon dioxide in acute mountain sickness

DEFF Research Database (Denmark)

Harvey, T C; Raichle, M E; Winterborn, M H

1988-01-01

of the respiratory alkalosis normally seen at high altitude. Symptoms of acute mountain sickness were rapidly relieved. In three subjects cerebral blood flow increased by 17-39%, so that oxygen delivery to the brain would have been considerably improved. This study confirms earlier suggestions of the beneficial...

[What you should know of the arterial blood gases during the watch].

Science.gov (United States)

Márquez-González, Horacio; Pámanes-González, Jesús; Márquez-Flores, Horacio; Gómez-Negrete, Alonso; Muñoz-Ramírez, Mireya C; Villa-Romero, Antonio Rafael

2012-01-01

Gasometry is the measurement of dissolved gases in the blood, by measuring pH, carbon dioxide pressure (pCO(2)), serum bicarbonate (HCO(3-)), and lactate and serum electrolytes: sodium, potassium and chlorine you can make a diagnosis, etiology and treatment in the critically ill patient. The aim is to provide five steps for the interpretation of blood gases by: 1. The definition of acidemia or acidosis, or alkalemia or alkalosis. 2. Defining the metabolic component or respiratory. 3. To determine the anion gap; levels above 15 ± 2 determine other likely causes of excess anions (methanol, uremia, diabetic ketoacidosis, paraldehyde, ionized, lactic acidosis, ethylene glycol and salicylates. 4. Compensation, using the Winter formula. 5. The delta gap, with the formula for determining intrinsic and metabolic alkalosis. When anion gap is normal, is calculated urinary anion gap; the value is negative if the loss is extrarenal, contrary to the positive result is renal etiology.

Neonatal Bartter Syndrome in association with congenital adrenal hyperplasia in a neonate - a rare combination.

Science.gov (United States)

Hussain, Shabbir

2016-05-01

Neonatal Bartter syndrome (NBS) is an autosomal recessive renal tubulopathy characterized by hypokalaemic, hypochloraemic metabolic alkalosis associated with increased urinary loss of sodium, potassium, calcium and chloride. There is hyperreninaemia and hyperaldosteronaemia but normotension. Congenital adrenal hyperplasia (CAH), another autosomal recessive condition, may present in the neonatal period with vomiting, hypovolaemia, failure to gain weight or ambiguous genitalia. We report a case of NBS and CAH combination in a neonate. A male neonate born at term was admitted with history of recurrent vomiting and dehydration episodes. Investigations revealed electrolytes imbalance, metabolic alkalosis, raised aldosterone and renin levels suggestive of NBS. He was treated successfully and discharged. He was re-admitted with the same symptoms. Further evaluation confirmed the presence of CAH as well. We report this case because of the rarity of this combination (NBS plus CAH) and to the best of our knowledge this is the first such case report from Pakistan.

A Rare Disorder with Common Clinical Presentation: Neonatal Bartter Syndrome.

Science.gov (United States)

Hussain, Shabbir; Tarar, Saba Haider; Al-Muhaizae, Muhammad

2015-04-01

Bartter syndrome is an autosomal recessive renal tubulopathy that presents with hypokalemic, hypochloremic metabolic alkalosis associated with increased urinary loss of sodium, potassium, calcium and chloride. There is hyperreninemia and hyperaldosteronemia but normotension. A full term male neonate was referred at 20-day of age with features of sepsis and respiratory distress. He was evaluated and managed as case of septicemia with all supportive paraphernalia including mechanical ventilation. Investigations revealed electrolytes imbalance and metabolic alkalosis suggestive of Neonatal Bartter Syndrome (NBS). Raised aldosterone and renin levels confirmed the diagnosis. Electrolyte imbalance was corrected with fluids and indomethacin, treated successfully, discharged and parents counseled. He was thriving well at 9 months of age. Another 2 months old male baby presented with recurrent episodes of lethargy with dehydration and failure to gain weight. Investigations confirmed the diagnosis of NBS. He was also successfully treated with same medication. We report these 2 cases because of the rarity of NBS, presentation of which may mimic common illnesses like sepsis and gastroenteritis.

Strong ion and weak acid analysis in severe preeclampsia: potential clinical significance.

Science.gov (United States)

Ortner, C M; Combrinck, B; Allie, S; Story, D; Landau, R; Cain, K; Dyer, R A

2015-08-01

The influence of common disturbances seen in preeclampsia, such as changes in strong ions and weak acids (particularly albumin) on acid-base status, has not been fully elucidated. The aims of this study were to provide a comprehensive acid-base analysis in severe preeclampsia and to identify potential new biological predictors of disease severity. Fifty women with severe preeclampsia, 25 healthy non-pregnant- and 46 healthy pregnant controls (26-40 weeks' gestation), were enrolled in this prospective case-control study. Acid-base analysis was performed by applying the physicochemical approach of Stewart and Gilfix. Mean [sd] base excess was similar in preeclamptic- and healthy pregnant women (-3.3 [2.3], and -2.8 [1.5] mEq/L respectively). In preeclampsia, there were greater offsetting contributions to the base excess, in the form of hyperchloraemia (BE(Cl) -2 [2.3] vs -0.4 [2.3] mEq/L, Palkalosis was associated with a non-reassuring/abnormal fetal heart tracing (Prespiratory and hypoalbuminaemic alkalosis that was metabolically offset by acidosis, secondary to unmeasured anions and dilution. While the overall base excess in severe preeclampsia is similar to that in healthy pregnancy, preeclampsia is associated with a greater imbalance offsetting hypoalbuminaemic alkalosis and hyperchloraemic acidosis. Rather than the absolute value of base excess, the magnitude of these opposing contributors may be a better indicator of the severity of this disease. Hypoalbuminaemic alkalosis may also be a predictor of fetal compromise. clinicaltrials.gov: NCT 02164370. © The Author 2015. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Effect of acute metabolic acid/base shifts on the human airway calibre.

NARCIS (Netherlands)

Brijker, F.; Elshout, F.J.J. van den; Heijdra, Y.F.; Bosch, F.H.; Folgering, H.T.M.

2001-01-01

Acute metabolic alkalosis (NaHCO(3)), acidosis (NH(4)Cl), and placebo (NaCl) were induced in 15 healthy volunteers (12 females, median age 34 (range 24-56) years) in a double blind, placebo controlled study to evaluate the presence of the effects on airway calibre. Acid-base shifts were determined

A New Therapeutic Strategy for Autosomal Dominant Polycystic Kidney Disease: Activation of AMP Kinase by Metformin

Science.gov (United States)

2012-07-01

role for CHOP during inhibition of the mitochondrial respiratory chain. J. Biochem. 146, 123–132. Joly, D., Ishibe, S., Nickel, C., Yu, Z., Somlo, S...urinary HCO3 excretion in response to an initial alkali load, resulting in compensated metabolic alkalosis . Therefore, it appears that the IRR may play a

The V-ATPase is expressed in the choroid plexus and mediates cAMP-induced intracellular pH alterations

DEFF Research Database (Denmark)

Christensen, Henriette L; Păunescu, Teodor G; Matchkov, Vladimir

2017-01-01

fraction in the luminal microvillus area. The vesicles did not translocate to the luminal membrane in two in vivo models of hypocapnia-induced alkalosis. The Na(+)-independent intracellular pH (pHi) recovery from acidification was studied in freshly isolated clusters of CPECs. At extracellular pH (pHo) 7...

Hypoxia silences retrotrapezoid nucleus respiratory chemoreceptors via alkalosis.

Science.gov (United States)

Basting, Tyler M; Burke, Peter G R; Kanbar, Roy; Viar, Kenneth E; Stornetta, Daniel S; Stornetta, Ruth L; Guyenet, Patrice G

2015-01-14

In conscious mammals, hypoxia or hypercapnia stimulates breathing while theoretically exerting opposite effects on central respiratory chemoreceptors (CRCs). We tested this theory by examining how hypoxia and hypercapnia change the activity of the retrotrapezoid nucleus (RTN), a putative CRC and chemoreflex integrator. Archaerhodopsin-(Arch)-transduced RTN neurons were reversibly silenced by light in anesthetized rats. We bilaterally transduced RTN and nearby C1 neurons with Arch (PRSx8-ArchT-EYFP-LVV) and measured the cardiorespiratory consequences of Arch activation (10 s) in conscious rats during normoxia, hypoxia, or hyperoxia. RTN photoinhibition reduced breathing equally during non-REM sleep and quiet wake. Compared with normoxia, the breathing frequency reduction (Δf(R)) was larger in hyperoxia (65% FiO2), smaller in 15% FiO2, and absent in 12% FiO2. Tidal volume changes (ΔV(T)) followed the same trend. The effect of hypoxia on Δf(R) was not arousal-dependent but was reversed by reacidifying the blood (acetazolamide; 3% FiCO2). Δf(R) was highly correlated with arterial pH up to arterial pH (pHa) 7.5 with no frequency inhibition occurring above pHa 7.53. Blood pressure was minimally reduced suggesting that C1 neurons were very modestly inhibited. In conclusion, RTN neurons regulate eupneic breathing about equally during both sleep and wake. RTN neurons are the first putative CRCs demonstrably silenced by hypocapnic hypoxia in conscious mammals. RTN neurons are silent above pHa 7.5 and increasingly active below this value. During hyperoxia, RTN activation maintains breathing despite the inactivity of the carotid bodies. Finally, during hypocapnic hypoxia, carotid body stimulation increases breathing frequency via pathways that bypass RTN. Copyright © 2015 the authors 0270-6474/15/350527-17$15.00/0.

[Acid-base homeostasis: metabolic acidosis and metabolic alkalosis].

Science.gov (United States)

Dussol, Bertrand

2014-07-01

Acid-base homeostasis ensured by the kidneys, which maintain the equilibrium between proton generation by cellular metabolism and proton excretion in urine. This requirement is lifesaving because of the protons' ability to bind to anionic proteins in the extracellular space, modifying their structure and functions. The kidneys also regenerate bicarbonates. The kidney is not the sole organ in charge of maintaining blood pH in a very narrow range; lungs are also involved since they allow a large amount of volatile acid generated by cellular respiration to be eliminated. Copyright © 2014 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.

Acid-base status determines the renal expression of Ca2+ and Mg2+ transport proteins.

NARCIS (Netherlands)

Nijenhuis, T.; Renkema, K.Y.; Hoenderop, J.G.J.; Bindels, R.J.M.

2006-01-01

Chronic metabolic acidosis results in renal Ca2+ and Mg2+ wasting, whereas chronic metabolic alkalosis is known to exert the reverse effects. It was hypothesized that these adaptations are mediated at least in part by the renal Ca2+ and Mg2+ transport proteins. The aim of this study, therefore, was

The effect of glutamine administration on urinary ammonium excretion in normal subjects and patients with renal disease.

Science.gov (United States)

Welbourne, T; Weber, M; Bank, N

1972-07-01

The effect of acute changes in the delivery rate of glutamine to the kidney on urinary ammonium excretion was studied in man. Healthy subjects and patients with intrinsic renal disease were studied under three different acid-base conditions: unaltered acid-base balance; NH(4)Cl-induced acidosis; and NaHCO(3)-induced alkalosis. Anhydrous L-glutamine was administered orally in a single dose of 260 mmoles during each of these three acid-base states. We found that endogenous venous plasma glutamine concentration fell during acidosis and rose during alkalosis in both healthy subjects and patients with renal disease. In healthy subjects, orally administered glutamine raised plasma glutamine concentration markedly over a 2-3 hr period. This was accompanied by an increase in urinary ammonium excretion and a rise in urine pH under normal acid-base conditions and during metabolic acidosis. No increase in ammonium excretion occurred when glutamine was administered during metabolic alkalosis in spite of an equivalent rise in plasma glutamine concentration. In patients with renal disease, endogenous venous plasma glutamine concentration was lower than in healthy subjects, perhaps as a result of mild metabolic acidosis. Acute oral glutamine loading failed to increase urinary ammonium excretion significantly during either unaltered acid-base conditions or after NH(4)Cl-induced acidosis, even though plasma glutamine rose as high as in healthy subjects. We conclude from these observations that glutamine delivery to the kidney is a rate-limiting factor for ammonium excretion in healthy subjects, both before and after cellular enzyme adaptation induced by metabolic acidosis. In contrast, in patients with renal disease, glutamine delivery is not rate-limiting for ammonium excretion. Presumably other factors, such as surviving renal mass and the activity of intracellular enzymes necessary for ammonia synthesis limit ammonium excretion in these patients.

Gastro-oesophageal reflux: An overview of the cost-effectiveness of ...

African Journals Online (AJOL)

with normal acid-base balance and cause metabolic alkalosis, or ... be dependent on the diagnosis, side-effects and cost-effectiveness of the .... care, e.g. time lost from work due to illness.5 When different ... negative impact on a patient's psychological well-being, than ... as well as the effects on the patient's quality of life.

Bartter's syndrome: A case report of nephrocalcinosis

OpenAIRE

KOŞAN, Celalettin

2014-01-01

Bartter's syndrome is characterized by generalized hyperplasia of juxtaglomerular apparatus, hyperreninism leading to secondary hyperaldesteronism, hypokalemic alkalosis and normal blood pressure. Although nephrocalcinosis has been described sporadically in patients with Barter's syndrome, this is still generally unrecognized. We reported a case of Barter's syndrome with nephrocalcinosis and discussed clinical significance of nephrocalcinosis in this syndrome.

Hypercapnea and Acidemia despite Hyperventilation following Endotracheal Intubation in a Case of Unknown Severe Salicylate Poisoning

Directory of Open Access Journals (Sweden)

Shannon M. Fernando

2017-01-01

Full Text Available Salicylates are common substances for deliberate self-harm. Acute salicylate toxicity is classically associated with an initial respiratory alkalosis, followed by an anion gap metabolic acidosis. The respiratory alkalosis is achieved through hyperventilation, driven by direct stimulation on the respiratory centers in the medulla and considered as a compensatory mechanism to avoid acidemia. However, in later stages of severe salicylate toxicity, patients become increasingly obtunded, with subsequent loss of airway reflexes, and therefore intubation may be necessary. Mechanical ventilation has been recommended against in acute salicylate poisoning, as it is believed to take away the compensatory hyperpnea and tachypnea. Despite the intuitive physiological basis for this recommendation, there is a paucity of evidence to support it. We describe a case of a 59-year-old male presenting with decreased level of consciousness and no known history of ingestion. He was intubated and experienced profound hypercarbia and acidemia despite mechanical ventilation with high minute ventilation and tidal volumes. This case illustrates the deleterious effects of intubation in severe salicylate toxicity.

Out of Warburg effect: An effective cancer treatment targeting the tumor specific metabolism and dysregulated pH.

Science.gov (United States)

Schwartz, Laurent; Seyfried, Thomas; Alfarouk, Khalid O; Da Veiga Moreira, Jorgelindo; Fais, Stefano

2017-04-01

As stated by Otto Warburg nearly a century ago, cancer is a metabolic disease, a fermentation caused by malfunctioning mitochondria, resulting in increased anabolism and decreased catabolism. Treatment should, therefore, aim at restoring the energy yield. To decrease anabolism, glucose uptake should be reduced (ketogenic diet). To increase catabolism, the oxidative phosphorylation should be restored. Treatment with a combination of α-lipoic acid and hydroxycitrate has been shown to be effective in multiple animal models. This treatment, in combination with conventional chemotherapy, has yielded extremely encouraging results in glioblastoma, brain metastasis and lung cancer. Randomized trials are necessary to confirm these preliminary data. The major limitation is the fact that the combination of α-lipoic acid and hydroxycitrate can only be effective if the mitochondria are still present and/or functional. That may not be the case in the most aggressive tumors. The increased intracellular alkalosis is a strong mitogenic signal, which bypasses most inhibitory signals. Concomitant correction of this alkalosis may be a very effective treatment in case of mitochondrial failure. Copyright © 2017 Elsevier Ltd. All rights reserved.

Expanding the spectrum of genetic mutations in antenatal Bartter syndrome type II.

Science.gov (United States)

Fretzayas, Andreas; Gole, Evangelia; Attilakos, Achilleas; Daskalaki, Anna; Nicolaidou, Polyxeni; Papadopoulou, Anna

2013-06-01

Bartter syndrome (BS) is a group of genetic disorders characterized by hypokalemic metabolic alkalosis, hyponatremia and elevated renin and aldosterone plasma concentrations. BS type II is caused by mutations in the KCNJ1 gene and usually presents with transient hyperkalemia. We report here a novel KCNJ1 mutation in a male neonate, prematurely born after a pregnancy complicated by polyhydramnios. The infant presented with typical clinical and laboratory findings of BS type II, such as hyponatremia, hypochloremic metabolic alkalosis, severe weight loss, elevated renin and aldosterone levels and transient hyperkalemia in the early postnatal period, which were later normalized. Molecular analysis revealed a compound heterozygous mutation in the KCNJ1 gene, consisting of a novel K76E and an already described V315G mutation, both affecting functional domains of the channel protein. Typical manifestations of antenatal BS in combination with hyperkalemia should prompt the clinician to search for mutations in the KCNJ1 gene first. © 2013 The Authors. Pediatrics International © 2013 Japan Pediatric Society.

Gitelman syndrome combined with complete growth hormone deficiency

Directory of Open Access Journals (Sweden)

Se Ra Min

2013-03-01

Full Text Available Gitelman syndrome is a rare autosomal recessive hereditary salt-losing tubulopathy, that manifests as hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria. It is caused by mutations in the solute carrier family 12(sodium/chloride transporters, member 3 (SLC12A3 gene encoding the thiazide-sensitive sodium chloride cotransporter channel (NCCT in the distal convoluted tubule of the kidney. It is associated with muscle weakness, cramps, tetany, vomiting, diarrhea, abdominal pain, and growth retardation. The incidence of growth retardation, the exact cause of which is unknown, is lower than that of Bartter syndrome. Herein, we discuss the case of an overweight 12.9-year-old girl of short stature presenting with hypokalemic metabolic alkalosis. The patient, on the basis of detection of a heterozygous mutation in the SLC12A3 gene and poor growth hormone (GH responses in two provocative tests, was diagnosed with Gitelman syndrome combined with complete GH deficiency. GH treatment accompanied by magnesium oxide and potassium replacement was associated with a good clinical response.

Prioritization of the Oral (Ingestive) Hazard of Industrial Chemicals

Science.gov (United States)

2011-10-28

or Respiration - respiratory obstruction VCVN1* "Vrednie chemichescie veshestva. Neorganicheskie soedinenia elementov I-IV groopp" (Hazardous...section Lungs, Thorax, or Respiration - respiratory depression Gastrointestinal - changes in structure or function of esophagus MJAUAJ Medical Journal...impaired Nutritional and Gross Metabolic - metabolic alkalosis JTCTDW Journal of Toxicology, Clinical Toxicology. 33 Sodium chloride #(T3) 7647-14-5 LD50

Reverse ventilation--perfusion mismatch

International Nuclear Information System (INIS)

Palmaz, J.C.; Barnett, C.A.; Reich, S.B.; Krumpe, P.E.; Farrer, P.A.

1984-01-01

Patients having lobar airway obstruction or consolidation usually have decreases of both ventilation and perfusion on lung scans. We report three patients in whom hypoxic vasoconstriction was apparently incomplete, resulting in a ''reversed'' ventilation-perfusion mismatch. Perfusion of the hypoxic lobe on the radionuclide scan was associated with metabolic alkalosis, pulmonary venous and pulmonary arterial hypertension in these patients

Evaluation of the Use of Capnography during the Transport of Critically Ill Mechanically Ventilated Patients.

Science.gov (United States)

1992-12-15

DISCUSSION: Gervais et a13 demonstrated that respiratory alkalosis developed when ICU patients were manually ventilated, without 7 spirometric...developed a respiratory acidosis. Use of the non-invasive monitor, the capnograph prevented this adverse effect and resulted in inIproved patient safety...ventilation, all patients developed respiratory acidoses. Capnography uniformly prevented the development of respiratory acidosis during transport. We

Pulmonary gas exchange and acid-base state at 5,260 m in high-altitude Bolivians and acclimatized lowlanders

DEFF Research Database (Denmark)

Wagner, Hans Peter; Araoz, Mauricio; Boushel, Robert Christopher

2002-01-01

hyperoxic work, capacity was 73% greater in N. Buffering of lactic acid was greater in N, with 20% less increase in base deficit per millimole per liter rise in lactate. These data show in L persistent alkalosis even after 9 wk at 5,260 m. In N, the data show 1) insignificant reduction in exercise capacity...

The formation and design of 'The Acute Admission Database'- a database including a prospective, observational cohort of 6279 patients triaged in the Emergency Department in a larger Danish hospital

DEFF Research Database (Denmark)

Barfod, Charlotte; Lauritzen, Marlene Mp; Danker, Jakob K

2012-01-01

of peripheral oxygen (9.2%), Glasgow Coma Score (6.6%) and respiratory rate (4.8%). A venous acid-base status was obtained in 43% of all patients. The majority (78%) had a pH within the normal range (7.35-7.45), 15% had acidosis (pH alkalosis (pH > 7.45). Median length of stay was 2 days...

Prevention and Management of Cold-Weather Injuries

Science.gov (United States)

2005-04-01

49 d. After an initial stimulation of respiration with mild hypothermia (leading to respiratory alkalosis ), there is a progressive decrease...nonevaporated sweat will reduce clothing insulation and possibly form ice crystals. Breathing cold air can slightly exacerbate respiratory water loss... Respiratory . (1) Upper airway temperatures, which normally remain unchanged during exercise under temperate conditions, can decrease substantially

Multiservice Tactics, Techniques, and Procedures for Treatment of Chemical Agent Casualties and Conventional Military Chemical Injuries

Science.gov (United States)

2007-09-01

breathing (too rapid and/or too deep) with a resultant decrease in carbon dioxide tension and respiratory alkalosis . hypopyon—Pus in the anterior...V-3 Effects of Sulfur Mustard on the Skin ................................................V-4 Effects of Sulfur Mustard on the Respiratory ...V-11 Effects of Arsenical Vesicants on the Respiratory Tract ..................V-12 Systemic Effects of Arsenical

Chronic mesenteric volvulus in a dog

Science.gov (United States)

Spevakow, Andrea B.; Nibblett, Belle Marie D.; Carr, Anthony P.; Linn, Kathleen A.

2010-01-01

A chronic, partial mesenteric volvulus was found on laparotomy of an adult Bernese mountain dog with a 4-month history of intermittent vomiting, diarrhea, and weight loss. The dog had elevated cholestatic and hepatocellular leakage enzymes, increased bile acids, azotemia, isosthenuria, and a hypokalemic, hypochloremic, metabolic alkalosis. The dog recovered fully following reduction of the volvulus. PMID:20357947

Effect of Acetazolamide vs Placebo on Duration of Invasive Mechanical Ventilation Among Patients With Chronic Obstructive Pulmonary Disease: A Randomized Clinical Trial.

Science.gov (United States)

Faisy, Christophe; Meziani, Ferhat; Planquette, Benjamin; Clavel, Marc; Gacouin, Arnaud; Bornstain, Caroline; Schneider, Francis; Duguet, Alexandre; Gibot, Sébastien; Lerolle, Nicolas; Ricard, Jean-Damien; Sanchez, Olivier; Djibre, Michel; Ricome, Jean-Louis; Rabbat, Antoine; Heming, Nicholas; Urien, Saïk; Esvan, Maxime; Katsahian, Sandrine

2016-02-02

Acetazolamide has been used for decades as a respiratory stimulant for patients with chronic obstructive pulmonary disease (COPD) and metabolic alkalosis, but no large randomized placebo-controlled trial is available to confirm this approach. To determine whether acetazolamide reduces mechanical ventilation duration in critically ill patients with COPD and metabolic alkalosis. The DIABOLO study, a randomized, double-blind, multicenter trial, was conducted from October 2011 through July 2014 in 15 intensive care units (ICUs) in France. A total of 382 patients with COPD who were expected to receive mechanical ventilation for more 24 hours were randomized to the acetazolamide or placebo group and 380 were included in an intention-to treat analysis. Acetazolamide (500-1000 mg, twice daily) vs placebo administered intravenously in cases of pure or mixed metabolic alkalosis, initiated within 48 hours of ICU admission and continued during the ICU stay for a maximum of 28 days. The primary outcome was the duration of invasive mechanical ventilation via endotracheal intubation or tracheotomy. Secondary outcomes included changes in arterial blood gas and respiratory parameters, weaning duration, adverse events, use of noninvasive ventilation after extubation, successful weaning, the duration of ICU stay, and in-ICU mortality. Among 382 randomized patients, 380 (mean age, 69 years; 272 men [71.6%]; 379 [99.7%] with endotracheal intubation) completed the study. For the acetazolamide group (n = 187), compared with the placebo group (n = 193), no significant between-group differences were found for median duration of mechanical ventilation (-16.0 hours; 95% CI, -36.5 to 4.0 hours; P = .17), duration of weaning off mechanical ventilation (-0.9 hours; 95% CI, -4.3 to 1.3 hours; P = .36), daily changes of minute-ventilation (-0.0 L/min; 95% CI, -0.2 to 0.2 L/min; P = .72), or partial carbon-dioxide pressure in arterial blood (-0.3 mm Hg; 95% CI, -0.8 to 0.2 mm

Mixed acid-base disorder secondary to topiramate use in traumatic brain injury

Directory of Open Access Journals (Sweden)

S Golla

2016-01-01

Full Text Available We report a case of a man with traumatic brain injury. He was started on to prophylactic topiramate which led to a mixed acid-base disorder. He had severe metabolic acidosis secondary to renal tubular acidification defect and respiratory alkalosis secondary to hyperventilation. Withdrawal of the offending drug led to the prompt resolution of the acid-base disturbance.

JPRS Report, Science & Technology, USSR: Space Biology & Aerospace Medicine, Vol. 21, No. 6, November-December 1987.

Science.gov (United States)

1988-03-11

that regulation of blood clotting under hypoxic conditions is consistent with tissular metabolism. Thus, tissue hypoxia and respiratory alkalosis ...79 Effect of Oxygen Inhalation on Respiratory Function During Exercise and Exposure to Added Resistance to Respiration 86 Polar Work Adaptability...cardiovascular, respiratory , digestive, ner- vous and endocrine systems, system of immune defense and metabolic processes. The first phase of the

Respiratory Adaptations in Acid-base Disturbances: Role of Cerebral Fluids,

Science.gov (United States)

1979-06-19

The respiratory and metabolic components of acid-base homeostasis are defined. A quantitative empirical description of the (incomplete) mutual...literature. Respiratory adaptations in steady acid-base disturbances of metabolic origin (hyperventilation with hypocapnia in primary metabolic acidosis, and...hypoventilation with hypercapnia in metabolic alkalosis ) are analyzed as a function of the acidity of the cerebral fluids (cerebrospinal and cerebral interstitial fluid). (Author)

A 37-year-old Woman with Altered Mental Status and Urinary Frequency

Directory of Open Access Journals (Sweden)

Deepa Ravikumar

2013-03-01

Full Text Available We present a case report of a patient who initially presented with altered mental status andsignificant urinary frequency. Over the course of her emergency department stay, she thendeveloped tachycardia out of proportion to a new fever along with a respiratory alkalosis. Althougheach objective finding has a broad differential diagnosis, thyroid storm was the only unifyingdiagnosis when all findings were present.

Metabolic, respiratory, and cardiological measurements during exercise and rest

Science.gov (United States)

1971-01-01

Low concentration effects of CO2 on metabolic respiration and circulation were measured during work and at rest. The relationship between heart rate and metabolic rate is examined, as well as calibration procedures, and rate measurement during submaximal and standard exercise tests. Alterations in acid base and electrolytes were found during exhaustive exercise, including changes in ECG and metabolic alkalosis effects.

Hereditary and acquired abnormalities in erythrocyte phosphofructokinase activity: the close association with altered 2,3-diphosphoglycerate levels.

Science.gov (United States)

Tarui, S; Kono, N; Kuwajima, M; Kitani, T

1980-01-01

Specific deficiency of erythrocyte phosphofructokinase (PFK) activity in Type VII glycogenosis presents a good model for the analysis of the relationship between 2,3 diphosphoglycerate (2,3 DPG) level and glycolysis in erythrocytes since glycolytic flow is partially blocked at the regulatory step. Enzymatic analyses of glycolytic intermediates of erythrocytes from a patient with Type VII glycogenosis demonstrated that 2,3 DPG is markedly decreased in parallel with fructose-1,6-phosphate (FDP). In acidosis including diabetic ketoacidosis and uremic acidosis a fall in 2,3 DPG is also associated with a marked reduction in FDP. On the other hand, in respiratory alkalosis glycolytic intermediates shift to the opposite direction and forward crossover at PFK step appears, being associated with an elevation of 2,3 DPG. These data indicate a close relationship between 2,3 DPG level and PFK activity in erythrocytes. At least in acidosis and alkalosis the alteration in 2,3 DPG level may well be explained by changes in PFK activity caused mainly through allosteric mechanism. In addition, twelve cases with hereditary PFK deficiency in muscle and erythrocytes reported in the world are reviewed and discussed briefly.

Treatment with 17-allylamino-17-demethoxygeldanamycin ameliorated symptoms of Bartter syndrome type IV caused by mutated Bsnd in mice.

Science.gov (United States)

Nomura, Naohiro; Kamiya, Kazusaku; Ikeda, Katsuhisa; Yui, Naofumi; Chiga, Motoko; Sohara, Eisei; Rai, Tatemitu; Sakaki, Sei; Uchida, Shinich

2013-11-22

Mutations of BSND, which encodes barttin, cause Bartter syndrome type IV. This disease is characterized by salt and fluid loss, hypokalemia, metabolic alkalosis, and sensorineural hearing impairment. Barttin is the β-subunit of the ClC-K chloride channel, which recruits it to the plasma membranes, and the ClC-K/barttin complex contributes to transepithelial chloride transport in the kidney and inner ear. The retention of mutant forms of barttin in the endoplasmic reticulum (ER) is etiologically linked to Bartter syndrome type IV. Here, we report that treatment with 17-allylamino-17-demethoxygeldanamycin (17-AAG), an Hsp90 inhibitor, enhanced the plasma membrane expression of mutant barttins (R8L and G47R) in Madin-Darby canine kidney cells. Administration of 17-AAG to Bsnd(R8L/R8L) knock-in mice elevated the plasma membrane expression of R8L in the kidney and inner ear, thereby mitigating hypokalemia, metabolic alkalosis, and hearing loss. These results suggest that drugs that rescue ER-retained mutant barttin may be useful for treating patients with Bartter syndrome type IV. Copyright © 2013 Elsevier Inc. All rights reserved.

Plasma Catecholamines and Stress Assessment in Men Exposed to Moderate Altitudes.

Science.gov (United States)

1982-01-01

posure, as evidenced by a significant fall in PC02 and a respiratory alkalosis , was able to improve blood oxygenation. Heart rate did not fall with...Survey . . . . 21 Oxygen Content and P02 ...... .. ..... 33 Venous PCO2 :’" 33 Venous pH . .. . . . . . . .. 37 Respiratory Rate ............. ... 37 Blood...a 68 L. Venous PC02 Levels . ... .............. 69 M. Venous pH. . .9. . . . . . .. . . . . . . . . . . . 70 N. Respiratory Rates

Book Analysis of Arms and Insecurity in the Persian Gulf.

Science.gov (United States)

1988-04-01

AND P. Exercise induced changes in blood ammonia levels in humans. Eur. VANAmEE. Respiratory alkalosis accompanying ammonia toxicity. J. AppL PhysioL...HA. to ensure uniform exercise intensity. Respiratory gas exchange and ventilation during ex- Submaximal Exercise ercise were measured using a...BTPS, 02 consumption (Vo 2) and CO2 group. Relative exercise intensity (%Vo, mx) was not production converted to STPD, and respiratory exchange

Clinical Management of Heat-Related Illnesses

Science.gov (United States)

2012-01-01

from CNS impairment.18,41,102 Hyperventilation and elevation of Tco primarily lead to respiratory alkalosis , which in EHS may be masked by metabolic...acute phase.69,102,116 Other common disturbances during the acute phase occur in the gastrointestinal and respiratory systems. Gastrointestinal dys...acidosis as a result of increased glycolysis and hyperlacticacidemia.26,74 Hypoxemia may be present in patients with respiratory complica- tions

Effect of Six Days of Staging on Physiologic Adjustments and Acute Mountain Sickness During Ascent to 4300 Meters

Science.gov (United States)

2009-01-01

respiratory alkalosis due to hyperventilation that was partially compensated for by increased excretion of HCO3 to maintain a normal pH following...carbon dioxide; RER, respiratory exchange quotient; Sao2, arterial oxygen saturation; Paco2, partial pressure of capillary-arterialized carbon dioxide...dioxide production; E=O2, ventilatory equivalent for oxygen; E=CO2, ventilatory equivalent for carbon dioxide; RER, respiratory exchange quotient

High-Frequency Percussive Ventilation Revisited

Science.gov (United States)

2010-01-01

be implemented. ‡ Follow the reverse of the ventilation sequence if respiratory alkalosis develops—however, start at ventilation goal sequence 1 not at...High-frequency percussive ventilation (HFPV) has demonstrated a potential role as a rescue option for refractory acute respiratory distress syndrome...frequency percussive ventilation (HFPV) has demon- strated a potential role as a salvage option for refrac- tory acute respiratory distress syndrome

USSR and Eastern Europe Scientific Abstracts, Biomedical and Behavioral Sciences, Number 84

Science.gov (United States)

1977-12-28

disease is attributable to the constantly stressed compensa- tory forces, respiratory alkalosis and metabolic acidosis, low arterial pressure, and...34 cells decreases as compared with the "bottom" cells. The higher respiratory indices of the "top" cells indicate predominance of anaerobic energy...Russian, 10 Western. 48 USSR UDC 591.1+12 INFLUENCE OF VAGUS AFFERENTATION UPON THE RESPIRATORY CENTER DURING HYPERVENTILATION Moscow

Antenatal Bartter syndrome presenting as hyperparathyroidism with hypercalcemia and hypercalciuria: a case report and review.

Science.gov (United States)

Gross, Itai; Siedner-Weintraub, Yael; Simckes, Ari; Gillis, David

2015-07-01

Antenatal type I Bartter syndrome (ABS) is usually identified by the presence of polyhydramnios, premature delivery, hypokalemia, metabolic alkalosis, hypercalciuria, and nephrocalcinosis caused by mutations in the Na-K-2Cl cotransporter (NKCC2)-encoding SLC12A1 gene. In this report, we describe a novel presentation of this syndrome with hypercalcemic hypercalciuric hyperparathyroidism, and review the literature of the variable atypical presentations of ABS.

Renal abnormalities in congenital chloride diarrhea

International Nuclear Information System (INIS)

Al-Hamad, Nadia M.; Al-Eisa, Amal A.

2004-01-01

Congenital chloride diarrhea CLD is a rare autosomal recessive disorder caused by a defect in the chloride/ bicarbonate exchange in the ileum and colon. It is characterized by watery diarrhea, abdominal distension, hypochloremic hypokalemic metabolic alkalosis with high fecal content of chloride >90 mmol/l. We report 3 patients with CLD associated with various renal abnormalities including chronic renal failure secondary to renal hypoplasia, nephrocalcinosis and congenital nephrotic syndrome. (author)

Ultrasound-guided paravertebral block for pyloromyotomy in 3 neonates with congenital hypertrophic pyloric stenosis

OpenAIRE

Mata-Gómez, Javier; Guerrero-Domínguez, Rosana; García-Santigosa, Marta; Ontanilla, Antonio

2015-01-01

BACKGROUND AND OBJECTIVES: Hypertrophic pyloric stenosis is a relatively common affection of gastrointestinal tract in childhood that results in symptoms, such as projectile vomiting and metabolic disorders that imply a high risk of aspiration during anesthetic induction. In this way, the carrying out of a technique with general anesthesia and intravenous rapid sequence induction, preoxygenation and cricoid pressure are recommended. After the correction of systemic metabolic alkalosis and pH ...

Training Supplement Winter 2010 Journal of Special Operations Medicine. A Peer Reviewed Journal for SOF Medical Professionals

Science.gov (United States)

2010-01-01

Alkalinization agent for specific toxins (salicylates, phenobarbital) Dose: o 1mEq/kg IV Contraindications: o Metabolic or respiratory alkalosis o...cause of death from altitude illness. 2. Usually occurs above 8,000ft. Respiratory distress at high altitude is HAPE until proven otherwise. 3...HAPE since this will exacerbate symptoms. 5. Treat per Pain Management Protocol, but avoid the use of narcotics since they may depress respiratory

Military Nutrition Research.

Science.gov (United States)

1983-10-01

Hypophosphatemia was exaggerated, possibly because of respiratory alkalosis . Phosphate losses in urine and sweat were minimal, preventing appreciable loss... respiratory gases, the newer modifications for simplification of the measurements, and the total errors that are anticipated in its use. Data are presented... respiratory requirements at the altitude of the V icecap (7,000 feet) with that of sea level (actually 165 feet). (3) Energy metabolism was measured for

Effects of a Taser: Conducted Energy Weapon on the Circulating Red-Blood-Cell Population and Other Factors in Sus scrofa

Science.gov (United States)

2013-03-30

changes had not been used in previous CEW studies. In the present studies, in addition to standard measurements (including heart and respiratory rates...our study favoring either young or old RBCs being released from the spleen is unknown. Since alkalosis (rather than acidosis) tends to result in...cardiovascular, respiratory , and metabolic effects of a long duration electronic control device exposure in human volunteers. Forensic Sci Med Pathol. 2010;6

Bench-to-bedside review: Treating acid–base abnormalities in the intensive care unit – the role of renal replacement therapy

OpenAIRE

Naka, Toshio; Bellomo, Rinaldo

2004-01-01

Acid–base disorders are common in critically ill patients. Metabolic acid–base disorders are particularly common in patients who require acute renal replacement therapy. In these patients, metabolic acidosis is common and multifactorial in origin. Analysis of acid–base status using the Stewart–Figge methodology shows that these patients have greater acidemia despite the presence of hypoalbuminemic alkalosis. This acidemia is mostly secondary to hyperphosphatemia, hyperlactatemia, and the accu...

Bartter's and Gitelman's syndromes: from gene to clinic

OpenAIRE

Naesens, Maarten; STEELS, Paul; Verberckmoes, René; Vanrenterghem, Yves; Kuypers, Dirk

2004-01-01

Bartter's and Gitelman's syndromes are characterized by hypokalemia, normal to low blood pressure and hypochloremic metabolic alkalosis. Recently, investigators have been able to demonstrate mutations of six genes encoding several renal tubular transporters and ion channels that can be held responsible for Bartter's and Gitelman's syndromes. Neonatal Bartter's syndrome is caused by mutations of NKCC2 or ROMK, classic Bartter's syndrome by mutations of ClC-Kb, Bartter's syndrome associated wit...

Nephrocalcinosis as adult presentation of Bartter syndrome type II.

Science.gov (United States)

Huang, L; Luiken, G P M; van Riemsdijk, I C; Petrij, F; Zandbergen, A A M; Dees, A

2014-02-01

Bartter syndrome consists a group of rare autosomal-recessive renal tubulopathies characterised by renal salt wasting, hypokalaemic metabolic alkalosis, hypercalciuria and hyperreninaemic hyperaldosteronism. It is classified into five types. Mutations in the KCNJ1 gene (classified as type II) usually cause the neonatal form of Bartter syndrome. We describe an adult patient with a homozygous KCNJ1 mutation resulting in a remarkably mild phenotype of neonatal type Bartter syndrome.

Association of Amelogenesis Imperfecta and Bartter's Syndrome.

Science.gov (United States)

Kumar, A C V; Alekya, V; Krishna, M S V V; Alekya, K; Aruna, M; Reddy, M H K; Sangeetha, B; Ram, R; Kumar, V S

2017-01-01

Bartter's syndrome is an autosomal recessive renal tubular disorder characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninemia with normal blood pressure. Bartter's syndrome is associated with hypercalciuria and nephrocalcinosis. Amelogenesis imperfecta (AI) is a group of hereditary disorders that affect dental enamel. AI could be part of several syndromes. The enamel renal syndrome is the association of AI and nephrocalcinosis. We report two patients of AI with Bartter's syndrome.

Calcium Unresponsive Hypocalcemic Tetany: Gitelman Syndrome with Hypocalcemia

Directory of Open Access Journals (Sweden)

Madhav Desai

2013-01-01

Full Text Available Introduction. Gitelman’s syndrome (GS is autosomal recessive renal tubular disorder characterized by hypokalemia, hypomagnesemia, hypocalciuria, metabolic alkalosis, and hyperreninemic hyperaldosteronism. It is usually associated with normal serum calcium. We report a patient presented with hypocalcemic tetany, and evaluation showed Gitelman’s syndrome with hypocalcemia. Case Report. A 28-year-old woman presented with cramps of the arms, legs, fatigue, and carpal spasms of one week duration. She has history of similar episodes on and off for the past two years. Her blood pressure was 98/66 mmHg. Chvostek’s sign and Trousseau’s sign were positive. Evaluation showed hypokalemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. Self-medication, diuretic use, laxative abuse, persistent vomiting, and diarrhoea were ruled out. Urinary prostaglandins and genetic testing could not be done because of nonavailability. To differentiate Gitelman syndrome from Bartter’s syndrome (BS, thiazide loading test was done. It showed blunted fractional chloride excretion. GS was confirmed and patient was treated with spironolactone along with magnesium, calcium, and potassium supplementation. Symptomatically, she improved and did not develop episodes of tetany again. Conclusion. In tetany patient along with serum calcium measurement, serum magnesium, serum potassium, and arterial blood gases should be measured. Even though hypocalcemia in Gitelman syndrome is rare, it still can occur.

The Role of Sodium Bicarbonate in the Management of Some Toxic Ingestions

Directory of Open Access Journals (Sweden)

Aibek E. Mirrakhimov

2017-01-01

Full Text Available Adverse reactions to commonly prescribed medications and to substances of abuse may result in severe toxicity associated with increased morbidity and mortality. According to the Center for Disease Control, in 2013, at least 2113 human fatalities attributed to poisonings occurred in the United States of America. In this article, we review the data regarding the impact of systemic sodium bicarbonate administration in the management of certain poisonings including sodium channel blocker toxicities, salicylate overdose, and ingestion of some toxic alcohols and in various pharmacological toxicities. Based on the available literature and empiric experience, the administration of sodium bicarbonate appears to be beneficial in the management of a patient with the above-mentioned toxidromes. However, most of the available evidence originates from case reports, case series, and expert consensus recommendations. The potential mechanisms of sodium bicarbonate include high sodium load and the development of metabolic alkalosis with resultant decreased tissue penetration of the toxic substance with subsequent increased urinary excretion. While receiving sodium bicarbonate, patients must be monitored for the development of associated side effects including electrolyte abnormalities, the progression of metabolic alkalosis, volume overload, worsening respiratory status, and/or worsening metabolic acidosis. Patients with oliguric/anuric renal failure and advanced decompensated heart failure should not receive sodium bicarbonate.

Population pharmacodynamic modeling and simulation of the respiratory effect of acetazolamide in decompensated COPD patients.

Directory of Open Access Journals (Sweden)

Nicholas Heming

Full Text Available Chronic obstructive pulmonary disease (COPD patients may develop metabolic alkalosis during weaning from mechanical ventilation. Acetazolamide is one of the treatments used to reverse metabolic alkalosis.619 time-respiratory (minute ventilation, tidal volume and respiratory rate and 207 time-PaCO2 observations were obtained from 68 invasively ventilated COPD patients. We modeled respiratory responses to acetazolamide in mechanically ventilated COPD patients and then simulated the effect of increased amounts of the drug.The effect of acetazolamide on minute ventilation and PaCO2 levels was analyzed using a nonlinear mixed effect model. The effect of different ventilatory modes was assessed on the model. Only slightly increased minute ventilation without decreased PaCO2 levels were observed in response to 250 to 500 mg of acetazolamide administered twice daily. Simulations indicated that higher acetazolamide dosage (>1000 mg daily was required to significantly increase minute ventilation (P0.75 L min(-1 in 60% of the population. The model also predicts that 45% of patients would have a decrease of PaCO2>5 mmHg with doses of 1000 mg per day.Simulations suggest that COPD patients might benefit from the respiratory stimulant effect after the administration of higher doses of acetazolamide.

Gitelman′s syndrome presenting with hypocalcemic tetany and hypokalemic periodic paralysis

Directory of Open Access Journals (Sweden)

Kunal Gandhi

2016-01-01

Full Text Available Gitelman′s syndrome is an autosomal recessive renal tubular disorder characterized by hypomagnesemia, hypokalemia, hypocalciuria, and metabolic alkalosis. Hypocalcemic tetany as a presentation of Gitelman′s syndrome has rarely been reported in literature. We report a rare case of Gitelman′s syndrome presenting with hypocalcemic tetany along with hypokalemic periodic paralysis. A 17-year-old female was admitted to our hospital with a history of perioral numbness and carpal spasms of five days duration with progressive quadriparesis developing over a period of few hours. Past history was significant for three episodes of transient lower limb weakness. On examination, blood pressure was 110/70 mm Hg. Chvostek′s sign and Trousseau′s sign were positive. Neurologically, she was fully oriented. She had Grade 3 power in all the four limbs with intact sensation. Laboratory tests showed hypocalcemia (7.8 mg/dL, hypokalemia (2.2 mEq/L, hypomagnesemia (0.9 mEq/L, and hypocalciuria (104 mg/day. Arterial blood gas showed mild metabolic alkalosis with respiratory compensation. Thus, a clinical diagnosis of GS was made. The patient made a remarkable recovery after the correction of electrolyte imbalance. The aim of this case report is to re-emphasize the fact that hypocalcemia can rarely occur in Gitelman′s syndrome.

Treatment of heartwater : potential adverse effects of furosemide administration on certain homeostatic parameters in normal sheep

Directory of Open Access Journals (Sweden)

A.S. Shakespeare

1998-07-01

Full Text Available Diuretics, in particular furosemide, are generally recommended as a supportive treatment in the advanced stages of heartwater in ruminants. However, after what appeared to be possible adverse effects accompanying its use in field cases of heartwater, the effects of this drug on certain blood and urine parameters were investigated in normal sheep at the same dose rates. Diuresis with concomitant natriuresis was significant after furosemide administration, as was the expected plasma volume decrease. Other significant changes included metabolic alkalosis, hypokalaemia and reduced blood ionised calcium. The difference in duration of the diuretic effect and the duration of the changes in blood parameters from c. 3 h and c. 6 h respectively make it difficult to determine a time interval between successive treatments with furosemide. It appears that the probable cause of death of sheep with heartwater is a drastic reduction in blood volume and decreased cardiac output that leads to general circulatory failure. A therapeutic approach that involves further loss of plasma volume due to diuresis appears contradictory. The added effects of potentiating respiratory alkalosis and the terminal drop in blood ionised calcium seen in heartwater-affected animals indicate that the use of furosemide in supportive treatment of this disease is not warranted.

[Clinical analysis of 6 cases of Bartter syndrome].

Science.gov (United States)

Yin, Fang-mei; Zheng, Fang-qiu; Zhang, Xin; Wu, Mei-jun; Wei, Hong-yan; Ma, Zhong-shu; Lu, Biao; Qiu, Ming-cai

2011-03-01

To summarize the clinical characteristics of Bartter syndrome and investigate its pathogenesis. The clinical data of 6 cases of Bartter syndrome at our hospital from November 2006 to May 2010 were analyzed retrospectively. The onset age of Bartter syndrome was 13-35 years old. The main symptoms included weakness (6/6), paralysis (1/6), numbness (5/6) and tetany (4/6). All patients had normal blood pressure. The biochemical tests showed persistent hypokalemia, metabolic alkalosis (6/6) and hyperreninemia. The pathological examination of deltoid muscle biopsy showed the swelling, degeneration and necrosis of myocytes and the deposition of immunocomplex in myolemma. And the pathological examination of renal biopsy showed the hyperplasia of juxtaglomerular apparatus (5/6) and the deposition of immunocomplex. All symptoms were relieved after a therapy of potassium supplementation or a combination of indomethacin, spironolactone and immunosuppressant. When such clinical features as weakness, paralysis, tetany, hypokalemic alkalosis and normotension are encountered, Bartter syndrome should be suspected. Serum electrolytes, blood gas analysis and activation of the renin-angiotensin-aldosterone system should be examined for a definite diagnosis. The treatment of choice includes potassium and magnesium supplementation or in combination with prostaglandin synthetase inhibitor, aldosterone antagonist and immunosuppressant. Immunologic mechanism may participate in the course of Bartter syndrome.

Cystinosis presenting with findings of Bartter syndrome.

Science.gov (United States)

Özkan, Behzat; Çayır, Atilla; Koşan, Celalettin; Alp, Handan

2011-01-01

A five-year-old boy was referred to our pediatric clinic for evaluation of failure to thrive, headache, intermittent high fever, restlessness, polyuria, and polydipsia. His weight and height measurements were under the 3rd percentile. Clinical findings consisted of frontal bossing, carious teeth, O-bain deformity of the lower extremities, and moderate dehydration. The presence of metabolic alkalosis, hypokalemia, hypochloremia, and high renin and aldosterone levels were suggestive of Bartter syndrome and a treatment regimen for Bartter syndrome was started. At follow-up, the polyuria and hyponatremia were found to persist. A reassessment of the patient revealed findings consistent with proximal renal tubular acidosis such as metabolic acidosis with a high urinary pH, proteinuria, aminoaciduria with phosphaturia and hypercalciuria. Based on the presence of parental consanguinity as well as polyuria, proteinuria, low tubular reabsorption of phosphorus, generalized aminoaciduria, light yellow skin and hair color, the probable diagnosis of cystinosis was established and was confirmed by slit-lamp examination of the cornea showing cystine crystal deposition. Our case is a good example demonstrating that development of metabolic alkalosis does not exclude cystinosis and that all findings of the patient should be thoroughly evaluated. ©Journal of Clinical Research in Pediatric Endocrinology, Published by Galenos Publishing.

A novel CLCN5 mutation in a boy with Bartter-like syndrome and partial growth hormone deficiency.

Science.gov (United States)

Bogdanović, Radovan; Draaken, Markus; Toromanović, Alma; Dordević, Maja; Stajić, Natasa; Ludwig, Michael

2010-11-01

Dent disease is an X-linked recessive disorder affecting the proximal tubule and is characterized by low-molecular-weight proteinuria (LMWP), hypercalciuria, nephrocalcinosis/nephrolithiasis with a variable number of features of Fanconi syndrome. It is most often associated with mutations in CLCN5, which encodes the endosomal electrogenic chloride/proton exchanger ClC-5. Renal acidification abnormalities are only rarely seen in Dent disease, whereas the hypokalemic metabolic alkalosis associated with hyperreninemic hyperaldosteronism (Bartter-like syndrome) has been reported in only one patient so far. We report on a 5-year-old boy with Dent disease caused by mutation in CLCN5 gene, c.1073G>A, who presented with hypokalemic metabolic alkalosis and hyperreninemic hyperaldosteronism persisting over the entire follow-up. No mutations were found in NKCC2, ROMK, NCCT, or ClC-Kb genes. In addition, the patient exhibited growth failure associated with partial growth hormone (GH) deficiency. Coexistence of Bartter-like syndrome features with LMWP should prompt a clinician to search for Dent disease. The Bartter syndrome phenotype seen in Dent disease patients may represent a distinct form of Bartter syndrome, the exact mechanism of which has yet to be fully elucidated. Growth delay that persists in spite of appropriate therapy should raise suspicion of other causes, such as GH deficiency.

The Role of Sodium Bicarbonate in the Management of Some Toxic Ingestions.

Science.gov (United States)

Mirrakhimov, Aibek E; Ayach, Taha; Barbaryan, Aram; Talari, Goutham; Chadha, Romil; Gray, Adam

2017-01-01

Adverse reactions to commonly prescribed medications and to substances of abuse may result in severe toxicity associated with increased morbidity and mortality. According to the Center for Disease Control, in 2013, at least 2113 human fatalities attributed to poisonings occurred in the United States of America. In this article, we review the data regarding the impact of systemic sodium bicarbonate administration in the management of certain poisonings including sodium channel blocker toxicities, salicylate overdose, and ingestion of some toxic alcohols and in various pharmacological toxicities. Based on the available literature and empiric experience, the administration of sodium bicarbonate appears to be beneficial in the management of a patient with the above-mentioned toxidromes. However, most of the available evidence originates from case reports, case series, and expert consensus recommendations. The potential mechanisms of sodium bicarbonate include high sodium load and the development of metabolic alkalosis with resultant decreased tissue penetration of the toxic substance with subsequent increased urinary excretion. While receiving sodium bicarbonate, patients must be monitored for the development of associated side effects including electrolyte abnormalities, the progression of metabolic alkalosis, volume overload, worsening respiratory status, and/or worsening metabolic acidosis. Patients with oliguric/anuric renal failure and advanced decompensated heart failure should not receive sodium bicarbonate.

Simulation Crisis Team Training Effect on Rural Hospital Safety Climate (SIMCRITTER)

Science.gov (United States)

2008-09-01

showed sinus tachycardia. ABG showed a mild respiratory and metabolic alkalosis , with adequate oxygenation on 6 liters nasal cannula. The chest x-ray is...Total Attending / Staff Physician 5 1.37% Physician In Training 0 0.00% Pharmacist 0 0.00% Respiratory Therapist 9 2.47% PT / OT / Speech 12 3.29...groups (e.g., nurses, physicians, and respiratory therapists). The unique aspects of the proposed project included the application of high-fidelity

A Stress Test to Evaluate the Physical Capacity of Performing L-1 Anti-G Straining Maneuvers

Science.gov (United States)

1988-09-01

similar to hyperventilation can produce respiratory alkalosis . Therefore, lowered G-tolerance may result from decreased cerebral blood flow. Another...VE), respiratory exchange ratio (RER) and heart rate (HR were determined for steady state exercise at AGSM duty cyclEs cf 2,, 215%, 33% and 50%. Thesc...V02, ml/kg/min), minute pulmonary ventilation (VE, I/min) and respiratory exchange ratio (RER, VCO 2/VO2) at each duty cycle of discontinuous AGSM

The United States Army Medical Department Journal. January-March 2013

Science.gov (United States)

2013-01-01

HEATSTROKE IN A MILITARY WORKING DOG January – March 2013 37 THE ARMY MEDICAL DEPARTMENT JOURNAL Respiratory alkalosis can develop as a result of...dropped to 99.1ºF within 35 minutes after presentation, and the pulse and respiratory rate normalized. The mu- cous membranes were pink, but tacky. The MWD...throughout the body, including blood cells, myocardium, skeletal muscle, soft tissues, and cells of the respiratory and nervous systems.5 Venom

VatuximabTM: Optimizing Therapeutic Strategies for Prostate Cancer Based on Dynamic MR Tumor Oximetry

Science.gov (United States)

2007-12-01

Ca2+ and pH in shaping myocardial contractile response to acute respiratory alkalosis , Am. J. Physiol. 265 (1993) H1696–1703. [313] H.L. Kirschenlohr...respect to growth and respiratory challenge. Int. J. Radiat. Oncol. Biol. Phys., 53: 744-756, 2002. 9. Zhao, D., Ran, S., Constantinescu, A., Hahn... respiratory challenge monitored with three oxygen-sensitive parameters. Applied Optics, 42, 2960-2967 (2003) 28. Brurberg, K. G., H. K. Skogmo, B. A. Graff

Quantified pH imaging with hyperpolarized 13C‐bicarbonate

DEFF Research Database (Denmark)

Scholz, David Johannes; Janich, Martin A.; Köllisch, Ulrich

2015-01-01

for various flip angles for bicarbonate (BiC) and CO2 with spectral‐spatial excitation and spiral readout in healthy Lewis rats in five slices. Acute subcutaneous sterile inflammation was induced with Concanavalin A in the right leg of Buffalo rats. pH and proton images were measured 2 h after induction...... and interpreted within inflammation and acute metabolic alkalosis models. Magn Reson Med 73:2274–2282, 2015. © 2014 Wiley Periodicals, Inc....

Classic Bartter syndrome: a rare cause of failure to thrive in a child

OpenAIRE

Vieira, Helena; Mendes, Leonor; Mendes, Patricia; da Silva, José Esteves

2012-01-01

Bartter syndrome is a group of rare autosomal-recessive disorders caused by a defect in distal tubule transport of sodium and chloride. Blood gases and plasma electrolytes raise suspicion of this diagnosis and the definitive diagnosis is made by genetic study. Early treatment improves prognosis. The authors present the case of an 11-month-old child with early failure to thrive and severe regurgitation. Blood gases revealed hypochloraemic metabolic alkalosis, hyponatraemia and hypokalaemia. Bl...

Acquired Bartter syndrome following gentamicin therapy.

Science.gov (United States)

Singh, J; Patel, M L; Gupta, K K; Pandey, S; Dinkar, A

2016-01-01

Aminoglycoside nephrotoxicity may manifest as nonoliguric renal failure or tubular dysfunction, such as Fanconi-like syndrome, Bartter-like syndrome (BS), or distal renal tubular acidosis. We report a case who developed severe renal tubular dysfunction on the the 7 th day of gentamicin therapy, resulting in metabolic alkalosis, refractory hypokalemia, hypocalcemia, hypomagnesemia, and polyuria. The patient was diagnosed as a case of transient BS associated with gentamicin exposure. The patient recovered with conservative management.

Association of amelogenesis imperfecta and Bartter's syndrome

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A. C. V. Kumar

2017-01-01

Full Text Available Bartter's syndrome is an autosomal recessive renal tubular disorder characterized by hypokalemia, hypochloremia, metabolic alkalosis, and hyperreninemia with normal blood pressure. Bartter's syndrome is associated with hypercalciuria and nephrocalcinosis. Amelogenesis imperfecta (AI is a group of hereditary disorders that affect dental enamel. AI could be part of several syndromes. The enamel renal syndrome is the association of AI and nephrocalcinosis. We report two patients of AI with Bartter's syndrome.

[Meeting point Stewart. Buffer bases, base excess and strong ions].

Science.gov (United States)

Lang, W

2007-04-01

Development of a two-buffer model which simulates the acid-base properties of blood and allows comparison of the different acidbase concepts according to Stewart and to Siggaard-Andersen. The two-buffer model consisted of different aqueous solutions of bicarbonate/CO(2) (pCO(2), sCO(2), pK(1)), HEPES buffer (A(tot), pK(a)) and electrolytes. These were used to calculate the pH from the independent variables according to Stewart - strong ion difference (SID), pCO(2) and total concentration of the weak acids (A(tot)) - from which all other dependent variables (cHCO(3)(-), cA(-), BB, BE) were obtained and compared with the measured values. The normal pH (7.408) was calculated from the normal values for SID (48 mmol/l), pCO(2) (40 mmHg) and A(tot) (45.2 mmol/l) and agreed perfectly with the measured value (7.409+/-0.001). This was also valid for all calculated and measured pH values when the SID was varied: non-respiratory alkalosis ( upward arrow) or acidosis ( downward arrow), pCO(2):respiratory acidosis ( upward arrow) or alkalosis ( downward arrow) and A(tot):hyperproteinemic acidosis ( upward arrow) or hypoproteinemic alkalosis ( downward arrow) were varied and the sum of the buffer bases (BB) was always equal to the SID. All changes and hence BE were also equal, providing that A(tot) was normal. This was not the case, however, if A(tot) was outside the normal range, when BE was then the difference from the normal BB at the respective reference point. Whereas the deviation of the measured pCO(2) was acceptable (1.74+/-0.86 mmHg), this was not the case for the SID (-6.18+/-3.58 mmol/l) calculated from the measured ion concentrations (Na, K, Ca, Cl). Despite controversial discussions, both concepts are much closer than might be expected. Whereas in the Stewart approach the focus of analysis is on plasma, with the Siggaard-Andersen approach it is on blood. Hence, a combined analysis of the blood gases (pH, pCO(2), pO(2), sO(2), cHb, BE) and of the strong ion gap (SIG

A Clinical Approach to the Diagnosis of Acid-Base Disorders

OpenAIRE

Bear, Robert A.

1986-01-01

The ability to diagnose and manage acid-base disorders rapidly and effectively is essential to the care of critically ill patients. This article presents an approach to the diagnosis of pure and mixed acid-base disorders, metabolic or respiratory. The approach taken is based on using the law of mass-action equation as it applies to the bicarbonate buffer system (Henderson equation), using sub-classifications for diagnostic purposes of causes of metabolic acidosis and metabolic alkalosis, and ...

Acquired Bartter syndrome following gentamicin therapy

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J Singh

2016-01-01

Full Text Available Aminoglycoside nephrotoxicity may manifest as nonoliguric renal failure or tubular dysfunction, such as Fanconi-like syndrome, Bartter-like syndrome (BS, or distal renal tubular acidosis. We report a case who developed severe renal tubular dysfunction on the the 7 th day of gentamicin therapy, resulting in metabolic alkalosis, refractory hypokalemia, hypocalcemia, hypomagnesemia, and polyuria. The patient was diagnosed as a case of transient BS associated with gentamicin exposure. The patient recovered with conservative management.

Unusual case of failure to thrive: Type III Bartter syndrome.

Science.gov (United States)

Agrawal, S; Subedi, K; Ray, P; Rayamajhi, A

2016-09-01

Bartter syndrome Type III is a rare autosomal recessive disorder resulting from an inherited defect in the thick ascending limb of the loop of henle of the nephrons in kidney. The typical clinical manifestations in childhood are failure to thrive and recurrent episodes of vomiting. Typical laboratory findings which help in the diagnosis are hypokalemic metabolic alkalosis, hypomagnesemia and hypercalciuria. We report a case of Type III Bartter syndrome not responding to repeated conventional treatment of failure to thrive.

Status epilepticus as the only presentation of the neonatal Bartter syndrome.

Science.gov (United States)

Patra, Soumya; Konar, Mithun C; Basu, Rajarshi; Khaowas, Ajoy K; Dutta, Soumyadeep; Sarkar, Debanjali

2012-03-01

Bartter syndrome is a rare hereditary (autosomal recessive) salt-losing tubulopathy characterized by hypokalemia, hypochloremia, metabolic alkalosis, and normal blood pressure with hyperreninemia, The underlying renal abnormality results in excessive urinary losses of sodium, chloride, and potassium. We report a case of a four-month-old infant with neonatal Bartter syndrome, who presented only with status epilepticus. To the best of our present knowledge, there is no reported case of Bartter syndrome who presented with status epilepticus.

Quantified pH imaging with hyperpolarized (13) C-bicarbonate.

Science.gov (United States)

Scholz, David Johannes; Janich, Martin A; Köllisch, Ulrich; Schulte, Rolf F; Ardenkjaer-Larsen, Jan H; Frank, Annette; Haase, Axel; Schwaiger, Markus; Menzel, Marion I

2015-06-01

Because pH plays a crucial role in several diseases, it is desirable to measure pH in vivo noninvasively and in a spatially localized manner. Spatial maps of pH were quantified in vitro, with a focus on method-based errors, and applied in vivo. In vitro and in vivo (13) C mapping were performed for various flip angles for bicarbonate (BiC) and CO2 with spectral-spatial excitation and spiral readout in healthy Lewis rats in five slices. Acute subcutaneous sterile inflammation was induced with Concanavalin A in the right leg of Buffalo rats. pH and proton images were measured 2 h after induction. After optimizing the signal to noise ratio of the hyperpolarized (13) C-bicarbonate, error estimation of the spectral-spatial excited spectrum reveals that the method covers the biologically relevant pH range of 6 to 8 with low pH error (< 0.2). Quantification of pH maps shows negligible impact of the residual bicarbonate signal. pH maps reflect the induction of acute metabolic alkalosis. Inflamed, infected regions exhibit lower pH. Hyperpolarized (13) C-bicarbonate pH mapping was shown to be sensitive in the biologically relevant pH range. The mapping of pH was applied to healthy in vivo organs and interpreted within inflammation and acute metabolic alkalosis models. © 2014 Wiley Periodicals, Inc.

Ultrasound-guided paravertebral block for pyloromyotomy in 3 neonates with congenital hypertrophic pyloric stenosis

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Javier Mata-Gómez

2015-08-01

Full Text Available BACKGROUND AND OBJECTIVES: Hypertrophic pyloric stenosis is a relatively common affection of gastrointestinal tract in childhood that results in symptoms, such as projectile vomiting and metabolic disorders that imply a high risk of aspiration during anesthetic induction. In this way, the carrying out of a technique with general anesthesia and intravenous rapid sequence induction, preoxygenation and cricoid pressure are recommended. After the correction of systemic metabolic alkalosis and pH normalization, cerebrospinal fluid can keep a state of metabolic alkalosis. This circumstance, in addition to the residual effect of neuromuscular blocking agents, inhalant anesthetics and opioids could increase the risk of postoperative apnea after a general anesthesia.CASE REPORT: We present the successful management in 3 neonates in those a pyloromyotomy was carried out because they had presented congenital hypertrophic pyloric stenosis. This procedure was done under general anesthesia with orotracheal intubation and rapid sequence induction. Then, ultrasound-guided paravertebral block was performed as analgesic method without the need for administrating opioids within intraoperative period and keeping an appropriate analgesic level.CONCLUSIONS: Local anesthesia has demonstrated to be safe and effective in pediatric practice. We consider the ultrasound-guided paravertebral block with one dose as a possible alternative for other local techniques described, avoiding the use of opioids and neuromuscular blocking agents during general anesthesia, and reducing the risk of central apnea within postoperative period.

Do over 200 million healthy altitude residents really suffer from chronic Acid-base disorders?

Science.gov (United States)

Zubieta-Calleja, Gustavo; Zubieta-Castillo, Gustavo; Zubieta-Calleja, Luis; Ardaya-Zubieta, Gustavo; Paulev, Poul-Erik

2011-01-01

As the oxygen tension of inspired air falls with increasing altitude in normal subjects, hyperventilation ensues. This acute respiratory alkalosis, induces increased renal excretion of bicarbonate, returning the pH back to normal, giving rise to compensated respiratory alkalosis or chronic hypocapnia. It seems a contradiction that so many normal people at high altitude should permanently live as chronic acid-base patients. Blood gas analyses of 1,865 subjects at 3,510 m, reported a P(a)CO(2) (arterial carbon dioxide tension ± SEM) = 29.4 ± 0.16 mmHg and pH = 7.40 ± 0.005. Base excess, calculated with the Van Slyke sea level equation, is -5 mM (milliMolar or mmol/l) as an average, suggesting chronic hypocapnia. THID, a new term replacing "Base Excess" is determined by titration to a pH of 7.40 at a P(a)CO(2) of 5.33 kPa (40 mmHg) at sea level, oxygen saturated and at 37°C blood temperature. Since our new modified Van Slyke equations operate with normal values for P(a)CO(2) at the actual altitude, a calculation of THID will always result in normal values-that is, zero.

Alkali-treated titanium selectively regulating biological behaviors of bacteria, cancer cells and mesenchymal stem cells.

Science.gov (United States)

Li, Jinhua; Wang, Guifang; Wang, Donghui; Wu, Qianju; Jiang, Xinquan; Liu, Xuanyong

2014-12-15

Many attentions have been paid to the beneficial effect of alkali-treated titanium to bioactivity and osteogenic activity, but few to the other biological effect. In this work, hierarchical micro/nanopore films were prepared on titanium surface by acid etching and alkali treatment and their biological effects on bacteria, cancer cells and mesenchymal stem cells were investigated. Gram-positive Staphylococcus aureus, Gram-negative Escherichia coli, and human cholangiocarcinoma cell line RBE were used to investigate whether alkali-treated titanium can influence behaviors of bacteria and cancer cells. Responses of bone marrow mesenchymal stem cells (BMMSCs) to alkali-treated titanium were also subsequently investigated. The alkali-treated titanium can potently reduce bacterial adhesion, inhibit RBE and BMMSCs proliferation, while can better promote BMMSCs osteogenesis and angiogenesis than acid-etched titanium. The bacteriostatic ability of the alkali-treated titanium is proposed to result from the joint effect of micro/nanotopography and local pH increase at bacterium/material interface due to the hydrolysis of alkali (earth) metal titanate salts. The inhibitory action of cell proliferation is thought to be the effect of local pH increase at cell/material interface which causes the alkalosis of cells. This alkalosis model reported in this work will help to understand the biologic behaviors of various cells on alkali-treated titanium surface and design the intended biomedical applications. Copyright © 2014 Elsevier Inc. All rights reserved.

Status epilepticus as the only presentation of the neonatal Bartter syndrome

Directory of Open Access Journals (Sweden)

Soumya Patra

2012-01-01

Full Text Available Bartter syndrome is a rare hereditary (autosomal recessive salt-losing tubulopathy characterized by hypokalemia, hypochloremia, metabolic alkalosis, and normal blood pressure with hyperreninemia, The underlying renal abnormality results in excessive urinary losses of sodium, chloride, and potassium. We report a case of a four-month-old infant with neonatal Bartter syndrome, who presented only with status epilepticus. To the best of our present knowledge, there is no reported case of Bartter syndrome who presented with status epilepticus.

Anesthetic management of a patient with Bartter’s syndrome: A case report

Directory of Open Access Journals (Sweden)

Harun Aydoğan

2012-09-01

Full Text Available Bartter’s syndrome is a rare disorder characterized bysevere hypochloremic metabolic alkalosis, hypokalemia,hyponatremia, hyperaldosteronism, elevation in plasmarenin activity and insensitivity to angiotensin II. Electrolyteimbalances such as hypomagnesemia, hyponatremiamight make anesthetic management difficult in Barttersyndrome. A 4 years old patient underwent surgery foringuinal hernia with caudal anesthesia using bupivacaine0.25%. In this case report, it was aimed to discuss the anestheticmanagement of a patient with Bartter syndrome.Key words: Regional anesthesia, Bartter syndrome, inguinalhernia surgery, pediatric anesthesia

(/sup 11/C )-DMO for evaluation of regional tissue pH in patients with hemispheric infarction using positron emission tomography

Energy Technology Data Exchange (ETDEWEB)

Castaing, M; Syrota, A; Rougemont, D; Berridge, M; Chretien, L; Baron, J C; Bousser, M G

1983-06-01

Changes in brain intracellular pH resulting from cerebral infarction were evaluated using the /sup 11/C-DMO (dimethyloxazolidine-dione) method, in 9 patients. A /sup 15/O/sub 2/-C/sup 15/O/sub 2/ study was performed the day following the DMO examination in order to obtain the values of cerebral blood flow, oxygen extraction and oxygen metabolic rate in the same regions-of-interest. The results emphasized the relationship between tissue alkalosis and luxury perfusion during recent infarction.

[Disorders of the acid-base balance and the anion gap].

Science.gov (United States)

Kimmel, Martin; Alscher, Mark Dominik

2016-10-01

The regulation of the acid-base balance and pH is critical for the organism. The most important buffer system is CO 2 / HCO 3 - . The kidney controls systemic bicarbonate and therefore the metabolic regulation and the lung is relevant for respiratory regulation by an effective CO 2 elimination. There are four acid-base disorders with two metabolic and two respiratory disorders (acidosis and alkalosis). The anion gap enables a further workup of metabolic acidosis. © Georg Thieme Verlag KG Stuttgart · New York.

Neonatal Bartter syndrome with cholelithiasis and hydrocephalus: Rare association.

Science.gov (United States)

Özdemir, Özmert Ma; Çıralı, Ceren; Yılmaz Ağladıoğlu, Sebahat; Evrengül, Havva; Tepeli, Emre; Ergin, Hacer

2016-09-01

Neonatal Bartter syndrome (NBS) is a rare autosomal recessive renal tubular disorder. This disease is characterized by hypokalemia, hypochloremia, and metabolic alkalosis that is often associated with failure to thrive and recurrent episodes of dehydration. The combination of BS and cholelithiasis in an infant is very rare. Herein, we report a premature male infant with NBS who developed cholelithiasis and hydrocephalus on clinical follow up. We recommend that periodic routine hepatobiliary ultrasonograpic screening for cholelithiasis should be performed in patients with NBS. © 2016 Japan Pediatric Society.

Antenatal Bartter syndrome.

Science.gov (United States)

Afzal, Muhammad; Khan, Ejaz A; Khan, Wisal A; Anwar, Viqas; Yaqoob, Asma; Rafiq, Shahid; Azam, Shaheena

2014-05-01

Antenatal Bartter syndrome is characterized by severe polyhydramnios in mother leading to premature delivery. Antenatal treatment has proven effective to prevent these problems. Postnatally newborns suffer from recurrent episodes of severe dehydration and electrolyte imbalance which can lead to fatal outcome. These manifestations are likely to be overlooked and missed under the umbrella of diagnosis of prematurity. This premature newborn with antenatal polyhydramnios had severe manifestations of polyuria, recurrent dehydration, electrolyte derangements and metabolic alkalosis. She was managed accordingly but unfortunately could not survive beyond 4 weeks.

Clinical observations and acid-base imbalances in sheep during chronic copper poisoningAvaliação clínica e hemogasométrica de ovinos com intoxicação cúprica acumulativa

Directory of Open Access Journals (Sweden)

Clara Satsuk Mori

2011-08-01

Full Text Available Twelve male sheep were intoxicated with copper and four served as controls. When hemoglobinuria was first diagnosed, the poisoned sheep were randomly distributed into two groups: 4 untreated and 8 tetratiomolybdate-treated. Blood samples and clinical evaluation were performed daily, from the onset of poisoning until the 30th day. Analysis of packed cell volume, plasma free hemoglobin, and blood gas were made. Elevated heart rates and rectal temperature, and reduced respiratory and ruminal movement rates were recorded in the intoxicated group. The poisoned sheep developed mild alkalosis caused by bicarbonate retention, while a short-periodic increase of pCO2 occurred to compensate the ongoing alkalosis. Elevated degree of anemia was directly proportional to heart rate, while high degree of alkalosis was inversely proportional to respiratory rate. Further, there was an elevated positive relationship between plasma free hemoglobin and rectal temperature, and an increase in rectal temperature accompanied a reduced ruminal movement.Foram utilizados 16 cordeiros, sendo 12 submetidos à intoxicação cúprica e quatro animais controle. Quando foi verificada a presença de hemoglobinúria, os animais intoxicados foram aleatoriamente distribuídos em dois grupos, quatro animais não tratados e oito animais tratados com tetratiomolybidato de amônia. Foi realizado exame clínico e coleta de sangue diariamente desde o início da intoxicação até 30 dias após. Foram analisados o volume globular, concentração de hemoglobina plasmática e avaliação hemogasométrica. Nos animais intoxicados, foi observado elevação da freqüência cardíaca e da temperatura retal e redução da freqüência respiratória e dos movimentos ruminais. Os ovinos intoxicados desenvolveram alcalose moderada causada por retenção de bicarbonato seguido de um aumento pontual da pCO2 para compensar a alcalose em curso. Quanto maior o grau de anemia foi maior a freqüência card

The influence of sodium bicarbonate on maximal force and rates of force development in the triceps surae and brachii during fatiguing exercise.

Science.gov (United States)

Siegler, Jason C; Mudie, Kurt; Marshall, Paul

2016-11-01

What is the central question of this study? Does metabolic alkalosis in humans, induced by sodium bicarbonate, affect rates of skeletal muscle fatigue differentially in muscle groups composed predominately of slow- and fast-twitch fibres? What is the main finding and its importance? Sodium bicarbonate exhibited no effect on the fatigue profile observed between triceps surae and brachii muscle groups during and after 2 min of tetanic stimulation. For the first time in exercising humans, we have profiled the effect of sodium bicarbonate on the voluntary and involuntary contractile characteristics of muscle groups representative of predominately slow- and fast-twitch fibres. The effect of metabolic alkalosis on fibre-specific maximal force production and rates of force development (RFD) has been investigated previously in animal models, with evidence suggesting an improved capacity to develop force rapidly in fast- compared with slow-twitch muscle. We have attempted to model in vivo the fatigue profile of voluntary and involuntary maximal force and RFD in the triceps surae and brachii after sodium bicarbonate (NaHCO 3 ) ingestion. In a double-blind, three-way repeated-measures design, participants (n = 10) ingested either 0.3 g kg -1 NaHCO 3 (ALK) or equivalent calcium carbonate (PLA) prior to 2 min of continuous (1 Hz) supramaximal stimulation (300 ms at 40 Hz) of the triceps surae or brachii, with maximal voluntary efforts (maximal voluntary torque) coupled with direct muscle stimulation also measured at baseline, 1 and 2 min. Metabolic alkalosis was achieved in both ALK trials but was not different between muscle groups. Regardless of the conditions, involuntary torque declined nearly 60% in the triceps brachii (P < 0.001) and ∼30% in the triceps surae (P < 0.001). In all trials, there was a significant decline in normalized involuntary RFD (P < 0.05). Maximal voluntary torque declined nearly 28% but was not different between conditions (P < 0

Hippocampal electrical activity of adult rabbits during moderate passive hyperventilation

International Nuclear Information System (INIS)

Touchard, Francoise

1982-01-01

The effects of a moderate passive hyperventilation (HV) were studied in immobilized un-anesthetized rabbits. Hypocapnia (PCO 2 = 23.3 ± 2.8 mm Hg) and alkalosis (pH = 7.54 ± 0.07) were measured on arterial samples. PO 2 remained stable. The following results were obtained. From the onset of HV, the mean discharge rate (F) of the pyramidal cells (CA 1 ) was modified. Several types of cellular behaviours were defined according to whether F decreased (51 pc of the neurons), increased (39 pc) or remained stable (6 pc). The most marked effect was observed 15 min after HV onset when 87 pc of cells showed a discharge rate lower than in controls. Whatever F variations, the temporal organization of the action potentials remained unchanged in 71 pc of cases. The evoked response resulting from the stimulation of the commissural inputs corresponded with the activity of GABA inhibitory neurons (basket cells). The response threshold, amplitude and latency were not modified by HV. Only the facilitation process resulting from paired pulses was modified in its late stage. These results as well as those concerning unit activity do not support various assumption such as trouble of the neuronal energetic metabolism due to hypoxia, modification of ionic exchanges (Na + , K + , Ca ++ ), or variations of neurotransmitter concentrations (especially GABA). The effects observed could be ascribed to modifications of neuronal membrane resting potential resulting from direct action of CO 2 and alkalosis. (author) [fr

Using omeprazole to link the components of the post-prandial alkaline tide in the spiny dogfish, Squalus acanthias.

Science.gov (United States)

Wood, Chris M; Schultz, Aaron G; Munger, R Stephen; Walsh, Patrick J

2009-03-01

After a meal, dogfish exhibit a metabolic alkalosis in the bloodstream and a marked excretion of basic equivalents across the gills to the external seawater. We used the H(+), K(+)-ATPase pump inhibitor omeprazole to determine whether these post-prandial alkaline tide events were linked to secretion of H(+) (accompanied by Cl(-)) in the stomach. Sharks were fitted with indwelling stomach tubes for pretreatment with omeprazole (five doses of 5 mg omeprazole per kilogram over 48 h) or comparable volumes of vehicle (saline containing 2% DMSO) and for sampling of gastric chyme. Fish were then fed an involuntary meal by means of the stomach tube consisting of minced flatfish muscle (2% of body mass) suspended in saline (4% of body mass total volume). Omeprazole pre-treatment delayed the post-prandial acidification of the gastric chyme, slowed the rise in Cl(-) concentration of the chyme and altered the patterns of other ions, indicating inhibition of H(+) and accompanying Cl(-) secretion. Omeprazole also greatly attenuated the rise in arterial pH and bicarbonate concentrations and reduced the net excretion of basic equivalents to the water by 56% over 48 h. Arterial blood CO(2) pressure (Pa(CO(2))) and plasma ions were not substantially altered. These results indicate that elevated gastric H(+) secretion (as HCl) in the digestive process is the major cause of the systemic metabolic alkalosis and the accompanying rise in base excretion across the gills that constitute the alkaline tide in the dogfish.

Population pharmacodynamic model of bicarbonate response to acetazolamide in mechanically ventilated chronic obstructive pulmonary disease patients

Science.gov (United States)

2011-01-01

Introduction Acetazolamide is commonly given to chronic obstructive pulmonary disease (COPD) patients with metabolic alkalosis. Little is known of the pharmacodynamics of acetazolamide in the critically ill. We undertook the pharmacodynamic modeling of bicarbonate response to acetazolamide in COPD patients under mechanical ventilation. Methods This observational, retrospective study included 68 invasively ventilated COPD patients who received one or multiple doses of 250 or 500 mg of acetazolamide during the weaning period. Among the 68 investigated patients, 207 time-serum bicarbonate observations were available for analysis. Population pharmacodynamics was modeled using a nonlinear mixedeffect model. The main covariates of interest were baseline demographic data, Simplified Acute Physiology Score II (SAPS II) at ICU admission, cause of respiratory failure, co-prescription of drugs interfering with the acid-base equilibrium, and serum concentrations of protein, creatinin, potassium and chloride. The effect of acetazolamide on serum bicarbonate levels at different doses and in different clinical conditions was subsequently simulated in silico. Results The main covariates interacting with acetazolamide pharmacodynamics were SAPS II at ICU admission (P = 0.01), serum chloride (P 500 mg twice daily is required to reduce serum bicarbonate concentrations > 5 mmol/L in the presence of high serum chloride levels or coadministration of systemic corticosteroids or furosemide. Conclusions This study identified several covariates that influenced acetazolamide pharmacodynamics and could allow a better individualization of acetazolamide dosing when treating COPD patients with metabolic alkalosis. PMID:21917139

Acute encephalopathy with concurrent respiratory and metabolic disturbances in first known parenteral human administration of flunixin meglumine and acepromazine maleate.

Science.gov (United States)

Kamali, Michael F; Wilson, Anwar C; Acquisto, Nicole M; Spillane, Linda; Schneider, Sandra M

2013-08-01

Flunexin is a nonsteroidal anti-inflammatory drug approved for veterinary use in horses and cattle. Acepromazine is a phenothiazine derivative used in horses, dogs, and cats. Human exposure to these substances is rare. We report a case of a human injection of two equine medications, flunixin and acepromazine, which resulted in altered mental status, respiratory alkalosis, gastrointestinal bleeding, and elevation of liver transaminases in a 43-year-old woman who worked as a horse trainer. The patient intentionally self-injected these medications and subsequently presented to the Emergency Department with altered mental status and lethargy. The patient required hospitalization for metabolic abnormalities, including respiratory alkalosis, and suffered a gastrointestinal bleed requiring blood transfusion. The patient ultimately recovered with supportive measures. We believe this to be the first case of concomitant injection of flunixin and acepromazine in a human. This report explains a case of parenteral administration of two equine medications and the subsequent complications in a patient that presented to the Emergency Department. Human exposure to veterinary medications cannot be predicted by their effect in animals due to variations in absorption, distribution, and metabolism. Physicians should be aware that individuals who work with animals may have access to large quantities of veterinary medicine. This case also exemplifies the challenges that Emergency Physicians face on a daily basis, and generates additional consideration for overdoses and intoxications from medications that are not considered commonplace in humans. Copyright © 2013 Elsevier Inc. All rights reserved.

Fanconi syndrome and severe polyuria: an uncommon clinicobiological presentation of a Gitelman syndrome.

Science.gov (United States)

Bouchireb, Karim; Boyer, Olivia; Mansour-Hendili, Lamisse; Garnier, Arnaud; Heidet, Laurence; Niaudet, Patrick; Salomon, Remi; Poussou, Rosa Vargas

2014-08-11

Gitelman syndrome is an autosomal recessive tubulopathy characterized by hypokalemia, hypomagnesemia, metabolic alkalosis and hypocalciuria. The majority of patients do not present with symptoms until late childhood or adulthood, and the symptoms are generally mild. We report here the first case of Gitelman syndrome presenting with the biological features of Fanconi syndrome and an early polyuria since the neonatal period. We discuss in this article the atypical electrolytes losses found in our patient, as well as the possible mechanisms of severe polyuria. A 6-year-old Caucasian girl was admitted via the Emergency department for vomiting, and initial laboratory investigations found hyponatremia, hypokalemia, metabolic acidosis with normal anion gap, hypophosphatemia, and hypouricemia. Urinalysis revealed Na, K, Ph and uric acid losses. Thus, the initial biological profile was in favor of a proximal tubular defect. However, etiological investigations were inconclusive and the patient was discharged with potassium chloride and phosphorus supplementation. Three weeks later, further laboratory analysis indicated persistent hypokalemia, a metabolic alkalosis, hypomagnesemia, and hypocalciuria. We therefore sequenced the SLC12A3 gene and found a compound heterozygosity for 2 known missense mutations. Gitelman syndrome can have varying and sometimes atypical presentations, and should be suspected in case of hypokalemic tubular disorders that do not belong to any obvious syndromic entity. In this case, the proximal tubular dysfunction could be secondary to the severe hypokalemia. This report emphasizes the need for clinicians to repeat laboratory tests in undiagnosed tubular disorders, especially not during decompensation episodes.

A patient with Bartter syndrome accompanying severe growth hormone deficiency and focal segmental glomerulosclerosis.

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Akil, Ipek; Ozen, Serkan; Kandiloglu, Ali Riza; Ersoy, Betul

2010-06-01

Bartter syndrome is a rare autosomal recessive, salt-losing disorder characterized by hypokalemic hypochloremic metabolic alkalosis. A 10-year-old boy had severe growth retardation (height standard deviation score -8.15). He had a thin, triangular face, prominent ears and forehead, and big eyes. Megacystis, bilateral hydroureteronephrosis, and residual urine were detected in ultrasonography, but there was no vesicoureteral reflux. Lumbosacral magnetic resonance (MR) showed posterior disc bulging at L4-5. Serum sodium and chloride levels were normal, but mild hypokalemia was overlooked initially. During follow-up, hypokalemic hypochloremic metabolic alkalosis developed, with high urinary chloride and potassium excretion (52 and 43 mEq/L, respectively). The patient, with renal salt loss, was thought to have classic Bartter syndrome due to absence of nephrocalcinosis, presence of persistent hypercalciuria and sensorineural deafness, and presence of relatively mild clinical and laboratory findings, except polyuria initially. The child was treated with indomethacin, spironolactone, and oral potassium in addition to growth hormone (GH). During treatment, he had considerable increase in weight and height compared with the period of GH therapy only. We present this case because, although growth retardation is a major feature of Bartter syndrome, associated GH deficiency is rarely reported in the literature. Diagnosis of Bartter syndrome was made later, as our patient was followed for megacystis and megaureter secondary to the neurogenic bladder and GH deficiency initially; and proteinuria associated with focal segmental glomerulosclerosis responded to treatment for Bartter syndrome.

17-α-Hydroxylase deficiency: An unusual case with primary amenorrhea and hypertension

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Sunil Kumar Kota

2011-01-01

Full Text Available A 14-year-old girl presented with acute onset quadriparesis and newly detected hypertension. Parental consanguinity, delayed puberty with normal stature form the additional information. Hypokalemia with metabolic alkalosis, low cortisol, high ACTH and FSH pointed to the possibility of CAH with 17α hydroxylase deficiency. 46XX karyotype and high progesterone supported this. Normalization of hypokalemia and hypertension with glucocorticoid treatment confirmed the diagnosis. In summary, the possibility of 17 OHD should be suspected in patients with hypokalemic myopathy, Hypertension and hypogonadism so that appropriate therapy can be implemented.

Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: The Role of Noninvasive Ventilation

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Terzano, Claudio; Di Stefano, Fabio; Conti, Vittoria; Di Nicola, Marta; Paone, Gregorino; Petroianni, Angelo; Ricci, Alberto

2012-01-01

Background Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Methods Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO2 and PaCO2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Results Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosis–metabolic alkalosis, 10/36 (27.8%) respiratory acidosis and 3/5 (60%) mixed respiratory-metabolic acidosis patients (p = 0.026), with durations of 45.1±9.8, 36.2±8.9 and 53.3±4.1 hours, respectively (p = 0.016). The duration of ventilation was associated with higher blood lactate (prespiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis–metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. Conclusions Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated. PMID:22539963

Experience of diagnosis and treatment of Gitelman syndrome

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Shuo TIAN

2017-12-01

Full Text Available Objective To analyze the clinical characteristics and provide the experiences in diagnosis and treatment of 3 cases of Gitelman syndrome (GitS. Methods Three patients diagnosed as GitS were selected as the objects in Tangshan gongren Hospital from Aug. 2010 to Jan. 2017. Their clinical data were retrospectively analyzed and combined with the related literatures, and the clinical characteristics and treatment experiences of the disease were discussed. Results Of the 3 patients, 2 were teenager onset and another one was adult onset. The blood pressure of the 3 patients was normal, and the clinical features were as paroxysmal weakness, tetany, polyuria and nocturia increased. Laboratory tests revealed low potassium, low sodium, low chlorine, hypomagnesemia, occasionally hypocalcemia, high urinary potassium, metabolic alkalosis, urine Ca/Cr ≤0.2, plasma rennin activity increased significantly and plasma aldosterone was normal. Being eliminated symptoms and phenomena were the potassium intake inadequate, loss of potassium in digestive tract, taking potassium excretion drugs, primary aldosteronism and Cushing syndrome. etc. Patients got symptoms relief and serum potassium level rose to near normal level after receiving the combined potassium and magnesium supplement. Conclusions The clinical characteristics of GitS manifest as fatigue, tetany, normal blood pressure, hypokalemia, hypomagnesemia, metabolic alkalosis, plasma rennin activity increases significantly and plasma aldosterone rises or normal. Treatment with combined potassium and magnesium supplement may lead to a good prognosis, but hypomagnesemia is harder to correct. Kidney damage can be avoided by early diagnosis and treatment. DOI: 10.11855/j.issn.0577-7402.2017.12.13

Control of rectal gland secretion by blood acid-base status in the intact dogfish shark (Squalus acanthias).

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Wood, Chris M; Munger, R Stephen; Thompson, Jill; Shuttleworth, Trevor J

2007-05-14

In order to address the possible role of blood acid-base status in controlling the rectal gland, dogfish were fitted with indwelling arterial catheters for blood sampling and rectal gland catheters for secretion collection. In intact, unanaesthetized animals, isosmotic volume loading with 500 mmol L-1 NaCl at a rate of 15 mL kg-1 h-1 produced a brisk, stable rectal gland secretion flow of about 4 mL kg-1 h-1. Secretion composition (500 mmol L-1 Na+ and Cl-; 5 mmol L-1 K+; <1 mmol L-1 Ca2+, Mg2+, SO(4)2-, or phosphate) was almost identical to that of the infusate with a pH of about 7.2, HCO3- mmol L-1<1 mmol L-1 and a PCO2 (1 Torr) close to PaCO2. Experimental treatments superimposed on the infusion caused the expected disturbances in systemic acid-base status: respiratory acidosis by exposure to high environmental PCO2, metabolic acidosis by infusion of HCl, and metabolic alkalosis by infusion of NaHCO3. Secretion flow decreased markedly with acidosis and increased with alkalosis, in a linear relationship with extracellular pH. Secretion composition did not change, apart from alterations in its acid-base status, and made negligible contribution to overall acid-base balance. An adaptive control of rectal gland secretion by systemic acid-base status is postulated-stimulation by the "alkaline tide" accompanying the volume load of feeding and inhibition by the metabolic acidosis accompanying the volume contraction of exercise.

Delayed Awakening from Anesthesia Following Electrolyte and Acid-Base Disorders, Two Cases

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Razavi M

2014-01-01

Full Text Available Introduction: Delayed awakening from anesthesia remains one of the biggest challenges that involve anesthesiologists. Most commonly, delayed awakening is due to drugs effects persistence. Metabolic (like hypo- hyperglycemia, electrolyte, acid-base disorders and hypothermia may cause delayed emergence from anesthesia. Structural disorders of cerebral nervous system (like increase in intracranial pressure, brain ischemia and psychological disorders can be regarded as other uncommon causes of this condition. Hypokalemia is induced by low potassium intake, excessive excretion from gastrointestinal (GI and kidneys (like using diuretics or a shift from extracellular space into intracellular space. Cases:  In these two reported cases, although proper measures had been taken to reverse the effects of anesthetic drugs, the patients did not regain their consciousness as fast as expected. The only significant finding in postoperative tests, along with respiratory alkalosis, was low serum potassium level (K=2.5 and K=2.9 in the first and the second patients, respectively. Correction of serum potassium (to K=3.3 and K=3.2 in the first and the second, respectively improved patients level of consciousness, and they were discharged from intensive care unit (ICU with good general condition. Conclusion: During surgery; pain, stress, sympathetic increase, catecholamine release and the consequent β-stimulation, certain drugs, and respiratory alkalosis due to hyperventilation may cause acute shift of potassium into the cells, which will be intensified in the patients with preoperative hypokalemia. Hypokalemia induces consciousness impairment and increases muscle relaxation, both of which affect patient awakening. Serum potassium evaluation is recommended in cases of delayed emergence from anesthesia.

Mixed acid-base disorders, hydroelectrolyte imbalance and lactate production in hypercapnic respiratory failure: the role of noninvasive ventilation.

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Terzano, Claudio; Di Stefano, Fabio; Conti, Vittoria; Di Nicola, Marta; Paone, Gregorino; Petroianni, Angelo; Ricci, Alberto

2012-01-01

Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO(2) and PaCO(2) and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosis-metabolic alkalosis, 10/36 (27.8%) respiratory acidosis and 3/5 (60%) mixed respiratory-metabolic acidosis patients (p = 0.026), with durations of 45.1 ± 9.8, 36.2 ± 8.9 and 53.3 ± 4.1 hours, respectively (p = 0.016). The duration of ventilation was associated with higher blood lactate (prespiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis-metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated.

Type IV neonatal Bartter syndrome complicated with congenital chloride diarrhea.

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Sakallı, Hale; Bucak, Hakan İbrahim

2012-01-01

Pseudo-Bartter syndrome encompasses a heterogenous group of disorders similar to Bartter syndrome. Sometimes a few status may be nested, as in our case presented here. An 8-month-old boy was referred to our hospital with of intractable diarrhea, polyuria, persistent hypokalemia, abdominal distension and failure to thrive. He was born in the 34 6/7 gestational week (GW) to consanguineous parents. In the 30(th) GW polyhydramnios was verified by ultrasonography. The laboratory results showed hypokalemic-hypochloremic metabolic alkalosis, hyponatremia, and increased urinary loss of chloride, potassium and calcium. An audiogram test revealed complete sensorineural deafness. Ultrasonography revealed medullary nephrocalcinosis in both kidneys. Elevated plasma renin activity and aldosterone were found and a provisional diagnosis of type-IV neonatal Bartter syndrome was made. Treatment with indomethacin, spironolactone and additional intake of NaCl/KCl was initiated. Despite these therapies, the child's diarrhea persisted but serum potassium concentration normalized, and hypercalciuria and urine output reduced. After determining the high fecal chloride concentration, there was an immediate decompensation of the disease on indomethacin withdrawal, thus a diagnosis of type IV neonatal Bartter syndrome complicated with congenital chloride diarrhea was considered. Indomethacin, spironolactone and supplementary therapies with NaCl/KCl were continued, which resulted in the normalization of serum electrolytes as well as his physical development, but high contents of chloride in urine and faeces and nephrocalcinosis remains unchanged during 1-year follow-up. Because of the clinical and laboratory simulations between the various diseases that lead to hypokalemic-hypochloremic metabolic alkalosis, patients must be evaluated carefully.

Vitamin C and sodium bicarbonate enhance the antioxidant ability of H9C2 cells and induce HSPs to relieve heat stress.

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Yin, Bin; Tang, Shu; Sun, Jiarui; Zhang, Xiaohui; Xu, Jiao; Di, Liangjiao; Li, Zhihong; Hu, Yurong; Bao, Endong

2018-02-13

Heat stress is exacerbated by global warming and affects human and animal health, leading to heart damage caused by imbalances in reactive oxygen species (ROS) and the antioxidant system, acid-base chemistry, electrolytes and respiratory alkalosis. Vitamin C scavenges excess ROS, and sodium bicarbonate maintains acid-base and electrolyte balance, and alleviates respiratory alkalosis. Herein, we explored the ability of vitamin C alone and in combination with equimolar sodium bicarbonate (Vitamin C-Na) to stimulate endogenous antioxidants and heat shock proteins (HSPs) to relieve heat stress in H9C2 cells. Control, vitamin C (20 μg/ml vitamin C for 16 h) and vitamin C-Na (20 μg/ml vitamin C-Na for 16 h) groups were heat-stressed for 1, 3 or 5 h. Granular and vacuolar degeneration, karyopyknosis and damage to nuclei and mitochondria were clearly reduced in treatment groups, as were apoptosis, lactate dehydrogenase activity and ROS and malondialdehyde levels, while superoxide dismutase activity was increased. Additionally, CRYAB, Hsp27, Hsp60 and Hsp70 mRNA levels were upregulated at 3 h (p < 0.01), and protein levels were increased for CRYAB at 0 h (p < 0.05) and 1 h (p < 0.01), and for Hsp70 at 3 and 5 h (p < 0.01). Thus, pre-treatment with vitamin C or vitamin C-Na might protect H9C2 cells against heat damage by enhancing the antioxidant ability and upregulating CRYAB and Hsp70.

Conn syndrome and Crohn disease in a pediatric case: an interesting parallel.

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Rodriguez, Manuel A; Alkhoury, Fuad; Malvezzi, Leopoldo; Diaz, Alejandro

2013-01-01

Conn syndrome is characterized by surreptitious secretion of aldosterone in which patients are found to have hypertension, hypokalemia, and metabolic alkalosis. Although rare, the most common presentation in the pediatric population is bilateral hyperplasia of the adrenal glands as opposed to an adenoma. Crohn disease is part of the spectrum of inflammatory bowel disease, which manifests in children as flare-ups of bloody diarrhea and abdominal pain. The association of concurrent Conn syndrome and Crohn disease has been previously presented in two cases in adults. This is the first pediatric case to be reported in the literature.

Intestinal Ileus as a Possible Cause of Hypobicarbonatemia

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Andres Serrano

2007-01-01

Full Text Available The possible occurrence of metabolic acidosis in patients with intestinal ileus is not well recognized. We describe a patient with acute alcohol-induced pancreatitis and a large transverse colon ileus in which plasma bicarbonate dropped rapidly in the absence of an increase in the plasma anion gap. The urinary anion gap and ammonium excretion were consistent with an appropriate renal response to metabolic acidosis and against the possibility of respiratory alkalosis. The cause of the falling plasma bicarbonate was ascribed to intestinal bicarbonate sequestration owing to the enhancement of chloride-bicarbonate exchange in a dilated paralyzed colon.

Reversible Hypokalemia and Bartter-Like Syndrome during Prolonged Systemic Therapy with Colistimethate Sodium in an Adult Patient.

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Kamal Eldin, Tarek; Tosone, Grazia; Capuano, Alfredo; Orlando, Raffaele

2017-12-01

We present the case of a 58-year-old woman who developed hypokalaemia and metabolic alkalosis 2 weeks after therapy with colistimethate sodium for the treatment of chronic lower limb ulcer infection by extensively drug-resistant (XDR) Pseudomonas aeruginosa. The metabolic changes observed resembled Bartter syndrome, a group of congenital disorders affecting the distal segments of the renal tubules. The metabolic abnormalities reversed spontaneously 6 days after drug discontinuation. Acquired forms of Bartter syndrome have been reported during courses of antibiotic therapy; however, to our knowledge, this is the first documented case associated with colistimethate therapy in an adult.

Anaesthetic management of a patient with Liddle's syndrome for emergency caesarean hysterectomy.

LENUS (Irish Health Repository)

Hayes, N E

2011-04-01

We describe the anaesthetic management of a patient with Liddle\\'s syndrome during caesarean section and emergency hysterectomy for placenta accreta associated with significant intrapartum haemorrhage. Liddle\\'s syndrome is a rare autosomal dominant disorder characterised by early onset arterial hypertension and hypokalaemic metabolic alkalosis. Additional issues were the presence of short stature, limb hypertonicity and preeclampsia. Initial management with a low-dose combined spinal-epidural technique was subsequently converted to general anaesthesia due to patient discomfort. The management of Liddle\\'s syndrome in the setting of neuraxial and general anaesthesia in a patient undergoing caesarean section is discussed.

Anaesthetic management of a patient with Liddle's syndrome for emergency caesarean hysterectomy.

LENUS (Irish Health Repository)

Hayes, N E

2012-02-01

We describe the anaesthetic management of a patient with Liddle\\'s syndrome during caesarean section and emergency hysterectomy for placenta accreta associated with significant intrapartum haemorrhage. Liddle\\'s syndrome is a rare autosomal dominant disorder characterised by early onset arterial hypertension and hypokalaemic metabolic alkalosis. Additional issues were the presence of short stature, limb hypertonicity and preeclampsia. Initial management with a low-dose combined spinal-epidural technique was subsequently converted to general anaesthesia due to patient discomfort. The management of Liddle\\'s syndrome in the setting of neuraxial and general anaesthesia in a patient undergoing caesarean section is discussed.

S737F is a new CFTR mutation typical of patients originally from the Tuscany region in Italy.

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Terlizzi, Vito; Di Lullo, Antonella Miriam; Comegna, Marika; Centrone, Claudia; Pelo, Elisabetta; Castaldo, Giuseppe; Raia, Valeria; Braggion, Cesare

2018-01-03

An increasing number of patients have been described as having a number of Cystic Fibrosis Transmembrane conductance Regulator (CFTR) variants for which it lacks a clear genotype-phenotype correlation. We assesses the clinical features of patients bearing the S737F (p.Ser737Phe) CFTR missense variant and evaluated the residual function of CFTR protein on nasal epithelial cells (NEC). A retrospective database was performed from individuals homozygous or compound heterozygous for the S737F variant followed in the Cystic Fibrosis (CF) Centre of Florence. We performed a nasal brushing in cooperating patients and compared the results with those of patients followed in the pediatric CF Centre of Naples. 9/295 (3%) subjects carrying at least S737F CFTR variant on one allele were identified. Patients were diagnosed in 7/9 cases by newborn screening and in two cases for dehydration with hypochloremic metabolic alkalosis; at diagnosis sweat chloride levels (SCL) were in the pathological range in only one case. After a mean follow up of 8,6 years (range 0,5-15,8), SCL were in the pathological range in 8/9 cases (mean age at CF diagnosis: 1,5 years), all patients were pancreatic sufficiency and respiratory function was normal. The gating activity on NEC was 15.6% and 12.7% in two patients compound heterozygous for W1282X and DelE22_24, while it was ranged between 6,2% and 9,8% in CF patients. S737F is a CFTR mutation associated to hypochloremic alkalosis in childhood, mild CF phenotype in teenage years and a residual function of CFTR protein.

Carbonic anhydrase 2-like and Na⁺-K⁺-ATPase α gene expression in medaka (Oryzias latipes) under carbonate alkalinity stress.

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Yao, Zongli; Lai, Qifang; Hao, Zhuoran; Chen, Ling; Lin, Tingting; Zhou, Kai; Wang, Hui

2015-12-01

High carbonate alkalinity is one of the major stress factors for living organisms in saline-alkaline water areas. Acute and chronic effects of carbonate alkalinity on expression of two genes, carbonic anhydrase 2-like (CA2-like) and Na(+)-K(+)-ATPase α subunit (NKA-α) mRNA in medaka (Oryzias latipes) were evaluated to better understand the responses important for coping with a carbonate alkalinity stress. In the acute exposure experiment, the expression of CA2-like and NKA-α mRNA in the gill and kidney of medaka were examined from 0 h to 7 days exposed to 30.4 mM carbonate alkalinity water. Exposure to high carbonate alkalinity resulted in a transitory alkalosis, followed by a transient increase in gill and kidney CA2-like and NKA-α mRNA expression. In the chronic exposure experiment, the expression of these two genes was examined in the gill and kidney at 50 days post-exposure to six different carbonate alkalinity concentrations ranging from 1.5 to 30.4 mM. Gill and kidney CA2-like mRNA levels in 30.4 mM were approximately 10 and 30 times higher than that of the control (1.5 mM), respectively. Less differences were found in NKA-α expression in the 50-days exposure. The results indicate that when transferred to high carbonate alkalinity water, a transitory alkalosis may occur in medaka, followed by compensatory acid-base and ion regulatory responses. Thus, CA2-like and NKA-α are at least two of the important factors that contribute to the regulation of alkalinity stress.

[A case of ammonium urate urinary stones with anorexia nervosa].

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Komori, K; Arai, H; Gotoh, T; Imazu, T; Honda, M; Fujioka, H

2000-09-01

A 27-year-old woman had been suffering from bulimia and habitual vomiting for about 7 years and was incidentally found to have right renal stones by computed tomography. She was referred to our hospital for the treatment of these caluculi. On admission, she presented with hypokalemia, hypochloremia and metabolic alkalosis and was diagnosed with anorexia nervosa. Following successful removal by percutaneous nephrolithotripsy and extracorporeal shockwave lithotripsy the stones were found to consist of pure ammonium urate. Since the urine of an anorexia nervosa patient tends to be rich in uric acid and ammonium, anorexia nervosa seems to be associated with ammonium urate urinary stones.

Respiratory Acid-Base Disorders in the Critical Care Unit.

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Hopper, Kate

2017-03-01

The incidence of respiratory acid-base abnormalities in the critical care unit (CCU) is unknown, although respiratory alkalosis is suspected to be common in this population. Abnormal carbon dioxide tension can have many physiologic effects, and changes in Pco 2 may have a significant impact on outcome. Monitoring Pco 2 in CCU patients is an important aspect of critical patient assessment, and identification of respiratory acid-base abnormalities can be valuable as a diagnostic tool. Treatment of respiratory acid-base disorders is largely focused on resolution of the primary disease, although mechanical ventilation may be indicated in cases with severe respiratory acidosis. Published by Elsevier Inc.

Hyperchloremia – Why and how

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Glenn T. Nagami

2016-07-01

Full Text Available Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance.

A case of Pseudo-Bartter syndrome

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Yang, Ik; Choi, Bo Whan; Lee, Yul; Chung, Soo Young

1994-01-01

Pseudo-Bartter Syndrome is a rare medical disease of the kidney characterized by normal blood pressure, hypokalemic metabolic alkalosis, hyperreninemia and hyperaldosteronism with drug history of diuretics. We report US, CT and MRI findings of a patients with clinically proved Pseudo-Bartter syndrome. The patient was a 37 year old woman with a history of long term ingestion of the diuretics(furosemide) for 20 years. Renal US revealed hyperechoic renal medulla at both kidneys. The resistive index(RI), calculated from the duplex doppler waveform is 0.61. Unenhanced CT revealed faint high attenuation along the medulla. T1-weighted MRI revealed indistinct corticomedullary differentiation

A case of Pseudo-Bartter syndrome

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Yang, Ik; Choi, Bo Whan; Lee, Yul; Chung, Soo Young [College of Medicine, Hallym University, Seoul (Korea, Republic of)

1994-10-15

Pseudo-Bartter Syndrome is a rare medical disease of the kidney characterized by normal blood pressure, hypokalemic metabolic alkalosis, hyperreninemia and hyperaldosteronism with drug history of diuretics. We report US, CT and MRI findings of a patients with clinically proved Pseudo-Bartter syndrome. The patient was a 37 year old woman with a history of long term ingestion of the diuretics(furosemide) for 20 years. Renal US revealed hyperechoic renal medulla at both kidneys. The resistive index(RI), calculated from the duplex doppler waveform is 0.61. Unenhanced CT revealed faint high attenuation along the medulla. T1-weighted MRI revealed indistinct corticomedullary differentiation.

Acid-Base and Electrolyte Disorders in Patients with and without Chronic Kidney Disease: An Update.

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Dhondup, Tsering; Qian, Qi

2017-12-01

Kidneys play a pivotal role in the maintenance and regulation of acid-base and electrolyte homeostasis, which is the prerequisite for numerous metabolic processes and organ functions in the human body. Chronic kidney diseases compromise the regulatory functions, resulting in alterations in electrolyte and acid-base balance that can be life-threatening. In this review, we discuss the renal regulations of electrolyte and acid-base balance and several common disorders including metabolic acidosis, alkalosis, dysnatremia, dyskalemia, and dysmagnesemia. Common disorders in chronic kidney disease are also discussed. The most recent and relevant advances on pathophysiology, clinical characteristics, diagnosis, and management of these conditions have been incorporated.

Anesthetic management of a patient with Bartter′s syndrome undergoing bilateral sagittal split osteotomy

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Nasser Nooh

2012-01-01

Full Text Available Bartter′s syndrome is an unusual (estimated incidence is 1.2 per million people but important congenital form of secondary hyperaldosteronism; due to abnormalities in renal handling of electrolytes. It is associated with hypertrophy and hyperplasia of the juxtaglomerular cells, normal blood pressure, and hypokalemic alkalosis withoutedema.We present a 22-year-old woman with Bartter′s syndrome underwent bilateral sagittal split osteotomy to correct mandibular prognathic. The anesthetic management of Bartter′s syndrome should be relevant to the pathophysiology of the syndrome. Therefore, it should be directed toward maintaining cardiovascular stability, control of associated fluid, electrolyte and acid-base derangements, and the prevention of renal damage.

Anaesthesia for laparoscopic cholecystectomy in Bartter′s syndrome

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Bala S Bhaskar

2010-01-01

Full Text Available Bartter′s syndrome is a rare inherited anamoly with defect in the thick segment of the ascending limb of the loop of Henle, with reduced reabsorption of potassium. Growth is affected with worsening renal function, hypokalaemia, hypochloraemic metabolic alkalosis, hypocalcemia, hypomagnesemia, increased levels of aldosterone, renin and angiotensin without hypertension and lack of responses to vasopressors. Treatment consists of potassium supplementation along with other medications. We present the case report, probably the first, of a child suffering from Bartter′s syndrome with gall stones posted for laparoscopic cholecystectomy. The pre-operative correction of hypokalemia and successful anaesthetic and fluid and electrolyte management of the patient are discussed.

Pseudo-Bartter’s syndrome in patients with cystic fibrosis: A case series and review of the literature

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Vilotijević-Dautović Gordana

2015-01-01

Full Text Available Introduction. Pseudo-Bartter syndrome (PBS is characterized by hyponatremic, hypochloremic metabolic alkalosis that mimics Bartter syndrome but with no pathology in the renal tubules. We present five patients with cystic fibrosis (CF and PBS. Cases Outline. Four children aged between three and five-and-one-half months with previously diagnosed CF and one aged 17 months with previously undiagnosed disease, were hospitalized during the summer season, with severe dehydration, oliguria, apathy and adynamia. Additionally, one of them had an ileostomy due to meconium ileus after birth. All children were on a diet without additional salt intake. Laboratory analysis on admission showed hyponatremia (115-133 mmol/L, mean 122.4 mmol/L, high plasma renin activity (229-500 pg/ml, mean 324 pg/ml and metabolic alkalosis (pH 7.5-7.6, mean 7.56 in all the patients, and in four of them high blood level of aldosterone (74-560 pg/ml, mean 295.9 pg/ml, hypokalemia (2.3-2.8 mmol/L, mean 2.6 mmol/L, hypochloremia (59-71 mmol/L, mean 66 mmol/L and low urinary sodium (5-12 mmol/L, mean 9 mmol/L. After intravenous rehydration followed by additional use of sodium and chloride in mean dosis of 1.78 mmol/kg per day, all the patients made a complete recovery. With advice for additional use of salt in the mentioned amount, the patients were discharged from the hospital. Conclusion. PBS is one of CF complications, especially in infants and young children in situations accompanied by increased sweating and/or other causes of additional loss of sodium and chlorine. Sometimes, as was the case with one of our patients, PBS may be the initial presentation form of the disease.

Sodium bicarbonate-augmented stress thallium myocardial scintigraphy

International Nuclear Information System (INIS)

Sarin, Badal; Chugh, Pradeep Kumar; Kaushal, Dinesh; Soni, Nakse Lal; Sawroop, Kishan; Mondal, Anupam; Bhatnagar, Aseem

2004-01-01

It is well known that sodium bicarbonate in pharmacological doses induces transient alkalosis, causing intracellular transport of serum potassium. The aims of this study were (a) to investigate whether, in humans, myocardial thallium-201 uptake can be augmented by pretreatment with a single bolus of sodium bicarbonate at a pharmacological dose, (b) to verify general safety aspects of the intervention and (c) to evaluate the clinical implications of augmentation of 201 Tl uptake, if any. Routine exercise myocardial scintigraphy was performed twice in eight adult volunteers (five normal and three abnormal), once without intervention and the second time (within a week) following intravenous administration of sodium bicarbonate (88 mEq in 50 ml) as a slow bolus 1 h prior to the injection of 201 Tl. Conventional myocardial thallium study was compared with sodium bicarbonate interventional myocardial scintigraphy with respect to myocardial uptake (counts per minute per mCi injected dose), washout patterns in normal and abnormal myocardial segments, and overall clinical interpretation based on planar and single-photon emission tomographic (SPET) images. All patients remained asymptomatic after the intervention. A mean increase of 53% in myocardial uptake of thallium was noted in post-exercise acquisitions after the intervention, confirming uptake of the tracer via the potassium-hydrogen pump and its augmentation by transient alkalosis. The washout pattern remained unchanged. The visual quality of planar and SPET images improved significantly after the intervention. Out of the five abnormal myocardial segments identified in three cases, four showed significant filling-in after the intervention, causing the diagnosis to be upgraded from ''partial scar'' to ''ischaemia'', or from ''ischaemia'' to ''normal''. The overall scan impression changed in two out of three such cases. Sodium bicarbonate augmentation may have significant implications for stress-thallium scintigraphy

Mixed acid-base disorders, hydroelectrolyte imbalance and lactate production in hypercapnic respiratory failure: the role of noninvasive ventilation.

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Claudio Terzano

Full Text Available BACKGROUND: Hypercapnic Chronic Obstructive Pulmonary Disease (COPD exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV when treating hypercapnic respiratory failure. METHODS: Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO(2 and PaCO(2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. RESULTS: Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7% mixed respiratory acidosis-metabolic alkalosis, 10/36 (27.8% respiratory acidosis and 3/5 (60% mixed respiratory-metabolic acidosis patients (p = 0.026, with durations of 45.1 ± 9.8, 36.2 ± 8.9 and 53.3 ± 4.1 hours, respectively (p = 0.016. The duration of ventilation was associated with higher blood lactate (p<0.001, lower pH (p = 0.016, lower serum sodium (p = 0.014 and lower chloride (p = 0.038. Hyponatremia without hypervolemic hypochloremia occurred in 11 respiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis-metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. CONCLUSIONS: Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated.

The use of the standard exercise test to establish the clinical significance of mild echocardiographic changes in a Thoroughbred poor performer : clinical communication

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C. Meyer

2004-06-01

Full Text Available A 4-year-old Thoroughbred gelding racehorse was referred to the Onderstepoort Veterinary Academic Hospital (OVAH with a history of post-race distress and collapse. In the absence of any obvious abnormalities in the preceding diagnostic work-up, a standard exercise test was performed to determine an underlying cause for the post-race distress reported. In this particular case oxygen desaturation became evident at speeds as slow as 6 m/s, where PO2 was measured at 82.3 mm Hg. Similarly at a blood pH of 7.28, PCO2 had dropped to 30.0mm Hg indicating a combined metabolic acidosis and respiratory alkalosis. The cause of the distress was attributed to a severe hypoxia, with an associated hypocapnoea, confirmed on blood gas analyses, where PO2 levels obtained were as low as 56.6 mm Hg with a mean PCO2 level of 25.4 mm Hg during strenuous exercise. Arterial oxygenation returned to normal immediately after cessation of exercise to 106.44 mm Hg, while the hypocapnoeic alkalosis, PCO2 25.67 mm Hg, persisted until the animal's breathing normalized. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise. The combination of an aortic stenosis and a mitral valve insufficiency may have resulted in a condition similar to that described as high-altitude pulmonary oedema, with respiratory changes and compensation as for acute altitude disease. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise and substantiate the fact that an extensive diagnostic regime may be required to establish a cause for poor performance and that the standard exercise test remains an integral part of this work-up.

Correlation between arterial blood gas analysis and peripheral blood gas analysis in acid-base unbalance state

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Hyun Lee Kim

2012-06-01

Full Text Available Acid-base unbalance is most common problem in severe ill patient, especially in condition of abnormal renal function state. Acid-base unbalances are respiratory acidosis, respiratory alkalosis, metabolic acidosis, and metabolic alkalosis. Metabolic acidosis is frequently appeared in clinical state. Arterial blood gas analysis is considered as a basic test to the intensive care unit patient and emergency state. Recently some researches were done, comparing with arterial blood gas analysis and venous blood gas analysis. Because of venous blood sampling is safer than arterial blood gas analysis, and beside not so different among them for detecting pH, pCO2, HCO3, except pO2 measuring. This research was done in emergency room, and for explaining no different between arterial blood gas analysis and peripheral blood gas analysis result in acid-base unbalance state patient. Especially in kidney functions decreased state. : The study was done from March, 2010 to January, 2011. The object was 89 peoples who came to emergency room for treating internal medicine problem. (Women 53, average age: 66.7±12.1 Then compare between arterial blood gas analysis and peripheral blood gas analysis. Result: The mean arterial minus venous difference for pH, pCO2, and bicarbonate was −0.0170, 2.6528, and 0.6124. Bland-Altman plot was done for predicting agreement of two groups, and the scale was pH −2.95 to 4.17, pCO2 −4.45 to 9.76, bicarbonate −2.95 to 4.16, in 95% relative. Conclusion: The peripheral blood gas pH, pCO2, bicarbonate level is almost same as arterial blood gas analysis results. And enough to measuring acid-base unbalance state, in absent of arterial blood testing.

Effect of acute acid-base disturbances on ErbB1/2 tyrosine phosphorylation in rabbit renal proximal tubules.

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Skelton, Lara A; Boron, Walter F

2013-12-15

The renal proximal tubule (PT) is a major site for maintaining whole body pH homeostasis and is responsible for reabsorbing ∼80% of filtered HCO3(-), the major plasma buffer, into the blood. The PT adapts its rate of HCO3(-) reabsorption (JHCO3(-)) in response to acute acid-base disturbances. Our laboratory previously showed that single isolated perfused PTs adapt JHCO3(-) in response to isolated changes in basolateral (i.e., blood side) CO2 and HCO3(-) concentrations but, surprisingly, not to pH. The response to CO2 concentration can be blocked by the ErbB family tyrosine kinase inhibitor PD-168393. In the present study, we exposed enriched rabbit PT suspensions to five acute acid-base disturbances for 5 and 20 min using a panel of phosphotyrosine (pY)-specific antibodies to determine the influence of each disturbance on pan-pY, ErbB1-specific pY (four sites), and ErbB2-specific pY (two sites). We found that each acid-base treatment generated a distinct temporal pY pattern. For example, the summated responses of the individual ErbB1/2-pY sites to each disturbance showed that metabolic acidosis (normal CO2 concentration and reduced HCO3(-) concentration) produced a transient summated pY decrease (5 vs. 20 min), whereas metabolic alkalosis produced a transient increase. Respiratory acidosis (normal HCO3(-) concentration and elevated CO2 concentration) had little effect on summated pY at 5 min but produced an elevation at 20 min, whereas respiratory alkalosis produced a reduction at 20 min. Our data show that ErbB1 and ErbB2 in the PT respond to acute acid-base disturbances, consistent with the hypothesis that they are part of the signaling cascade.

[Acid-base status in patients treated with peritoneal dialysis].

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Katalinić, Lea; Blaslov, Kristina; Pasini, Eva; Kes, Petar; Bašić-Jukić, Nikolina

2014-04-01

When compared to hemodialysis, peritoneal dialysis is very simple yet low cost method of renal replacement therapy. Series of studies have shown its superiority in preserving residual renal function, postponing uremic complications, maintaining the acid-base balance and achieving better post-transplant outcome in patients treated with this method. Despite obvious advantages, its role in the treatment of chronic kidney disease is still not as important as it should be. Metabolic acidosis is an inevitable complication associated with progressive loss of kidney function. Its impact on mineral and muscle metabolism, residual renal function, allograft function and anemia is very complex but can be successfully managed. The aim of our study was to evaluate the efficiency in preserving the acid-base balance in patients undergoing peritoneal dialysis at Zagreb University Hospital Center. Twenty-eight patients were enrolled in the study. The mean time spent on the treatment was 32.39 ± 43.43 months. Only lactate-buffered peritoneal dialysis fluids were used in the treatment. Acid-base balance was completely maintained in 73.07% of patients; 11.54% of patients were found in the state of mild metabolic acidosis, and the same percentage of patients were in the state of mild metabolic alkalosis. In one patient, mixed alkalosis with respiratory and metabolic component was present. The results of this study showed that acid-base balance could be maintained successfully in patients undergoing peritoneal dialysis, even only with lactate-buffered solutions included in the treatment, although they were continuously proclaimed as inferior in comparison with bicarbonate-buffered ones. In well educated and informed patients who carefully use this method, accompanied by the attentive and thorough care of their physicians, this method can provide quality continuous replacement of lost renal function as well as better quality of life.

The acid-base effects of continuous hemofiltration with lactate or bicarbonate buffered replacement fluids.

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Tan, H K; Uchino, S; Bellomo, R

2003-06-01

To evaluate, quantify and compare the effects of continuous veno-venous hemofiltration (CVVH) with lactate or bicarbonate-buffered replacement fluids on acid-base balance. Randomized double crossover study. Intensive Care Unit of Tertiary Medical Center. Eight patients with severe acute renal failure. Random allocation to either 2 hours of isovolemic lactate-buffered (treatment A) CVVH or 2 hours of bicarbonate-buffered (treatment B) CVVH with cross over and with same procedure repeated the following day (double cross over). Timed collections of arterial blood and ultrafiltrate (UF), measurement of blood and UF gases and lactate concentrations and calculation of buffer-base mass balance. At baseline, both groups of patients had a similar, slight metabolic alkalosis (pH: 7.45 vs. 7.45; BE 3.9 mEq/L for treatment A and 4.0 for treatment B) and a serum bicarbonate of 28.1 mmol/L for treatment A vs. 28.3 mmol/L for treatment B; all NS. This alkalosis was present despite slight hyperlactatemia in both groups (A: 2.4 mmol/L vs. B 2.8 mmol/; NS). Within 60 minutes of treatment, however, treatment A led to a significantly higher lactate concentration (3.9 vs 2.5 mmol/L; p = 0.0011), a significantly lower BE (2.3 vs 4.1 mEq/L; p = 0.0019) and a significantly lower bicarbonate concentration (26.7 vs. 28.3 mmol/L; p = 0.0038) in the presence of an unchanged PaCO2. These differences persisted during the study period. The UF of patients receiving treatment A contained more lactate (10.2 vs 2.9 mmol/L; p buffer-base balance of +20.4 mEq/h compared to -2.6 mEq/h for treatment B; p buffered replacement fluids induces iatrogenic hyperlactatemia. Such hyperlactatemia is associated with an acidifying effect despite a positive buffer-base balance.

Hypokalemic paralysis in a middle-aged female with classic Bartter syndrome.

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Chiang, Wen-Fang; Lin, Shih-Hung; Chan, Jenq-Shyong; Lin, Shih-Hua

2014-02-01

Inherited classic Bartter syndrome (cBS) is an autosomal recessive renal tubular disorder resulting from inactivating mutations in the asolateral chloride channel (C1C-Kb) and usually presents in early infancy or childhood with mild to moderate hypokalemia. Profound hypokalemic paralysis in patients with cBS is extremely rare, especially in middle age. A 45-year-old Chinese female patient was referred for evaluation of chronic severe hypokalemia despite regular K+ supplementation (1 mmol/kg/d). She had had two episodes of muscle paralysis due to severe hypokalemia (K+ 1.9 - 2.1 mmol/l) in the past 3 years. She denied vomiting, diarrhea, or the use of laxatives or diuretics. Her blood pressure was normal. Biochemical studies showed hypokalemia (K+ 2.5 mmol/l) with renal potassium wasting, metabolic alkalosis (HCO3- 32 mmol/l), normomagnesemia (Mg2+ 0.8 mmol/l), hypercalciuria (calcium to creatinine ratio 0.5 mmol/mmol; normal < 0.22 mmol/mol), high plasma renin activity, but normal plasma aldosterone concentration. Abdominal sonography revealed neither renal stones nor nephrocalcinosis. Acquired causes of cBS such as autoimmune disease and drugs were all excluded. Molecular analysis of the CLCNKB gene, encoding ClC-Kb, and SLC12A3, encoding the thiazide-sensitive sodium chloride cotransporter (NCC), revealed compound heterozygous mutations in CLCNKB (L335P and G470E) inherited from her parents; her SLC12A3 was normal. These two mutations were not identified in 100 healthy subjects. Her plasma K+ concentration rose to 3 - 3.5 mmol/l after the addition of spironolactone. Inherited cBS may present with hypokalemic paralysis and should be considered in adult patients with hypokalemia and metabolic alkalosis.

Persistent severe hypokalemia: Gitelman syndrome and differential diagnosis

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Christine Zomer Dal Molin

Full Text Available Abstract The main causes of hypokalemia are usually evident in the clinical history of patients, with previous episodes of vomiting, diarrhea or diuretic use. However, in some patients the cause of hypokalemia can become a challenge. In such cases, two major components of the investigation must be performed: assessment of urinary excretion potassium and the acid-base status. This article presents a case report of a patient with severe persistent hypokalemia, complementary laboratory tests indicated that's it was hypomagnesaemia and hypocalciuria associated with metabolic alkalosis, and increase of thyroid hormones. Thyrotoxic periodic paralysis was included in the differential diagnosis, but evolved into euthyroid state, persisting with severe hypokalemia, which led to be diagnosed as Gitelman syndrome.

Mineralocorticoid hypertension: clinical and laboratory studies with special reference to selective percutaneous venography combined with aldosterone assay in the adrenal venous blood

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Wajchenberg, B.L.; Liberman, B.; Novaes, M.

1977-01-01

With the purpose of demonstrating the presence of hypertension, hypokalemia and alkalosis were studied. The presence of daily aldosteronism was verified in five patients; the sixth one presented no daily aldosteronism but an increase of 18-OH-DOCA production, an ACTH dependente mineralocorticoid. The presence of tumor (less than 0.9cm) could not be shown in two patients by bilateral selective adrenal venography. The aldosterone assay during catherization of adrenal vein of those patients permitted to determine the tumoral side. Attention must be given to the fact that the blood collection of adrenal vein must always be made during adrenal venography to demonstrate the presence of short unilateral tumor or bilateral disease [pt

Bartter syndrome associated with nephropathic cystinosis.

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Osman, Nader M; Sanosi, Ali Al

2016-01-01

Bartter syndrome is a rare inherited defect in the thick ascending limb of the loop of Henle. It is characterized by low potassium levels (hypokalaemia), increased blood pH (alkalosis) and normal to low blood pressure. There are three types of Bartter syndrome: neonatal, the classic type and Gitelman syndrome. Nephropathic cystinosis is an autosomal recessive disorder characterized by accumulation of free cystine in lysosomes due to disorder of lysosomal transport that can lead to end stage renal failure within 10 years and multiorgan impairment. We report a 5 year 9 month old child with Bartter syndrome associated with nephropathic cystinosis, hypothyroidism and rickets. Hitherto, only a handful of similar cases have been reported in the literature.

Adult presentation of Bartter syndrome type IV with erythrocytosis.

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Heilberg, Ita Pfeferman; Tótoli, Cláudia; Calado, Joaquim Tomaz

2015-01-01

Bartter syndrome comprises a group of rare autosomal-recessive salt-losing disorders with distinct phenotypes, but one unifying pathophysiology consisting of severe reductions of sodium reabsorption caused by mutations in five genes expressed in the thick ascending limb of Henle, coupled with increased urinary excretion of potassium and hydrogen, which leads to hypokalemic alkalosis. Bartter syndrome type IV, caused by loss-of-function mutations in barttin, a subunit of chloride channel CLC-Kb expressed in the kidney and inner ear, usually occurs in the antenatal-neonatal period. We report an unusual case of late onset presentation of Bartter syndrome IV and mild phenotype in a 20 years-old man who had hypokalemia, deafness, secondary hyperparathyroidism and erythrocytosis.

Episodic seasonal Pseudo-Bartter syndrome in cystic fibrosis.

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Kintu, Brett; Brightwell, Alex

2014-06-01

Pseudo-Bartter syndrome (PBS) describes an uncommon but well recognised complication of cystic fibrosis leading to hypochloraemic, hypokalaemic metabolic alkalosis. Pseudo-Bartter syndrome is usually seen at initial presentation or within the first two years of life in children with cystic fibrosis. Risk factors for development of PBS include warm weather conditions, severe respiratory or pancreatic disease and gastrointestinal losses (e.g. vomiting and diarrhoea). PBS is rare in older children and adolescents although epidemics have been associated with heat wave conditions in warmer climates. In this era of climate change, it is crucial that clinicians consider Pseudo-Bartter syndrome when patients with cystic fibrosis present unwell during summer. Copyright © 2014 Elsevier Ltd. All rights reserved.

A Basic Therapy Gone Awry.

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Galinko, Laura B; Hsu, Steven H; Gauran, Cosmin; Fingerhood, Michael L; Pastores, Stephen M; Halpern, Neil A; Chawla, Sanjay

2017-11-01

Baking soda (sodium bicarbonate) is a common household item that has gained popularity as an alternative cancer treatment. Some have speculated that alkali therapy neutralizes the extracellular acidity of tumor cells that promotes metastases. Internet blogs have touted alkali as a safe and natural alternative to chemotherapy that targets cancer cells without systemic effects. Sodium bicarbonate overdose is uncommon, with few reports of toxic effects in humans. The case described here is the first reported case of severe metabolic alkalosis related to topical use of sodium bicarbonate as a treatment for cancer. This case highlights how a seemingly benign and readily available product can have potentially lethal consequences. ©2017 American Association of Critical-Care Nurses.

Hyperventilation-induced respiratory alkalosis falls short of countering fatigue during repeated maximal isokinetic contractions.

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Sakamoto, Akihiro; Naito, Hisashi; Chow, Chin Moi

2015-07-01

Hyperventilation, implemented during recovery of repeated maximal sprints, has been shown to attenuate performance decrement. This study evaluated the effects of hyperventilation, using strength exercises, on muscle torque output and EMG amplitude. Fifteen power-trained athletes underwent maximal isokinetic knee extensions consisting of 12 repetitions × 8 sets at 60°/s and 25 repetitions × 8 sets at 300°/s. The inter-set interval was 40 s for both speeds. For the control condition, subjects breathed spontaneously during the interval period. For the hyperventilation condition, subjects hyperventilated for 30 s before each exercise set (50 breaths/min, PETCO2: 20-25 mmHg). EMG was recorded from the vastus medialis and lateralis muscles to calculate the mean amplitude for each contraction. Hyperventilation increased blood pH by 0.065-0.081 and lowered PCO2 by 8.3-10.3 mmHg from the control values (P < 0.001). Peak torque declined with repetition and set numbers for both speeds (P < 0.001), but the declining patterns were similar between conditions. A significant, but small enhancement in peak torque was observed with hyperventilation at 60°/s during the initial repetition phase of the first (P = 0.032) and fourth sets (P = 0.040). EMG amplitude also declined with set number (P < 0.001) for both speeds and muscles, which was, however, not attenuated by hyperventilation. Despite a minor ergogenic effect in peak torque at 60°/s, hyperventilation was not effective in attenuating the decrement in torque output at 300°/s and decrement in EMG amplitude at both speeds during repeated sets of maximal isokinetic knee extensions.

Alkalosis and Dialytic Clearance of Phosphate Increases Phosphatase Activity: A Hidden Consequence of Hemodialysis.

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Ricardo Villa-Bellosta

Full Text Available Extracellular pyrophosphate is a potent endogenous inhibitor of vascular calcification, which is degraded by alkaline phosphatase (ALP and generated by hydrolysis of ATP via ectonucleotide pyrophosphatase/phosphodiesterase 1 (eNPP1. ALP activity (as routinely measured in clinical practice represents the maximal activity (in ideal conditions, but not the real activity (in normal or physiological conditions. For the first time, the present study investigated extracellular pyrophosphate metabolism during hemodialysis sessions (including its synthesis via eNPP1 and its degradation via ALP in physiological conditions.45 patients in hemodialysis were studied. Physiological ALP activity represents only 4-6% of clinical activity. ALP activity increased post-hemodialysis by 2% under ideal conditions (87.4 ± 3.3 IU/L vs. 89.3 ± 3.6 IU/L and 48% under physiological conditions (3.5 ± 0.2 IU/L vs. 5.2 ± 0.2 IU/L. Pyrophosphate synthesis by ATP hydrolysis remained unaltered post-hemodialysis. Post-hemodialysis plasma pH (7.45 ± 0.02 significantly increased compared with the pre-dialysis pH (7.26 ± 0.02. The slight variation in pH (~0.2 units induced a significant increase in ALP activity (9%. Addition of phosphate in post-hemodialysis plasma significantly decreased ALP activity, although this effect was not observed with the addition of urea. Reduction in phosphate levels and increment in pH were significantly associated with an increase in physiological ALP activity post-hemodialysis. A decrease in plasma pyrophosphate levels (3.3 ± 0.3 μmol/L vs. 1.9 ± 0.1 μmol/L and pyrophosphate/ATP ratio (1.9 ± 0.2 vs. 1.4 ± 0.1 post-hemodialysis was also observed.Extraction of uremic toxins, primarily phosphate and hydrogen ions, dramatically increases the ALP activity under physiological conditions. This hitherto unknown consequence of hemodialysis suggests a reinterpretation of the clinical value of this parameter.

Forty Years Abuse of Baking Soda, Rhabdomyolysis, Glomerulonephritis, Hypertension Leading to Renal Failure: A Case Report

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Terje Forslund M.D., Ph.D.

2008-01-01

Full Text Available We present a patient who had ingested sodium bicarbonate for treatment of alcoholic dyspepsia during forty years at increasing doses. During the last year he had used more than 50 grams daily. He presented with metabolic alkalosis, epileptic convulsions, subdural hematoma, hypertension and rhabdomyolysis with end stage renal failure, for which he had to be given regular intermittent hemodialysis treatment. Untreated hypertension and glomerulonephritis was probably present prior to all these acute incidents. Examination of the kidney biopsy revealed mesangial proliferative glomerulonephritis and arterial wall thickening causing nephrosclerosis together with interstitial calcinosis. The combination of all these pathologic changes might be responsible for the development of progressive chronic renal failure ending up with the need for continuous intermittent hemodialysis treatment.

Colorectal injury by compressed air--a report of 2 cases.

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Suh, H. H.; Kim, Y. J.; Kim, S. K.

1996-01-01

We report two colorectal trauma patients whose rectosigmoid region was ruptured due to a jet of compressed air directed to their anus while they were playing practical jokes with their colleagues in their place of work. It was difficult to diagnose in one patient due to vague symptoms and signs and due to being stunned by a stroke of the compressed air. Both patients suffered from abdominal pain and distension, tension pneumoperitoneum and mild respiratory alkalosis. One patient was treated with primary two layer closure, and the other with primary two layer closure and sigmoid loop colostomy. Anorectal manometry and transanal ultrasonography checked 4 weeks after surgery, revealed normal anorectal function and anatomy. The postoperative courses were favorable without any wound infection or intraabdominal sepsis. PMID:8835767

Maintaining K+ balance on the low-Na+, high-K+ diet

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Cornelius, Ryan J.; Wang, Bangchen; Wang-France, Jun

2016-01-01

A low-Na+, high-K+ diet (LNaHK) is considered a healthier alternative to the “Western” high-Na+ diet. Because the mechanism for K+ secretion involves Na+ reabsorptive exchange for secreted K+ in the distal nephron, it is not understood how K+ is eliminated with such low Na+ intake. Animals on a LNaHK diet produce an alkaline load, high urinary flows, and markedly elevated plasma ANG II and aldosterone levels to maintain their K+ balance. Recent studies have revealed a potential mechanism involving the actions of alkalosis, urinary flow, elevated ANG II, and aldosterone on two types of K+ channels, renal outer medullary K+ and large-conductance K+ channels, located in principal and intercalated cells. Here, we review these recent advances. PMID:26739887

Acid-base balance of dairy cows and its relationship with alcoholic stability and mineral composition of milk

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Rafael Fagnani

2014-05-01

Full Text Available This study aimed to associate the occurrence of acid-base disorders with the alcoholic stability of milk from animals in the field, and to evaluate differences between the mineral composition of milk that was both stable and unstable in alcohol. The sample comprised 96 dairy cows, where the milk and blood of each corresponding animal was collected. The mineral composition of stable and unstable milk in alcohol was different and may be related to acid-base disturbances. The average amount of phosphate was lower in the milk that was unstable in alcohol, while potassium was greater. Frequency of the alcoholically unstable milk cases was higher in the cows with acid-base disturbances. Respiratory alkalosis was the disorder that was most observed.

A typical presentation of acute myeloid leukemia

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Udayakumar N

2006-01-01

Full Text Available A young man who presented with fever, altered sensorium and sudden onset tachypnea, is described. Arterial blood gas analysis, revealed the presence of severe high anion gap metabolic acidosis, with compensatory respiratory alkalosis and normal oxygen saturation. A detailed neurological, nephrological, biochemical and hematological evaluation, revealed the presence of Acute myeloid leukemia, with lactic acidosis and hyponatremia. There are very few reports of presentation of leukemia as lactic acidosis. This case report highlights the need for emergency room physicians, to consider the possibility of lactic acidosis, as one of the causes of high anion gap acidosis and to meticulously investigate the cause of lactic acidosis. We describe a rare clinical instance of lactic acidosis as the presenting manifestation of Acute myeloid leukemia.

Forty years abuse of baking soda, rhabdomyolysis, glomerulonephritis, hypertension leading to renal failure: a case report.

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Forslund, Terje; Koistinen, Arvo; Anttinen, Jorma; Wagner, Bodo; Miettinen, Marja

2008-01-01

We present a patient who had ingested sodium bicarbonate for treatment of alcoholic dyspepsia during forty years at increasing doses. During the last year he had used more than 50 grams daily. He presented with metabolic alkalosis, epileptic convulsions, subdural hematoma, hypertension and rhabdomyolysis with end stage renal failure, for which he had to be given regular intermittent hemodialysis treatment. Untreated hypertension and glomerulonephritis was probably present prior to all these acute incidents. Examination of the kidney biopsy revealed mesangial proliferative glomerulonephritis and arterial wall thickening causing nephrosclerosis together with interstitial calcinosis. The combination of all these pathologic changes might be responsible for the development of progressive chronic renal failure ending up with the need for continuous intermittent hemodialysis treatment.

Nephropathic Cystinosis Mimicking Bartter Syndrome: a Novel Mutation.

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Bastug, Funda; Nalcacioglu, Hulya; Ozaltin, Fatih; Korkmaz, Emine; Yel, Sibel

2018-01-01

Cystinosis is a rare autosomal recessive disorder resulting from defective lysosomal transport of cystine due to mutations in the cystinosin lysosomal cystine transporter (CTNS) gene. The clinical phenotype of nephropathic cystinosis is characterized by renal tubular Fanconi syndrome and development of end-stage renal disease during the first decade. Although metabolic acidosis is the classically prominent finding of the disease, a few cases may present with hypokalemic metabolic alkalosis mimicking Bartter syndrome. Bartter-like presentation may lead to delay in diagnosis and initiation of specific treatment for cystinosis. We report a case of a 6-year-old girl initially presenting with the features of Bartter syndrome that was diagnosed 2 years later with nephropathic cystinosis and a novel CTNS mutation.

Inherited renal tubular defects with hypokalemia

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Muthukrishnan J

2009-01-01

Full Text Available Bartter′s and Gitelman′s syndrome are two ends of a spectrum of inherited renal tubular disorders that present with hypokalemic metabolic alkalosis of varying severity. Clinical features and associated calcium and magnesium ion abnormalities are used to diagnose these cases after excluding other commoner causes. We report on two cases, the first being a young boy, born of pregnancy complicated by polyhydramnios, who had classical dysmorphic features, polyuria, hypokalemia and hypercalciuria and was diagnosed as having Bartter′s syndrome. The second patient is a lady who had recurrent tetany as the only manifestation of Gitelman′s syndrome, which is an unusual presentation. Potassium replacement with supplementation of other deficient ions led to satisfactory clinical and biochemical response.

Variability of Acid-Base Status in Acetate-Free Biofiltration 84% versus Bicarbonate Dialysis

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Harzallah Kais

2008-01-01

Full Text Available The ultimate goal of hemodialysis (HD treatment is to achieve the highest level of efficacy in the presence of maximal clinical tolerance. With an aim to offer good hemodynamic stability, as observed during the acetate-free biofiltration 14% (AFB 14% to patients who are intolerant to bicarbonate dialysis (BD and with less cost, we have developed since June 1994, a new HD technique, namely AFB 84%. This study was carried out to analyze acid-base variations during the AFB 84% in comparison to BD in hemodynamically stable patients on regular HD. This was a prospective randomized crossover study carried out on 12 patients (6 males and 6 females for a total of 144 HD sessions (72 BD and 72 AFB 84%. Patients with decompensated cardiomyopathy, respiratory diseases or uncontrolled hypertension were not included in the trial. All the patients were treated with BD or AFB 84%; the latter is characterized by the absence of acetate in the dialysate and a complete correction of buffer balance by post-dilutional infusion of bicarbonate-based replacement solution. The comparison of pre-dialysis arterial acid-base and blood-gas parameters revealed no significant differences of pH, HCO 3 - and paCO 2 levels between the two techniques. Analysis of post-dialysis parameters showed that, among patients dialyzed with BD, there was over correction of metabolic acidosis with a tendency towards metabolic alkalosis. In contrast, in patients dialyzed with AFB 84%, we observed a significant improvement in pH and HCO 3 - levels but the increase in paCO2 level was not significant. A comparison of these parameters between the two techniques showed statistically significant difference in pH, HCO3 - and paCO2 levels, but not for paO2 level. AFB 84% can offer some important advantages with the complete absence of acetate from the substitution fluids, and permits a better correction of metabolic acidosis than BD, without causing alkalosis.

Functional and molecular characterization of transmembrane intracellular pH regulators in human dental pulp stem cells.

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Chen, Gunng-Shinng; Lee, Shiao-Pieng; Huang, Shu-Fu; Chao, Shih-Chi; Chang, Chung-Yi; Wu, Gwo-Jang; Li, Chung-Hsing; Loh, Shih-Hurng

2018-06-01

Homeostasis of intracellular pH (pH i ) plays vital roles in many cell functions, such as proliferation, apoptosis, differentiation and metastasis. Thus far, Na + -H + exchanger (NHE), Na + -HCO 3 - co-transporter (NBC), Cl - /HCO 3 - exchanger (AE) and Cl - /OH - exchanger (CHE) have been identified to co-regulate pH i homeostasis. However, functional and biological pH i -regulators in human dental pulp stem cells (hDPSCs) have yet to be identified. Microspectrofluorimetry technique with pH-sensitive fluorescent dye, BCECF, was used to detect pH i changes. NH 4 Cl and Na + -acetate pre-pulse were used to induce intracellular acidosis and alkalosis, respectively. Isoforms of pH i -regulators were detected by Western blot technique. The resting pH i was no significant difference between that in HEPES-buffered (nominal HCO 3 - -free) solution or CO 2 /HCO 3 -buffered system (7.42 and 7.46, respectively). The pH i recovery following the induced-intracellular acidosis was blocked completely by removing [Na + ] o , while only slowed (-63%) by adding HOE694 (a NHE1 specific inhibitor) in HEPES-buffered solution. The pH i recovery was inhibited entirely by removing [Na + ] o , while adding HOE 694 pulse DIDS (an anion-transporter inhibitor) only slowed (-55%) the acid extrusion. Both in HEPES-buffered and CO 2 /HCO 3 -buffered system solution, the pH i recovery after induced-intracellular alkalosis was entirely blocked by removing [Cl - ] o . Western blot analysis showed the isoforms of pH i regulators, including NHE1/2, NBCe1/n1, AE1/2/3/4 and CHE in the hDPSCs. We demonstrate for the first time that resting pH i is significantly higher than 7.2 and meditates functionally by two Na + -dependent acid extruders (NHE and NBC), two Cl - -dependent acid loaders (CHE and AE) and one Na + -independent acid extruder(s) in hDPSCs. These findings provide novel insight for basic and clinical treatment of dentistry. Copyright © 2018 Elsevier Ltd. All rights reserved.

Sodium bicarbonate-augmented stress thallium myocardial scintigraphy

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Sarin, Badal; Chugh, Pradeep Kumar; Kaushal, Dinesh; Soni, Nakse Lal; Sawroop, Kishan; Mondal, Anupam; Bhatnagar, Aseem [Department of Nuclear Medicine, Institute of Nuclear Medicine and Allied Sciences, Brig. S. K. Mazumdar Road, 110054, Delhi (India)

2004-04-01

It is well known that sodium bicarbonate in pharmacological doses induces transient alkalosis, causing intracellular transport of serum potassium. The aims of this study were (a) to investigate whether, in humans, myocardial thallium-201 uptake can be augmented by pretreatment with a single bolus of sodium bicarbonate at a pharmacological dose, (b) to verify general safety aspects of the intervention and (c) to evaluate the clinical implications of augmentation of {sup 201}Tl uptake, if any. Routine exercise myocardial scintigraphy was performed twice in eight adult volunteers (five normal and three abnormal), once without intervention and the second time (within a week) following intravenous administration of sodium bicarbonate (88 mEq in 50 ml) as a slow bolus 1 h prior to the injection of {sup 201}Tl. Conventional myocardial thallium study was compared with sodium bicarbonate interventional myocardial scintigraphy with respect to myocardial uptake (counts per minute per mCi injected dose), washout patterns in normal and abnormal myocardial segments, and overall clinical interpretation based on planar and single-photon emission tomographic (SPET) images. All patients remained asymptomatic after the intervention. A mean increase of 53% in myocardial uptake of thallium was noted in post-exercise acquisitions after the intervention, confirming uptake of the tracer via the potassium-hydrogen pump and its augmentation by transient alkalosis. The washout pattern remained unchanged. The visual quality of planar and SPET images improved significantly after the intervention. Out of the five abnormal myocardial segments identified in three cases, four showed significant filling-in after the intervention, causing the diagnosis to be upgraded from ''partial scar'' to ''ischaemia'', or from ''ischaemia'' to ''normal''. The overall scan impression changed in two out of three such cases. Sodium

Gitelman's syndrome in pregnancy: case report and review of the literature.

LENUS (Irish Health Repository)

McCarthy, Fergus P

2012-01-31

Gitelman\\'s syndrome (GS), a rare renal disorder, results in hypokalaemia, hypomagnesaemia, hypocalciuria and a metabolic alkalosis. It is unclear if an alteration in management is necessary or beneficial during pregnancy. A 32-year-old woman with GS was managed in her second pregnancy. Antenatally, the patient required 39 (principally day case) admissions to the hospital for intravenous (IV) therapy and received a cumulative total of 47 l of IV 0.9% saline solution, 47 doses of 20 mmol magnesium chloride and 46 doses of 80 mmol potassium chloride. She delivered a 2940-g female infant in excellent condition by caesarean section. We would suggest that close attention to maternal weight gain during pregnancy is an easily available clinical tool to assess adequacy of fluid and electrolyte repletion in this condition.

Stress of formalin treatment in juvenile spring chinook salmon (Oncorhynchus tshawytscha) and steelhead trout (Salmo gairdneri)

Science.gov (United States)

Wedemeyer, Gary; Yasutake, W.T.

1973-01-01

The physiological stress of 200 ppm formalin treatments at 10 C is more severe in the juvenile steelhead trout (Salmo gairdneri) than in the spring chinook salmon (Oncorhynchus tshawytscha). In the steelhead, a marked hypochloremia follows a 1-hr treatment and recovery requires about 24 hr. During longer treatments, hypercholesterolemia together with reduced regulatory precision, hypercortisolemia, alkaline reserve depletion, and hypocapnia unaccompanied by a fall in blood pH occur — suggestive of compensated respiratory alkalosis. In the spring chinook, hypochloremia and reduced plasma cholesterol regulatory precision are the significant treatment side effects but recovery requires only a few hours.Formalin treatments also cause epithelial separation, hypertrophy, and necrosis in the gills of both fishes but again, consistent with the physiological dysfunctions, these are more severe in the steelhead.

Infantile variant of Bartter syndrome and sensorineural deafness: A new autosomal recessive disorder

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Landau, D.; Shalev, H.; Carmi, Rivka; Ohaly, M. [Univ. of the Negev, Ashkelon (Israel)

1995-12-04

The infantile variant of Bartter syndrome (IBS) is usually associated with maternal polyhydramnios, premature birth, postnatal polyuria and hypokalemic hypochloremic metabolic alkalosis and a typical appearance. IBS is thought to be an autosomal recessive trait. Several congenital tubular defects are associated with sensorineural deafness (SND). However, an association between the IBS and SND has not been reported so far. Here we describe 5 children of an extended consanguineous Bedouin family with IBS and SND. In 3 of the cases, the typical electrolyte imbalance and facial appearance were detected neonatally. SND was detected as early as age 1 month, suggesting either coincidental homozygotization of 2 recessive genes or a pleiotropic effect of one autosomal recessive gene. This association suggests that evaluation of SND is warranted in every case of IBS. 35 refs., 2 figs., 2 tabs.

Acute toxicity from baking soda ingestion.

Science.gov (United States)

Thomas, S H; Stone, C K

1994-01-01

Sodium bicarbonate is an extremely well-known agent that historically has been used for a variety of medical conditions. Despite the widespread use of oral bicarbonate, little documented toxicity has occurred, and the emergency medicine literature contains no reports of toxicity caused by the ingestion of baking soda. Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The case of a patient with three hospital admissions in 4 months, all the result of excessive oral intake of bicarbonate for symptomatic relief of dyspepsia is reported. Evaluation and treatment of patients with acute bicarbonate ingestion is discussed.

Bartter syndrome and growth hormone deficiency: three cases.

Science.gov (United States)

Buyukcelik, Mithat; Keskin, Mehmet; Kilic, Beltinge Demircioglu; Kor, Yilmaz; Balat, Ayse

2012-11-01

Bartter syndrome is a rare autosomal recessive disorder characterized by hypokalemia, salt loss, and metabolic alkalosis. Short stature is one of the clinical manifestations in these children. Although polyuria, polydipsia, hypokalemia, and salt loss may be responsible for growth retardation, the exact pathogenesis of short stature in Bartter syndrome is not known. In this study, we present three children diagnosed as having Bartter syndrome with short stature and growth hormone (GH) deficiency. After recombinant human growth hormone therapy (rhGH), their growth velocities were improved. These results indicate that GH deficiency may contribute to short stature in children with Bartter syndrome, and rhGH therapy would be an excellent adjunctive treatment for short children with this syndrome whose condition is resistant to conventional therapies in terms of growth.

Bartter syndrome type III and congenital anomalies of the kidney and urinary tract: an antenatal presentation.

Science.gov (United States)

Westland, Rik; Hack, Wilfried W; van der Horst, Henricus J R; Uittenbogaard, Lukas B; van Hagen, Johanna M; van der Valk, Paul; Kamsteeg, Erik J; van den Heuvel, Lambert P; van Wijk, Joanna A E

2012-12-01

Bartter syndrome encompasses a variety of inheritable renal tubular transport disorders characterized by hypokalemia and hypochloremic metabolic alkalosis. Bartter syndrome Type III is caused by genetic alterations in the chloride channel kidney B (CLCNKB) gene and often presents in the first 2 years of life, known as classic Bartter syndrome. However, in rare cases Bartter syndrome Type III has an antenatal presentation with polyhydramnios, premature delivery and severe dehydration in the first weeks of life. Associations between congenital anomalies of the kidney and urinary tract and Bartter syndrome are extremely rare. This case report presents a girl with Bartter syndrome Type III due to a homozygous CLCNKB mutation and bilateral congenital anomalies of the kidney and urinary tract. In addition, we describe the antenatal presentation as well as its perinatal management.

Acid-alkaline state of the blood in chronic combined effect of silicon dioxide, radon and tobacco smoke

International Nuclear Information System (INIS)

Ivanov, Z.; Charykchiev, D.

1987-01-01

Experimental observations were carried out on rats, subjected to inhalaion of radon-222 and combination of radon-222 with intratracheally introduced free silicon dioxide and tobacco smoke. A special method was used for anaerobic and narcosis-free taking of arterial blood from the left cardiac ventricle, the animals being investigated on the 2nd and the 6th month from the start of the experiment. In all tested animals a tendency to respiratory hypercapneic acidosis was established, particularly to the end of the experiment and in the group treated only with radon-222. In these animals a marked non-respiratory alkalosis with deviation of pH to alkaline direction was added. It is assumed that above-mentioned acid-alkaline disturbances could be due to the found morphological changes in the respiratory system, the liver and kidneys

Amitraz poisoning: case report

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Jaime Alexander Molina-Bolaños

2017-10-01

Full Text Available Amitraz is an insecticide compound used worldwide for controlling pests, especially in agricultural and livestock areas. However, amitraz poisoning in Colombia is rare. This article reports the case of an 18-year-old female patient who was admitted in the emergency service 3 hours after the intake of an unknown amount of Triatox® (amitraz. The patient presented with a depressed level of consciousness, respiratory distress, hypotension, bradycardia, myosis and metabolic acidosis compensated with respiratory alkalosis. Initial treatment was provided using life support measures in the emergency ward, and subsequent transfer and support in the intensive care unit. She was discharged 24 hours after admission. This case considers the clinical similarity between amitraz poisoning and poisoning caused by other more frequent toxic compounds such as carbamates, organophosphates and opioids, which require different management.

Neonatal bartter syndrome

International Nuclear Information System (INIS)

Parkash, J.; Salat, S. M.; Khan, I.A.

2006-01-01

A pre-term baby girl was born following a pregnancy complicated by severe polyhydramnios at a gestational age of 36 weeks. She was initially suffering from respiratory distress consistent with idiopathic respiratory distress syndrome, and altered electrolyte imbalance with hyponatremia, hypokalemia and hypochloremic metabolic alkalosis. However, during the third week of life when she had dehydration along with significant electrolyte imbalance, Bartter's syndrome was considered which was supported by findings of high renin and aldosterone levels. Treatment was done by correction of electrolytes and dehydration along with indomethacin. The drug was well tolerated. The infant showed correction of electrolyte imbalance. The features of this case suggest an extreme form of Bartter's syndrome presenting from the early days of life. The syndrome is reported because of it's rarity and alerts pediatricians to the antenatal and neonatal variant of Bartter's syndrome. (author)

Opiate Withdrawal Complicated by Tetany and Cardiac Arrest

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Irfanali R. Kugasia

2014-01-01

Full Text Available Patients with symptoms of opiate withdrawal, after the administration of opiate antagonist by paramedics, are a common presentation in the emergency department of hospitals. Though most of opiate withdrawal symptoms are benign, rarely they can become life threatening. This case highlights how a benign opiate withdrawal symptom of hyperventilation led to severe respiratory alkalosis that degenerated into tetany and cardiac arrest. Though this patient was successfully resuscitated, it is imperative that severe withdrawal symptoms are timely identified and immediate steps are taken to prevent catastrophes. An easier way to reverse the severe opiate withdrawal symptom would be with either low dose methadone or partial opiate agonists like buprenorphine. However, if severe acid-base disorder is identified, it would be safer to electively intubate these patients for better control of their respiratory and acid-base status.

Genetic analysis in Bartter syndrome from India.

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Sharma, Pradeep Kumar; Saikia, Bhaskar; Sharma, Rachna; Ankur, Kumar; Khilnani, Praveen; Aggarwal, Vinay Kumar; Cheong, Hae

2014-10-01

Bartter syndrome is a group of inherited, salt-losing tubulopathies presenting as hypokalemic metabolic alkalosis with normotensive hyperreninemia and hyperaldosteronism. Around 150 cases have been reported in literature till now. Mutations leading to salt losing tubulopathies are not routinely tested in Indian population. The authors have done the genetic analysis for the first time in the Bartter syndrome on two cases from India. First case was antenatal Bartter syndrome presenting with massive polyuria and hyperkalemia. Mutational analysis revealed compound heterozygous mutations in KCNJ1(ROMK) gene [p(Leu220Phe), p(Thr191Pro)]. Second case had a phenotypic presentation of classical Bartter syndrome however, genetic analysis revealed only heterozygous novel mutation in SLC12A gene p(Ala232Thr). Bartter syndrome is a clinical diagnosis and genetic analysis is recommended for prognostication and genetic counseling.

Relationship of metabolic alkalosis, azotemia and morbidity in patients with chronic obstructive pulmonary disease and hypercapnia.

Science.gov (United States)

Ucgun, Irfan; Oztuna, Funda; Dagli, Canan Eren; Yildirim, Huseyin; Bal, Cengiz

2008-01-01

Exacerbation of chronic obstructive pulmonary disease (COPD) is an important cause of morbidity and mortality, but the effect of metabolic compensation of respiratory acidosis (RA) on mortality is not fully understood. To investigate the relationship between metabolic compensation and mortality in COPD patients with RA. We prospectively investigated all COPD patients with RA admitted to the respiratory intensive care unit between February 2001 and March 2007. Two hundred and thirteen patients (159 male, 54 female; mean age 65 +/- 10.8 years) were divided into three groups (71 patients each) according to base excess (BE) levels: (1) low BE, (2) medium BE, and (3) high BE. H(+) concentration was calculated according to their standard formula and BE was calculated according to the Van Slyke equation. The overall mortality rate was 24.9%. The group mortality rates were 32, 17 and 25% in the low, medium and high BE groups, respectively (p = 0.001). When patients were divided into three groups according to the HCO(3)(-) levels, the group mortality rate was 59.1% in the low HCO(3)(-) group and 19.8% in the high HCO(3)(-) group. Based on univariate analysis, six factors affecting mortality were identified. However, multivariate analysis showed that the levels of serum HCO(3)(-) (p = 0.013; OR: 0.552; CI: 0.345-0.882) and creatinine (p = 0.019; OR: 2.114; CI: 1.132-3.949) had an independent effect. In patients with COPD exacerbation and hypercapnia, the development of sufficient metabolic compensation and adequate renal function significantly decreases mortality. Copyright 2008 S. Karger AG, Basel.

Gitelman syndrome manifesting in early childhood and leading to delayed puberty: a case report

Directory of Open Access Journals (Sweden)

Raza Farhan

2012-10-01

Full Text Available Abstract Introduction Gitelman syndrome is an inherited autosomal recessive renal salt-wasting disorder. It presents with variable clinical symptoms including muscle weakness and fatigue, and the diagnosis is based on metabolic alkalosis, hypokalemia, hypomagnesemia and hypocalciuria. It is usually diagnosed incidentally in early adulthood. There are rare cases of Gitelman syndrome presenting in early childhood; however, to the best of our knowledge it has not previously been associated with delayed puberty. Case presentation A 17-year-old South Asian man with recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years was admitted for further workup. Before the age of 12 years, the episodes had been mild, but they then got progressively worse. Other symptoms include polyuria, polydipsia, nocturia, paresthesia and occasional watery diarrhea. He also had a history of short stature, poor weight gain and delayed developmental landmarks. His family history was unremarkable except for the consanguineous marriage of his parents. An examination revealed a thin and lean man with blood pressure of 95/60mmHg. His height and weight were below the third percentile and his sexual development was at Tanner Stage II. Laboratory work revealed serum sodium of 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and magnesium of 1.2mg/dL. His testosterone level was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL with normal levels of luteinizing hormone and follicle-stimulating hormone. The sex hormone findings were attributed to delayed puberty. A 24-hour urinary analysis revealed decreased excretion of calcium (25.9mg/24 hours. Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of Gitelman syndrome was made. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake

Pattern of acid base abnormalities in critically ill patinets

International Nuclear Information System (INIS)

Ahmad, T.M.; Mehmood, A.; Malik, T.M.

2015-01-01

To find out the pattern of acid base abnormalities in critically ill patients in a tertiary care health facility. Study Design: A descriptive study. Place and Duration of Study: The study was carried out in the department of pathology, Combined Military Hospital Kharian from January 2013 to June 2013. Patients and Methods: Two hundred and fifty patients suffering from various diseases and presenting with exacerbation of their clinical conditions were studied. These patients were hospitalized and managed in acute care units of the hospital. Arterial blood gases were analysed to detect acid base status and their correlation with their clinical condition. Concomitant analysis of electrolytes was carried out. Tests related to concurrent illnesses e.g. renal and liver function tests, cardiac enzymes and plasma glucose were assayed by routine end point and kinetic methods. Standard reference materials were used to ensure internal quantify control of analyses. Results: Two hundred and fifteen patients out of 250 studied suffered from acid base disorders. Gender distribution showed a higher percentage of male patients and the mean age was 70.5 ± 17.4 years. Double acid base disorders were the commonest disorders (34%) followed by metabolic acidosis (30%). Anion gap was calculated to further stratify metabolic acidosis and cases of diabetic ketoacidosis were the commonest in this category (47%). Other simple acid base disorders were relatively less frequent. Delta bicarbonate was calculated to unmask the superimposition of respiratory alkalosis or acidosis with metabolic acidosis and metabolic alkalosis. Though triple acid base disorders were noted in a small percentage of cases (05%), but were found to be the most complicated and challenging. Mixed acid base disorders were associated with high mortality. Conclusion: A large number of critically ill patients manifested acid base abnormalities over the full spectrum of these disorders. Mixed acid base disorders were

Hypoxia and Its Acid-Base Consequences: From Mountains to Malignancy.

Science.gov (United States)

Swenson, Erik R

Hypoxia, depending upon its magnitude and circumstances, evokes a spectrum of mild to severe acid-base changes ranging from alkalosis to acidosis, which can alter many responses to hypoxia at both non-genomic and genomic levels, in part via altered hypoxia-inducible factor (HIF) metabolism. Healthy people at high altitude and persons hyperventilating to non-hypoxic stimuli can become alkalotic and alkalemic with arterial pH acutely rising as high as 7.7. Hypoxia-mediated respiratory alkalosis reduces sympathetic tone, blunts hypoxic pulmonary vasoconstriction and hypoxic cerebral vasodilation, and increases hemoglobin oxygen affinity. These effects and others can be salutary or counterproductive to tissue oxygen delivery and utilization, based upon magnitude of each effect and summation. With severe hypoxia either in the setting of profound arterial hemoglobin desaturation and reduced O2 content or poor perfusion (ischemia) at the global or local level, metabolic and hypercapnic acidosis develop along with considerable lactate formation and pH falling to below 6.8. Although conventionally considered to be injurious and deleterious to cell function and survival, both acidoses may be cytoprotective by various anti-inflammatory, antioxidant, and anti-apoptotic mechanisms which limit total hypoxic or ischemic-reperfusion injury. Attempts to correct acidosis by giving bicarbonate or other alkaline agents under these circumstances ahead of or concurrent with reoxygenation efforts may be ill advised. Better understanding of this so-called "pH paradox" or permissive acidosis may offer therapeutic possibilities. Rapidly growing cancers often outstrip their vascular supply compromising both oxygen and nutrient delivery and metabolic waste disposal, thus limiting their growth and metastatic potential. However, their excessive glycolysis and lactate formation may not necessarily represent oxygen insufficiency, but rather the Warburg effect-an attempt to provide a large amount

The role of acid-base imbalance in statin-induced myotoxicity.

Science.gov (United States)

Taha, Dhiaa A; De Moor, Cornelia H; Barrett, David A; Lee, Jong Bong; Gandhi, Raj D; Hoo, Chee Wei; Gershkovich, Pavel

2016-08-01

Disturbances in acid-base balance, such as acidosis and alkalosis, have potential to alter the pharmacologic and toxicologic outcomes of statin therapy. Statins are commonly prescribed for elderly patients who have multiple comorbidities such as diabetes mellitus, cardiovascular, and renal diseases. These patients are at risk of developing acid-base imbalance. In the present study, the effect of disturbances in acid-base balance on the interconversion of simvastatin and pravastatin between lactone and hydroxy acid forms have been investigated in physiological buffers, human plasma, and cell culture medium over pH ranging from 6.8-7.8. The effects of such interconversion on cellular uptake and myotoxicity of statins were assessed in vitro using C2C12 skeletal muscle cells under conditions relevant to acidosis, alkalosis, and physiological pH. Results indicate that the conversion of the lactone forms of simvastatin and pravastatin to the corresponding hydroxy acid is strongly pH dependent. At physiological and alkaline pH, substantial proportions of simvastatin lactone (SVL; ∼87% and 99%, respectively) and pravastatin lactone (PVL; ∼98% and 99%, respectively) were converted to the active hydroxy acid forms after 24 hours of incubation at 37°C. At acidic pH, conversion occurs to a lower extent, resulting in greater proportion of statin remaining in the more lipophilic lactone form. However, pH alteration did not influence the conversion of the hydroxy acid forms of simvastatin and pravastatin to the corresponding lactones. Furthermore, acidosis has been shown to hinder the metabolism of the lactone form of statins by inhibiting hepatic microsomal enzyme activities. Lipophilic SVL was found to be more cytotoxic to undifferentiated and differentiated skeletal muscle cells compared with more hydrophilic simvastatin hydroxy acid, PVL, and pravastatin hydroxy acid. Enhanced cytotoxicity of statins was observed under acidic conditions and is attributed to increased

Gitelman syndrome manifesting in early childhood and leading to delayed puberty: a case report.

Science.gov (United States)

Raza, Farhan; Sultan, Mubashar; Qamar, Khola; Jawad, Ali; Jawa, Ali

2012-10-02

Gitelman syndrome is an inherited autosomal recessive renal salt-wasting disorder. It presents with variable clinical symptoms including muscle weakness and fatigue, and the diagnosis is based on metabolic alkalosis, hypokalemia, hypomagnesemia and hypocalciuria. It is usually diagnosed incidentally in early adulthood. There are rare cases of Gitelman syndrome presenting in early childhood; however, to the best of our knowledge it has not previously been associated with delayed puberty. A 17-year-old South Asian man with recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years was admitted for further workup. Before the age of 12 years, the episodes had been mild, but they then got progressively worse. Other symptoms include polyuria, polydipsia, nocturia, paresthesia and occasional watery diarrhea. He also had a history of short stature, poor weight gain and delayed developmental landmarks. His family history was unremarkable except for the consanguineous marriage of his parents. An examination revealed a thin and lean man with blood pressure of 95/60mmHg. His height and weight were below the third percentile and his sexual development was at Tanner Stage II. Laboratory work revealed serum sodium of 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and magnesium of 1.2mg/dL. His testosterone level was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL) with normal levels of luteinizing hormone and follicle-stimulating hormone. The sex hormone findings were attributed to delayed puberty. A 24-hour urinary analysis revealed decreased excretion of calcium (25.9mg/24 hours). Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of Gitelman syndrome was made. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake. Diagnosis of Gitelman syndrome is usually made incidentally

Bilateral acute lupus pneumonitis in a case of rhupus syndrome

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Supriya Sarkar

2012-01-01

Full Text Available Rhupus syndrome, the overlap of rheumatoid arthritis (RA and systemic lupus erythematosus (SLE, is an extremely uncommon condition. Organ damages found due to SLE are usually mild in rhupus. Lupus pneumonitis in rhupus syndrome has not been reported worldwide. We are reporting a 23-year-old female with bilateral symmetric erosive arthritis, oral ulcer, alopecia, polyserositis, anemia, leucopenia, positive RA-factor, anti nuclear antibody (ANA and anti ds-DNA. She presented with acute onset dyspnea, high fever, chest pain, tachycardia, tachypnea, hypoxia and respiratory alkalosis. High resolution computed tomography (HRCT-thorax showed bilateral, basal consolidation with air bronchogram. Repeated sputum and single broncho alveolar lavage (BAL fluid examination revealed no organism or Hemosiderin-laden macrophage. The diagnosis of rhupus was confirmed by combined manifestations of RA and SLE, and the diagnosis of acute lupus pneumonitis was established by clinico-radiological picture and by excluding other possibilities.

Hypokalemic paralysis and respiratory failure due to excessive intake of licorice syrup

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Mehmet Oguzhan Ay

2014-04-01

Full Text Available Licorice is the root of Glycyrrhiza glabra, which has a herbal ingredient, glycyrrhizic acid. Excessive intake of licorice may cause a hypermineralocorticoidism-like syndrome characterized by sodium and water retention, hypokalemia, hypertension, metabolic alkalosis, low-renin activity, and hypoaldosteronism. In this paper, an 34 years old man who admitted to the emergency department with respiratory failure and marked muscle weakness of all extremities that progressed to paralysis after excessive intake of licorice syrup was presented. It was aimed to draw attention to the necessity of questioning whether there is excessive intake of licorice or not in patients who admitted to emergency department with paralysis and dyspnea. Plasma potassium concentration of the patient was 1.4 mmol/L. The patient\\'s respiratory distress and loss of muscle strength recovered completely after potassium replacement. [Cukurova Med J 2014; 39(2.000: 387-391

Amikacin-induced type 5 Bartter-like syndrome with severe hypocalcemia

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Chrispal A

2009-01-01

Full Text Available Aminoglycoside-induced renal toxicity is well known and may manifest with nonoliguric renal failure or renal tubular dysfunction. Aminoglycoside-induced renal tubular dysfunction could result in diffuse damage or manifest as a Fanconi-like syndrome, Bartter-like syndrome, or distal renal tubular acidosis. We discuss a patient who developed severe renal tubular dysfunction secondary to short-term therapy with Amikacin, resulting in refractory hypokalemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, and polyuria. This constellation of biochemical abnormalities mimic Type 5 Bartter′s syndrome, where there is activating mutation of the calcium sensing receptor in the thick ascending loop of Henle and the distal tubule. In this case this activation of the calcium sensing receptor was triggered by amikacin. This phenomenon has been described with gentamicin though never with amikacin. Recovery of the tubular dysfunction took 15 days following cessation of the offending drug, Amikacin.

Sodium bicarbonate intake improves high-intensity intermittent exercise performance in trained young men

DEFF Research Database (Denmark)

Krustrup, Peter; Ermidis, Georgios; Mohr, Magni

2015-01-01

Background Sodium bicarbonate intake has been shown to improve exercise tolerance, but the effects on high-intensity intermittent exercise are less clear. Thus, the aim of the present study was to determine the effect of sodium bicarbonate intake on Yo-Yo intermittent recovery level 2 test......) prior intake of sodium bicarbonate (0.4 g · kg−1 body weight). Heart rate and rating of perceived exertion (RPE) were measured during the test and venous blood samples were taken frequently. Results Yo-Yo IR2 performance was 14 % higher (P = 0.04) in SBC than in CON (735 ± 61 vs 646 ± 46 m, respectively......-intensity intermittent exercise performance is improved by prior intake of sodium bicarbonate in trained young men, with concomitant elevations in blood alkalosis and peak blood lactate levels, as well as lowered rating of perceived exertion....

Adrenocortical carcinoma, an unusual cause of secondary hypertension.

Science.gov (United States)

Veron Esquivel, Daniel; Batiz, Fernando; Farias Vega, Alfonso; Carrillo Gonzalez, Perla A

2016-12-07

We present the case of a female patient aged 39 years who was admitted to our hospital due to hypertension, severe hypokalaemia and metabolic alkalosis; physical examination was remarkable for plethoric moon face, centripetal obesity and bilateral lower extremity oedema. She was admitted for intravenous potassium replacement and further assessment of hypertension and associated clinical findings. Laboratory testing showed increased levels of aldosterone, renin, cortisol, testosterone and androstenedione. An abdominal CT revealed a large mass in the right adrenal gland with hepatic involvement. The patient was started on antihypertensive medications and underwent laparoscopic surgery for mass and liver biopsy. The pathological diagnosis was adrenocortical carcinoma with liver metastasis. Hyperaldosteronism is a cause of secondary hypertension and its diagnosis is usually benign. Adrenocortical carcinoma is a rare condition and aldosterone secreting tumours are even rarer; associated hypertension usually improves after tumour resection, but with the presence of metastasis, blood pressure control is difficult. 2016 BMJ Publishing Group Ltd.

[Comparative studies on toxicity of various dielectrics, petroleum derivatives, used in electroerosion technology. IV. Morphological and cytoenzymatic changes in the lungs and acid-base imbalance in rats chronically exposed to petroleum hydrocarbons].

Science.gov (United States)

Starek, A; Kamiński, M

1981-01-01

In rats exposed to odourless kerosene of 75 and 300 mg/m3 concentration, for 14 weeks, morphologic and cytoenzymatic examinations of lungs have been carried out and acid-base equilibrium indices in blood have been determined. Passive congestion of lung parenchyma, subpleural blood extravasation, atelectasis foci, thickened interalveolar septa with infiltrates from neutrophils, lymphocytes, eosinophils and macrophages have been found. In addition a decrease in succinic dehydrogenase activity, NADPH -- tetrazolium reductase, and Mg++-ATP-ase and increase in acid phosphatase activity have been revealed. Those have been focal changes, involving, apart from bronchial tree (low exposure -- 75 mg/m3), the remaining lung parenchyma segments (high exposure -- 300 mg/m3). In addition, disturbances in acid-base equilibrium in form of compensated metabolic alkalosis (75 mg/m3) and compensated metabolic acidosis (300 mg/m3) have occurred. The obtained results demonstrate toxic effects of kerosene hydrocarbons on the function and structure of lungs.

in Critically Ill Patients: Success and Limits

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Filippo Mariano

2011-01-01

Full Text Available Citrate anticoagulation has risen in interest so it is now a real alternative to heparin in the ICUs practice. Citrate provides a regional anticoagulation virtually restricted to extracorporeal circuit, where it acts by chelating ionized calcium. This issue is particularly true in patients ongoing CRRT, when the “continuous” systemic anticoagulation treatment is per se a relevant risk of bleeding. When compared with heparin most of studies with citrate reported a longer circuit survival, a lower rate of bleeding complications, and transfused packed red cell requirements. As anticoagulant for CRRT, the infusion of citrate is prolonged and it could potentially have some adverse effects. When citrate is metabolized to bicarbonate, metabolic alkalosis may occur, or for impaired metabolism citrate accumulation leads to acidosis. However, large studies with dedicated machines have indeed demonstrated that citrate anticoagulation is well tolerated, safe, and an easy to handle even in septic shock critically ill patients.

A dangerous mixture

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Anna Piva

2014-03-01

Full Text Available A 59-year old woman was admitted for fatigue and arm paresthesias with Trousseau sign. Her medical history included thyroidectomy and hypercholesterolemia recently treated with simvastatin. Laboratory tests showed severe hypokalemia and hypocalcemia, severe increase in muscle enzymes, metabolic alkalosis; low plasma renin activity, increased thyroid-stimulating hormone, normal free thyroxine, increased parathyroid hormone, decreased vitamin D3; alterations in electrolyte urinary excretion, cortisol and aldosterone were excluded. Hypothesizing a statin-related myopathy, simvastatin was suspended; the patient reported use of laxatives containing licorice. Electrolytes normalized with intravenous supplementation. Among many biochemical alterations, none stands out as a major cause for muscular and electrolyte disorders. All co-factors are inter-connected, starting with statin-induced myopathy, worsened by hypothyroidism, secondary hyperaldosteronism and vitamin D deficiency, leading to hypocalcemia and hypokalemia, perpetrating muscular and electrolyte disorders. The importance of considering clinical conditions as a whole emerges with multiple co-factors involved. Another issue concerns herbal products and their potential dangerous effects.

A Case of Paraneoplastic Cushing Syndrome Presenting as Hyperglycemic Hyperosmolar Nonketotic Syndrome

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Christina E. Brzezniak

2017-04-01

Full Text Available Carcinoid tumors are neuroendocrine tumors that mainly arise in the gastrointestinal tract, lungs, and bronchi. Bronchopulmonary carcinoids have been associated with Cushing syndrome, which results from ectopic adrenocorticotrophic hormone (ACTH secretion. We report the case of a 65-year-old man, a colonel in the US Air Force, with metastatic bronchopulmonary carcinoid tumors treated on a clinical trial who was hospitalized for complaints of increasing thirst, polydipsia, polyuria, weakness, and visual changes. Decompensated hyperglycemia suggested a diagnosis of hyperglycemic hyperosmolar nonketotic syndrome (HHNS. Additional findings, which included hypokalemia, hypernatremia, hypertension, metabolic alkalosis, moon facies, and striae, raised a red flag for an ectopic ACTH syndrome. Elevated ACTH levels confirmed Cushing syndrome. Treatment with a fluid replacement and insulin drip resulted in immediate symptomatic improvement. Cushing syndrome should be considered in carcinoid patients with physical stigmata such as moon facies and striae. HHNS may be the presenting clinical feature in patients with impaired glucose metabolism.

The increased concentration of 2,3-diphosphoglycerate in red blood cells of spontaneously hypertensive rats.

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Przybylski, J; Skotnicka-Fedorowicz, B; Lisiecka, A; Siński, M; Abramczyk, P

1997-12-01

It has been recognised that high haemoglobin oxygen capacity is essential for the development of high blood pressure in spontaneously hypertensive rats. In the present study we have found increased concentration of 2,3 diphosphoglycerate (2,3-DPG) in red blood cells of spontaneously hypertensive rats (SHR) of Okamoto-Aoki strain. As 2,3-DPG is the major factor decreasing haemoglobin affinity to oxygen, our finding suggests that at given value of pO2 oxygen delivery to the tissue of SHR would be increased. Therefore increased concentration of 2,3-DPG in red blood cells of SHR would be of the pathophysiological meaning by promoting autoregulatory increase in total vascular resistance in this strain of rats. The mechanism responsible for enhanced synthesis of 2,3-DPG in SHR remains unclear. Intracellular alkalosis due to either hypocapnia and/or an enhanced activity of Na+/H+ antiporter occurring in SHR are the most plausible explanations for the above finding.

Apparent mineralocorticoid excess: time of manifestation and complications despite treatment.

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Knops, Noël B B; Monnens, Leo A; Lenders, Jacques W; Levtchenko, Elena N

2011-06-01

Here we describe the case of a patient followed from birth because of a positive family history for apparent mineralocorticoid excess (AME) in an older brother. The patient, a girl, had normal serum electrolyte and blood pressure measurements in the first months after birth. Not until the age of 11 months did she develop anorexia and failure to thrive in combination with hypertension, hypokalemia, and metabolic alkalosis, which are consistent with the diagnosis of AME. This diagnosis was confirmed by mutation analysis of the HSD11B2 gene (C1228T). Treatment with amiloride and furosemide electrolyte disturbances normalized her blood pressure. At the age of 19 years she unexpectedly suffered a stroke. Additional investigations revealed no accepted risk factor for stroke. We discuss the possible underlying mechanisms for the delayed manifestation of hypertension and electrolyte disturbances in AME, propose an additional explanation for the stroke in this patient, and advise treatment with a mineralocorticoid receptor antagonist to reduce stroke risk in patients with AME.

Type III Bartter-like syndrome in an infant boy with Gitelman syndrome and autosomal dominant familial neurohypophyseal diabetes insipidus.

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Brugnara, Milena; Gaudino, Rossella; Tedeschi, Silvana; Syrèn, Marie-Louise; Perrotta, Silverio; Maines, Evelina; Zaffanello, Marco

2014-09-01

We report the case of an infant boy with polyuria and a familial history of central diabetes insipidus. Laboratory blood tests disclosed hypokalemia, metabolic alkalosis, hyperreninemia, and hyperaldosteronism. Plasma magnesium concentration was slightly low. Urine analysis showed hypercalciuria, hyposthenuria, and high excretion of potassium. Such findings oriented toward type III Bartter syndrome (BSIII). Direct sequencing of the CLCNKB gene revealed no disease-causing mutations. The water deprivation test was positive. Magnetic resonance imaging showed a lack of posterior pituitary hyperintensity. Finally, direct sequencing of the AVP-NPII gene showed a point mutation (c.1884G>A) in a heterozygous state, confirming an autosomal dominant familial neurohypophyseal diabetes insipidus (adFNDI). This condition did not explain the patient's phenotype; thus, we investigated for Gitelman syndrome (GS). A direct sequencing of the SLC12A3 gene showed c.269A>C and c.1205C>A new mutations. In conclusion, the patient had a genetic combination of GS and adFNDI with a BSIII-like phenotype.

Antenatal Bartter syndrome presenting with vomiting and constipation mimicking subacute intestinal obstruction in a 20-day-old neonate.

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Abdelgadir, Ibtihal Siddiq; Elgharbawy, Fawzia; Salameh, Khalil Mohamad; Juma, Baha Eldin

2017-11-14

Antenatal Bartter syndrome is a rare condition that can present with different clinical features. These features include early onset maternal polyhydramnios, failure to thrive, prematurity and nephrocalcinosis.We are presenting this 20-day-old girl who had an antenatal history of polyhydramnios. She developed persistent non-bilious vomiting that was associated with constipation soon after birth. She presented with failure to thrive and features suggestive of intestinal obstruction. On the initial evaluation, she was noted to have hypokalaemic, hyponatraemic metabolic alkalosis. The initial work-up was done to exclude surgical and renal causes of her presentation, and the diagnosis was confirmed by gene analysis to be type III-classic Bartter syndrome. She was closely monitored for her growth and development with the appropriate salt replacement therapy. © BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

[A clinical and hereditary analysis of novel complex heterozygous KCNJ1 mutation in a Bartter syndrome type Ⅱ patient].

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Li, X Y; Jiang, Y; Xu, L J; Duan, L; Peng, X Y; Chen, L M; Xia, W B; Xing, X P

2017-10-01

Bartter syndrome (BS) is a hereditary condition transmitted as an autosomal recessive (Bartter type 1 to 4) or dominant trait (Bartter type 5). The disease associates hypokalemic alkalosis with varying degrees of hypercalciuria. Here we presented a case (BS type Ⅱ) of a 17 years old female presented with polyhydramnios, polyuria, nephrocalcinosis and hypokalemia, which was alleviated after treatment with celecoxib and vitamin D(3). DNA sequencing identified compound heterozygous KCNJ 1 gene mutations, c. 931C >T (p.R311W) and c. 445-446insCCTGAACAC (p.V149Afs, 150X), with the latter a novel mutation. Her father and mother were heterozygous carriers of c. 931C >T (p.R311W) and c. 445-446insCCTGAACAC (p.V149Afs, 150X), respectively. In conclusion, this case of BS type Ⅱ is caused by a novel compound heterozygous KCNJ 1 mutation. Further studies are needed to verify the effect of celecoxib in BS patients.

Hypercholermic metabolic alcalsosis as a presentation of cystic fibrosis: presentation of two cases = Alcalosis metabólica hipoclorémica como presentación de la fibrosis quística. Informe de dos casos

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Olga Lucía Morales Múnera

2013-07-01

Full Text Available Introduction: We describe two cases of patients with hyperchloremic metabolic acidosis as an initial presentation of cystic fibrosis (CF or as part of a second CF exacerbation. Clinical Cases: Two patients, 6 and 9 months old, consulted for cough, fever, and dyspnea. The first had syndrome of recurrent bronchial obstruction, without a diagnosis of CF on admission. Both presented with difficulty breathing, dehydration, and malnutrition. Arterial blood gases showed metabolic acidosis, hypokalemia, and severe hypochloremia. Treatment with sodium chloride and potassium improved their electrolyte balance and acid-base status. They did not present with renal or gastrointestinal losses of chloride. CF and pseudo-Barter’s Syndrome were diagnosed. Conclusion: Metabolic alkalosis can present as an initial manifestation of CF in infants with recurrent bronchiolitis and short stature suspected of having CF: equally it can be an acute exacerbation in patients with known CF. Your recognition and treatment are an opportunity to decrease morbidity.

Construction and validation of a decision tree for treating metabolic acidosis in calves with neonatal diarrhea

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Trefz Florian M

2012-12-01

Full Text Available Abstract Background The aim of the present prospective study was to investigate whether a decision tree based on basic clinical signs could be used to determine the treatment of metabolic acidosis in calves successfully without expensive laboratory equipment. A total of 121 calves with a diagnosis of neonatal diarrhea admitted to a veterinary teaching hospital were included in the study. The dosages of sodium bicarbonate administered followed simple guidelines based on the results of a previous retrospective analysis. Calves that were neither dehydrated nor assumed to be acidemic received an oral electrolyte solution. In cases in which intravenous correction of acidosis and/or dehydration was deemed necessary, the provided amount of sodium bicarbonate ranged from 250 to 750 mmol (depending on alterations in posture and infusion volumes from 1 to 6.25 liters (depending on the degree of dehydration. Individual body weights of calves were disregarded. During the 24 hour study period the investigator was blinded to all laboratory findings. Results After being lifted, many calves were able to stand despite base excess levels below −20 mmol/l. Especially in those calves, metabolic acidosis was undercorrected with the provided amount of 500 mmol sodium bicarbonate, which was intended for calves standing insecurely. In 13 calves metabolic acidosis was not treated successfully as defined by an expected treatment failure or a measured base excess value below −5 mmol/l. By contrast, 24 hours after the initiation of therapy, a metabolic alkalosis was present in 55 calves (base excess levels above +5 mmol/l. However, the clinical status was not affected significantly by the metabolic alkalosis. Conclusions Assuming re-evaluation of the calf after 24 hours, the tested decision tree can be recommended for the use in field practice with minor modifications. Calves that stand insecurely and are not able to correct their position if pushed

Nitric oxide rectifies acid-base disturbance and modifies thyroid hormone activity during net confinement of air-breathing fish (Anabas testudineus Bloch).

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Peter, Valsa S

2013-01-15

Nitric oxide (NO), a short-lived freely diffusible radical gas that acts as an important biological signal, regulates an impressive spectrum of physiological functions in vertebrates including fishes. The action of NO, however, on thyroid hormone status and its role in the integration of acid-base, osmotic and metabolic balances during stress are not yet delineated in fish. Sodium nitroprusside (SNP), a NO donor, was employed in the present study to investigate the role of NO in the stressed air-breathing fish Anabas testudineus. Short-term SNP treatment (1 mM; 30 min) interacted negatively with thyroid axis, as evident in the fall of plasma thyroxine in both stressed and non-stressed fish. In contrast, the cortisol responsiveness to NO was negligible. SNP challenge produced systemic alkalosis, hypocapnia and hyperglycemia in non-stressed fish. Remarkable acid-base compensation was found in fish kept for 60 min net confinement where a rise in blood pH and HCO(3) content occurred with a reduction in PCO(2) content. SNP challenge in these fish, on the contrary, produced a rise in oxygen load together with hypocapnia but without an effect on HCO(3) content, indicating a modulator role of NO in respiratory gas transport during stress response. SNP treatment reduced Na(+), K(+) ATPase activity in the gill, intestine and liver of both stressed and non-stressed fish, and this suggests that stress state has little effect on the NO-driven osmotic competence of these organs. On the other hand, a modulatory effect of NO was found in the kidney which showed a differential response to SNP, emphasizing a key role of NO in kidney ion transport and its sensitivity to stressful condition. H(+)-ATPase activity, an index of H(+) secretion, downregulated in all the organs of both non-stressed and stressed fish except in the gill of non-stressed fish and this supports a role for NO in promoting alkalosis. The data indicate that, (1) NO interacts antagonistically with T(4), (2) modifies

Gitelman syndrome

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Levtchenko Elena N

2008-07-01

Full Text Available Abstract Gitelman syndrome (GS, also referred to as familial hypokalemia-hypomagnesemia, is characterized by hypokalemic metabolic alkalosis in combination with significant hypomagnesemia and low urinary calcium excretion. The prevalence is estimated at approximately 1:40,000 and accordingly, the prevalence of heterozygotes is approximately 1% in Caucasian populations, making it one of the most frequent inherited renal tubular disorders. In the majority of cases, symptoms do not appear before the age of six years and the disease is usually diagnosed during adolescence or adulthood. Transient periods of muscle weakness and tetany, sometimes accompanied by abdominal pain, vomiting and fever are often seen in GS patients. Paresthesias, especially in the face, frequently occur. Remarkably, some patients are completely asymptomatic except for the appearance at adult age of chondrocalcinosis that causes swelling, local heat, and tenderness over the affected joints. Blood pressure is lower than that in the general population. Sudden cardiac arrest has been reported occasionally. In general, growth is normal but can be delayed in those GS patients with severe hypokalemia and hypomagnesemia. GS is transmitted as an autosomal recessive trait. Mutations in the solute carrier family12, member 3 gene, SLC12A3, which encodes the thiazide-sensitive NaCl cotransporter (NCC, are found in the majority of GS patients. At present, more than 140 different NCC mutations throughout the whole protein have been identified. In a small minority of GS patients, mutations in the CLCNKB gene, encoding the chloride channel ClC-Kb have been identified. Diagnosis is based on the clinical symptoms and biochemical abnormalities (hypokalemia, metabolic alkalosis, hypomagnesemia and hypocalciuria. Bartter syndrome (especially type III is the most important genetic disorder to consider in the differential diagnosis of GS. Genetic counseling is important. Antenatal diagnosis for GS

Adrenal Mass Causing Secondary Hypertension.

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Robinson, Darlene Y

2015-11-01

Most hypertensive patients have essential (primary) hypertension; only 5% to 10% have a secondary cause. Two clinical characteristics suggestive of secondary hypertension are early onset (hypertension (>180/110 mm Hg). When faced with these findings, clinicians should consider a secondary cause of hypertension. A 22-year-old woman being evaluated for asthma exacerbation in the emergency department was noted to have severe persistent hypertension. Additional evaluation revealed severe hypokalemia, metabolic alkalosis, and hypernatremia. The patient was admitted to the hospital for blood pressure management, electrolyte replacement, and further evaluation of presumed hyperaldosteronism. Diagnostic imaging revealed a large adrenal mass. Surgical resection was performed, leading to a diagnosis of hyperaldosteronism caused by adrenal carcinoma. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Secondary hypertension is far less common than essential hypertension; however, considering the large volume of patients seen in emergency departments, it is likely that some will have secondary hypertension. Emergency physicians should be aware of the clinical characteristics that suggest secondary hypertension so that the appropriate diagnostic and treatment pathways can be pursued. Copyright © 2015 Elsevier Inc. All rights reserved.

Liddle Syndrome: Review of the Literature and Description of a New Case

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Martina Tetti

2018-03-01

Full Text Available Liddle syndrome is an inherited form of low-renin hypertension, transmitted with an autosomal dominant pattern. The molecular basis of Liddle syndrome resides in germline mutations of the SCNN1A, SCNN1B and SCNN1G genes, encoding the α, β, and γ-subunits of the epithelial Na+ channel (ENaC, respectively. To date, 31 different causative mutations have been reported in 72 families from four continents. The majority of the substitutions cause an increased expression of the channel at the distal nephron apical membrane, with subsequent enhanced renal sodium reabsorption. The most common clinical presentation of the disease is early onset hypertension, hypokalemia, metabolic alkalosis, suppressed plasma renin activity and low plasma aldosterone. Consequently, treatment of Liddle syndrome is based on the administration of ENaC blockers, amiloride and triamterene. Herein, we discuss the genetic basis, clinical presentation, diagnosis and treatment of Liddle syndrome. Finally, we report a new case in an Italian family, caused by a SCNN1B p.Pro618Leu substitution.

Successful pregnancy in a female patient with congenital chloride diarrhea (CLD) and renal impairment.

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Shimizu, Yoshio; Kamoda, Tomohiro; Nagata, Michio; Yoh, Keigyo; Hashimoto, Yuko; Matsui, Akira; Yoshikawa, Hiroyuki; Yamagata, Kunihiro; Koyama, Akio

2009-01-01

We report a successful case of pregnancy in a female patient with congenital chloride diarrhea (CLD) and reduced renal function due to interruption of treatment. CLD is an autosomal recessive disorder of intestinal electrolyte absorption caused by mutations in the solute carrier family 26, member 3 (SLC26A3) gene, and continuous production of watery diarrhea induces dehydration, metabolic alkalosis and many kinds of electrolyte disturbances in CLD patients. The patient in our case was a 24-year-old female CLD patient with moderate renal impairment; a renal biopsy specimen showed minimal glomerular changes, but tubulointerstitial damage by crystal formation, consistent with renal function data. One year after our initial examination and reinstitution of therapy, the patient got married and soon conceived. There were no major problems during the course of pregnancy, and the patient successfully delivered a healthy full-term infant vaginally. The symptoms and clinical course of the patient were particularly mild, and we discuss possible reasons for these observations from a perspective of genotype, phenotype and environmental conditions.

Recurrent urinary tract infections in an infant with antenatal Bartter syndrome.

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Tasic, Velibor; Pota, Liljana; Gucev, Zoran

2011-02-01

antenatal variant of Bartter syndrome is characterized by a history of polyhydramnios, premature birth, metabolic alkalosis, hypokalemia, polyuria and renal salt wasting. In this report we present a premature female baby with antenatal Barter syndrome who had three episodes of urinary tract infection (UTI), without evidence for congenital anomaly of the kidneys or urinary tract. antenatal Bartter syndrome was diagnosed according to the standard criteria. Ultrasound scan and voiding cystourethrography were performed to exclude congenital anomaly of the kidneys and urinary tract. the baby presented with early hyperkalemia and acidosis. The typical biochemical features of the Bartter syndrome were observed in the second month. Despite appropriate treatment she had persistent hypercalciuria. The clinical course was complicated with recurrent episodes of febrile UTIs. Urinary tract system imaging did not demonstrate congenital anomalies. She finally died of severe dehydration, acidosis and renal failure. since no congenital anomaly of the kidneys or urinary tract was demonstrated in our patient, we believe that severe, persistent hypercalciuria is the most important risk factor for development of recurrent UTIs.

ACUTE MOUNTAIN SICKNESS

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Jakub Krzeszowiak

2012-03-01

Full Text Available This paper presents the most likely pathophysiological causes of the development of acute mountain sickness (AMS, also known as altitude sickness, its pulmonary form i.e. high altitude pulmonary edema (HAPE, and high altitude cerebral edema (HACE. These diseases constitute extraordinary environmental hazards because they are directly connected with low atmospheric pressure, and thus low partial oxygen pressure. The above adverse atmospheric conditions start to affect humans already at an altitude of 2,500 meters above the sea level and, coupled with extreme physical exertion, can quickly lead to respiratory alkalosis, which is not present under any other conditions in the lowlands. Mountaineering above 4,500 m a.s.l. leads to hypoxia of internal organs and, primarily, reduced renal perfusion with all its consequences. The above adverse changes, combined with inadequate acclimatization, can lead to a situation of imminent danger to life and health. This paper describes in detail the consequences of acute mountain sickness, which can ultimately lead to the development of AMS and one of severe forms of HACE and/or HAPE.

Physiologic and Pharmacokinetic Changes in Pregnancy

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Maged eCostantine

2014-04-01

Full Text Available Physiologic changes in pregnancy induce profound alterations to the pharmacokinetic properties of many medications. These changes affect distribution, absorption, metabolism, and excretion of drugs, and thus may impact their pharmacodynamic properties during pregnancy. Pregnant women undergo several adaptations in many organ systems. Some adaptations are secondary to hormonal changes in pregnancy, while others occur to support the gravid woman and her developing fetus. Some of the changes in maternal physiology during pregnancy include, for example, increased maternal fat and total body water, decreased plasma protein concentrations, especially albumin, increased maternal blood volume, cardiac output and blood flow to the kidneys and uteroplacental unit, and decreased blood pressure. The maternal blood volume expansion occurs at a larger proportion than the increase in red blood cell mass, which results in physiologic anemia and hemodilution. Other physiologic changes include increased tidal volume, partially compensated respiratory alkalosis, delayed gastric emptying and gastrointestinal motility, and altered activity of hepatic drug metabolizing enzymes. Understating these changes and their profound impact on the pharmacokinetic properties of drugs in pregnancy is essential to optimize maternal and fetal health.

Responses of serum electrolytes of goats to twelve hours of road transportation during the hot-dry season in Nigeria, and the effect of pretreatment with ascorbic acid

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J.O. Ayo

2009-09-01

Full Text Available Twenty goats which served as the experimental group were administered ascorbic acid (AA per os at a dosage rate of 100 mg/kg body mass, while 20 others served as controls and were given 10 mt each of sterile water. Forty minutes after the administration and loading, the goats were transported for 12 h. Handling and loading of the experimental and control groups of goats decreased (P < 0.05 the potassium and sodium serum concentrations. The concentration of serum chloride, sodium and calcium increased significantly (P< 0.05 immediately post-transportation, while potassium and magnesium decreased (P < 0.05 in the control goats. In AA-treated goats sodium and magnesium concentrations decreased abruptly (P< 0.05, while calcium increased significantly (P< 0.05 after transportation. Handling, loading and transportation adversely affected the electrolyte balance of the goats which suggested respiratory alkalosis, dehydration and muscular damage in the transported goats, and the administration of AA alleviated the adverse effects of road transportation stress on serum electrolytes.

A urolith of biogenic dolomite - another clue in the dolomite mystery

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Mansfield, Charles F.

1980-06-01

A male Dalmatian, Canis familiaris, produced uroliths of almost pure dolomite, 3-8 mm across, in his urinary bladder in less than 8 months at 38°C and about 1 atm. The X-ray diffractogram identified the predominant mineral as dolomite, and the sharp (01.5) peak showed it is ordered dolomite, not the disordered form, protodolomite. Geochemically and biologically plausible causes include (1) renal, respiratory, or metabolic alkalosis, (2) infection by urease-producing (urea-splitting) fungi or bacteria and (3) infection by uric acid-fermenting bacteria. Hematological, bacteriological, urological and geochemical considerations most strongly implicate infection by either anaerobic, urease-producing bacteria or anaerobic, uric acid-fermenting bacteria. The physical and chemical conditions of this urinary system more closely approximate modern and inferred ancient carbonate depositional settings than most previous laboratory experiments, especially in terms of temperature, pressure, total salinity and, possibly, biota. The presence of urease-producing and/or uric acid-fermenting bacteria in urea- and/or acid-containing sediment, such as fecal pellets and algal mats, could promote formation of authigenic dolomite or other carbonates.

Early neuro-vegetative responses to head irradiation of the rabbit at mean absorbed doses of 1000 and 150 rads

International Nuclear Information System (INIS)

Dufour, Raymond.

1977-10-01

Head irradiation was studied in order to back up a previous assumption on the kinetics of vegetative responses to whole-body exposure: the earliest response might have a central origin and explain the slight increase of blood pressure, tachycardia, hyperthermia and hyperventilation. Following head exposure at a mean absorbed dose of 1000 rads, blood pressure increased on the 15 th min, reaching 0.8 - 1 cm Hg on the 30th min and during 7 - 8 hours. The increase of heart rate occured as early and was about 40% and lasted for 24 hours. Body temperature increased as early as the end of exposure, was highest within 2 - 2.30 hours and decreased on the 6th hour. Arterial blood showed a respiratory alkalosis on the 1st hour, lasting after the 6th hour and disappeared within 24 hours. At a dose of 150 rads, the changes were lasting but of lower importance and duration. The results show that early changes following whole-body exposure also occur after head exposure and are magnified. The kinetics involved are discussed [fr

Effect of Modified Alkaline Supplementation on Syngenic Melanoma Growth in CB57/BL Mice.

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Azzarito, Tommaso; Lugini, Luana; Spugnini, Enrico Pierluigi; Canese, Rossella; Gugliotta, Alessio; Fidanza, Stefano; Fais, Stefano

2016-01-01

Tumor extracellular acidity is a hallmark of malignant cancers. Thus, in this study we evaluated the effects of the oral administration of a commercially available water alkalizer (Basenpulver®) (BP) on tumor growth in a syngenic melanoma mouse model. The alkalizer was administered daily by oral gavage starting one week after tumor implantation in CB57/BL mice. Tumors were calipered and their acidity measured by in vivo MRI guided 31P MRS. Furthermore, urine pH was monitored for potential metabolic alkalosis. BP administration significantly reduced melanoma growth in mice; the optimal dose in terms of tolerability and efficacy was 8 g/l (p< 0.05). The in vivo results were supported by in vitro experiments, wherein BP-treated human and murine melanoma cell cultures exhibited a dose-dependent inhibition of tumor cell growth. This investigation provides the first proof of concept that systemic buffering can improve tumor control by itself and that this approach may represent a new strategy in prevention and/or treatment of cancers.

Antenatal Bartter Syndrome: A Review

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Y. Ramesh Bhat

2012-01-01

Full Text Available Antenatal Bartter syndrome (ABS is a rare autosomal recessive renal tubular disorder. The defective chloride transport in the loop of Henle leads to fetal polyuria resulting in severe hydramnios and premature delivery. Early onset, unexplained maternal polyhydramnios often challenges the treating obstetrician. Increasing polyhydramnios without apparent fetal or placental abnormalities should lead to the suspicion of this entity. Biochemical analysis of amniotic fluid is suggested as elevated chloride level is usually diagnostic. Awareness, early recognition, maternal treatment with indomethacin, and amniocentesis allow the pregnancy to continue. Affected neonates are usually born premature, have postnatal polyuria, vomiting, failure to thrive, hypercalciuria, and subsequently nephrocalcinosis. Hypokalemia, metabolic alkalosis, secondary hyperaldosteronism and hyperreninaemia are other characteristic features. Volume depletion due to excessive salt and water loss on long term stimulates renin-angiotensin-aldosterone system resulting in juxtaglomerular hyperplasia. Clinical features and electrolyte abnormalities may also depend on the subtype of the syndrome. Prenatal diagnosis and timely indomethacin administration prevent electrolyte imbalance, restitute normal growth, and improve activity. In this paper, authors present classification, pathophysiology, clinical manifestations, laboratory findings, complications, and prognosis of ABS.

Secretin stimulates HCO3(-) and acetate efflux but not Na+/HCO3(-) uptake in rat pancreatic ducts

DEFF Research Database (Denmark)

Novak, I; Christoffersen, B C

2001-01-01

to be important in HCO3(-) -transporting epithelia. pHi was measured with BCECF in freshly isolated intralobular ducts. A reduction in extracellular Na+ concentration or application of HOE 694 (1 microM) decreased pHi by 0.1 to 0.6 pH units, demonstrating Na+/H+ exchanger activity. A reduction in extracellular Cl......- concentration or addition of H2DIDS (10 microM) increased pHi by 0.1 to 0.5 pH units, demonstrating Cl-/ HCO(3)- (OH ) exchanger activity. In experimental acidosis, extracellular HCO3(-)/CO2 buffer did not increase the rate of pHi recovery, indicating that provision of HCO3(-) by the Na+/HCO3(-) cotransporter...... was not apparent. Most importantly, Na+/HCO3(-) cotransport was not stimulated by secretin (1 nM). In contrast, in experimental alkalosis the pHi recovery was increased in HCO3(-)/CO2 buffer, possibly due to Na+/HCO3(-) cotransport in the efflux mode. Secretin (1 nM) and carbachol (1 microM) stimulated HCO3...

A novel mutation of CLCNKB in a Korean patient of mixed phenotype of Bartter-Gitelman syndrome.

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Cho, Hee-Won; Lee, Sang Taek; Cho, Heeyeon; Cheong, Hae Il

2016-11-01

Bartter syndrome (BS) is an inherited renal tubular disorder characterized by low or normal blood pressure, hypokalemic metabolic alkalosis, and hyperreninemic hyperaldosteronism. Type III BS is caused by loss-of-function mutations in CLCNKB encoding basolateral ClC-Kb. The clinical phenotype of patients with CLCNKB mutations has been known to be highly variable, and cases that are difficult to categorize as type III BS or other hereditary tubulopathies, such as Gitelman syndrome, have been rarely reported. We report a case of a 10-year-old Korean boy with atypical clinical findings caused by a novel CLCNKB mutation. The boy showed intermittent muscle cramps with laboratory findings of hypokalemia, severe hypomagnesemia, and nephrocalcinosis. These findings were not fully compatible with those observed in cases of BS or Gitelman syndrome. The CLCNKB mutation analysis revealed a heterozygous c.139G>A transition in exon 13 [p.Gly(GGG)465Glu(GAG)]. This change is not a known mutation; however, the clinical findings and in silico prediction results indicated that it is the underlying cause of his presentation.

Antenatal Bartter Syndrome: A Review

Science.gov (United States)

Bhat, Y. Ramesh; Vinayaka, G.; Sreelakshmi, K.

2012-01-01

Antenatal Bartter syndrome (ABS) is a rare autosomal recessive renal tubular disorder. The defective chloride transport in the loop of Henle leads to fetal polyuria resulting in severe hydramnios and premature delivery. Early onset, unexplained maternal polyhydramnios often challenges the treating obstetrician. Increasing polyhydramnios without apparent fetal or placental abnormalities should lead to the suspicion of this entity. Biochemical analysis of amniotic fluid is suggested as elevated chloride level is usually diagnostic. Awareness, early recognition, maternal treatment with indomethacin, and amniocentesis allow the pregnancy to continue. Affected neonates are usually born premature, have postnatal polyuria, vomiting, failure to thrive, hypercalciuria, and subsequently nephrocalcinosis. Hypokalemia, metabolic alkalosis, secondary hyperaldosteronism and hyperreninaemia are other characteristic features. Volume depletion due to excessive salt and water loss on long term stimulates renin-angiotensin-aldosterone system resulting in juxtaglomerular hyperplasia. Clinical features and electrolyte abnormalities may also depend on the subtype of the syndrome. Prenatal diagnosis and timely indomethacin administration prevent electrolyte imbalance, restitute normal growth, and improve activity. In this paper, authors present classification, pathophysiology, clinical manifestations, laboratory findings, complications, and prognosis of ABS. PMID:22518185

Bartter Syndrome Type 3: Phenotype-Genotype Correlation and Favorable Response to Ibuprofen

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Xuejun Yang

2018-05-01

Full Text Available Objective: To investigate the phenotype-genotype correlation in different genetic kinds of Bartter syndrome type 3 in children.Methods: Clinical and genetic data of 2 patients with different mutations in Bartter syndrome type 3 was analyzed while the prognosis was compared after a 6-year follow-up or 2-year follow-up, respectively.Results: Bartter syndrome is a kind of autosomal recessive inherited renal disorder. The manifestation and prognosis of Bartter syndrome change with mutation types, and severe mutation were often accompanied with unfavorable prognosis. Comprehensive therapy with ibuprofen, antisterone, captopril, and potassium have remarkable effect, while ibuprofen may improve growth retardation partly.Conclusion: Bartter syndrome should be considered when children have unreasonable continuous electrolyte disturbance, metabolic alkalosis and growth retardation.As a genetic disease, its clinical features depend on the mutation type. It can be ameliorated by electrolyte supplementation, prostaglandin synthetase inhibitors, angiotensin-converting enzyme inhibitors and potassium-sparing diuretic. Considering the following electrolyte disturbances, infections, growth retardation, kidney failure and even death, Bartter syndrome need lifelong treatment, early diagnosis and treatment is the most important.

Effect of Modified Alkaline Supplementation on Syngenic Melanoma Growth in CB57/BL Mice.

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Tommaso Azzarito

Full Text Available Tumor extracellular acidity is a hallmark of malignant cancers. Thus, in this study we evaluated the effects of the oral administration of a commercially available water alkalizer (Basenpulver® (BP on tumor growth in a syngenic melanoma mouse model. The alkalizer was administered daily by oral gavage starting one week after tumor implantation in CB57/BL mice. Tumors were calipered and their acidity measured by in vivo MRI guided 31P MRS. Furthermore, urine pH was monitored for potential metabolic alkalosis. BP administration significantly reduced melanoma growth in mice; the optimal dose in terms of tolerability and efficacy was 8 g/l (p< 0.05. The in vivo results were supported by in vitro experiments, wherein BP-treated human and murine melanoma cell cultures exhibited a dose-dependent inhibition of tumor cell growth. This investigation provides the first proof of concept that systemic buffering can improve tumor control by itself and that this approach may represent a new strategy in prevention and/or treatment of cancers.

Fluid, electrolyte, and acid-base balances in three-day, combined-training horses.

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White, S L

1998-04-01

Horses competing in 3-day, combined-training events develop a metabolic acidosis that is partially compensated for by a respiratory alkalosis immediately after phases B and D. By the end of phase C and 30 minutes to 2 hours after phase D, the acidosis is resolved by the oxidation of lactate, and a metabolic alkalosis prevails. A reduction in TBW and cation content occurs, which often is not replenished 12 to 24 hours after the event, even though the serum or plasma concentration of various constituents may be within normal limits. Hypochloremia and hypocalcemia, however, may persist 12 or more hours after the speed and endurance test. All of the data cited in this article are from horses that successfully completed their respective tests. Nevertheless, some horses developed substantial fluid and cation losses. In horses that are not well conditioned or in competitions in which terrain, footing, or hot environments increase the thermal load or decrease heat loss, greater losses of fluids and electrolytes can be expected. Body weight losses exceeding 5% and cation losses exceeding 4000 mEq/L occur in endurance horses suffering from exhaustion and synchronous diaphragmatic flutter. In one study, two thirds of the Na+ lost during exercise-induced sweating in cool, dry conditions was replenished from salt supplements added to a balanced forage and concentrated diet. Consequently, horses in regular training and competition may benefit from salt supplementation. The composition of the salt supplement and the amount fed should be based on the composition of the horse's diet, degree of work, and environmental conditions. Horses competing in a 3-day, combined-training event may be expected to have persistent losses of weight and cations, particularly if conditions result in heavy sweating. Many horses in the field studies had minimal changes in weight and cation balance compared with pre-event values. The diet and electrolyte supplementation of the horses in the majority of

The physiological stress response to high-intensity sprint exercise following the ingestion of sodium bicarbonate.

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Peart, Daniel J; Kirk, Richard J; Hillman, Angela R; Madden, Leigh A; Siegler, Jason C; Vince, Rebecca V

2013-01-01

The purpose of this study was to investigate the effects of pre-exercise alkalosis on the physiological stress response to high-intensity exercise. Seven physically active males (age 22 ± 3 years, height 1.82 ± 0.06 m, mass 81.3 ± 8.4 kg and peak power output 300 ± 22 W) performed a repeated sprint cycle exercise following a dose of 0.3 g kg(-1) body mass of sodium bicarbonate (NaHCO(3)) (BICARB), or a placebo of 0.045 g kg(-1) body mass of sodium chloride (PLAC). Monocyte-expressed heat shock protein 72 (HSP72) and plasma thiobarbituric acid reactive substances (TBARS) were significantly attenuated in BICARB compared to PLAC (p = 0.04 and p = 0.039, respectively), however total anti-oxidant capacity, the ratio of oxidised to total glutathione, cortisol, interleukin 6 and interleukin 8 were not significantly induced by the exercise. In conclusion, monocyte-expressed HSP72 is significantly increased following high-intensity anaerobic exercise, and its attenuation following such exercise with the ingestion of NaHCO(3) is unlikely to be due to a decreased oxidative stress.

Hypokalemic salt-losing tubulopathy with chronic renal failure and sensorineural deafness.

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Jeck, N; Reinalter, S C; Henne, T; Marg, W; Mallmann, R; Pasel, K; Vollmer, M; Klaus, G; Leonhardt, A; Seyberth, H W; Konrad, M

2001-07-01

To characterize a rare inherited hypokalemic salt-losing tubulopathy with linkage to chromosome 1p31. We conducted a retrospective analysis of the clinical data for 7 patients in whom cosegregation of the disease with chromosome 1p31 had been demonstrated. In addition, in 1 kindred, prenatal diagnosis in the second child was established, allowing a prospective clinical evaluation. Clinical presentation of the patients was homogeneous and included premature birth attributable to polyhydramnios, severe renal salt loss, normotensive hyperreninemia, hypokalemic alkalosis, and excessive hyperprostaglandin E-uria, which suggested the diagnosis of hyperprostaglandin E syndrome/antenatal Bartter syndrome. However, the response to indomethacin was only poor, accounting for a more severe variant of the disease. The patients invariably developed chronic renal failure. The majority had extreme growth retardation, and motor development was markedly delayed. In addition, all patients turned out to be deaf. The hypokalemic salt-losing tubulopathy with chronic renal failure and sensorineural deafness represents not only genetically but also clinically a disease entity distinct from hyperprostaglandin E syndrome/antenatal Bartter syndrome. A pleiotropic effect of a single gene defect is most likely causative for syndromic hearing loss.

Electrolyte and Acid-Base Disturbances in End-Stage Liver Disease: A Physiopathological Approach.

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Jiménez, José Víctor; Carrillo-Pérez, Diego Luis; Rosado-Canto, Rodrigo; García-Juárez, Ignacio; Torre, Aldo; Kershenobich, David; Carrillo-Maravilla, Eduardo

2017-08-01

Electrolyte and acid-base disturbances are frequent in patients with end-stage liver disease; the underlying physiopathological mechanisms are often complex and represent a diagnostic and therapeutic challenge to the physician. Usually, these disorders do not develop in compensated cirrhotic patients, but with the onset of the classic complications of cirrhosis such as ascites, renal failure, spontaneous bacterial peritonitis and variceal bleeding, multiple electrolyte, and acid-base disturbances emerge. Hyponatremia parallels ascites formation and is a well-known trigger of hepatic encephalopathy; its management in this particular population poses a risky challenge due to the high susceptibility of cirrhotic patients to osmotic demyelination. Hypokalemia is common in the setting of cirrhosis: multiple potassium wasting mechanisms both inherent to the disease and resulting from its management make these patients particularly susceptible to potassium depletion even in the setting of normokalemia. Acid-base disturbances range from classical respiratory alkalosis to high anion gap metabolic acidosis, almost comprising the full acid-base spectrum. Because most electrolyte and acid-base disturbances are managed in terms of their underlying trigger factors, a systematic physiopathological approach to their diagnosis and treatment is required.

Changes of arterial blood pressure, heart rate, internal body temperature, and blood acido-basic balance in the unanaesthetized rabbit following whole-body gamma irradiation at a mean absorbed dose of 250 rads

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Dufour, R.; Court, L.

1973-09-01

The general effects of whole-body gamma -irradiation at a mean absorbed dose of 250 rads were studied simultaneously in the unanaesthetized rabbit for 48 hours. They occurred early, with the following characteristics: arterial blood pressure decreased steadily as early as the 2nd hour and reached its minimum value on the 5th hour with a decrease of about 14%; it remained low during the following two days. Heart rate increased during the first hour, was the highest by the end of the second hour, and resumed normal value on the 24th hour. Internal body temperature increased during the 1st hour and was maximum by the end of the 2nd hour, with a mean increase of 1.2 deg C; hyperthermia steadily decreased between the 4th and the 6th hours and had completely disappeared by the 24th hour. Respiratory alkalosis is shown in the acido-basic balance by a raise of pH, a decrease of PCO/sub 2/ and arterial blood bicarbonates. These various changes seem to indicate a double origin, both central and peripheral. (FR)

Modulation of erythropoietin concentrations by manipulation of hypercarbia

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Miller, M.E.; Howard, D.

1979-01-01

The present studies were done to determine whether preventing the respiratory alkalosis, which is known to occur with acute hypoxic stimuli, would lead to alterations in plasma concentrations of erythropoietin (Ep). Rats were subjected to two acute stresses, hypoxia and blood loss, separately and in combination, with and without the added stress of hypercarbia. Hypercarbia in all experimental groups was associated with a decrease in plasma concentrations of Ep. This reduction in plasma Ep with hypercarbia could not be fully explained by the higher arterial pO/sub 2/s or p50s of the hypercarbic rats. Hypercarbia may have indirectly suppressed Ep production by increasing blood flow to the site of Ep production. Alternatively, the cell of origin of Ep could be sensitive to changes in pH and/or pCO/sub 2/. It was further demonstrated that neither the onset nor the degree of reticulocytosis could be predicted by the plasma Ep concentrations. It is likely that the removal of red blood cells led to a decrease in marrow transit time with the early emergence of reticulocytes after acute blood loss.

Renal acidification responses to respiratory acid-base disorders.

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Madias, Nicolaos E

2010-01-01

Respiratory acid-base disorders are those abnormalities in acid-base equilibrium that are expressed as primary changes in the arterial carbon dioxide tension (PaCO2). An increase in PaCO2 (hypercapnia) acidifies body fluids and initiates the acid-base disturbance known as respiratory acidosis. By contrast, a decrease in PaCO2 (hypocapnia) alkalinizes body fluids and initiates the acid-base disturbance known as respiratory alkalosis. The impact on systemic acidity of these primary changes in PaCO2 is ameliorated by secondary, directional changes in plasma [HCO3¯] that occur in 2 stages. Acutely, hypercapnia or hypocapnia yields relatively small changes in plasma [HCO3¯] that originate virtually exclusively from titration of the body's nonbicarbonate buffers. During sustained hypercapnia or hypocapnia, much larger changes in plasma [HCO3¯] occur that reflect adjustments in renal acidification mechanisms. Consequently, the deviation of systemic acidity from normal is smaller in the chronic forms of these disorders. Here we provide an overview of the renal acidification responses to respiratory acid-base disorders. We also identify gaps in knowledge that require further research.

Bartter's Syndrome with Type 2 Diabetes Mellitus

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Ting-Ting See

2009-02-01

Full Text Available We report a rare case of Bartter's syndrome in a 35-year-old woman with type 2 diabetes mellitus. The patient presented with leg weakness, fatigue, polyuria and polydipsia. Hypokalemia, metabolic alkalosis, and high renin and aldosterone concentrations were present, but the patient was normotensive. Gitelman's syndrome was excluded because of the presence of hypercalciuria, secondary hyperparathyroidism and bilateral nephrocalcinosis. The patient's condition improved upon administration of a prostaglandin synthetase inhibitor (acemetacin, oral potassium chloride and potassium-sparing diuretics. Five months later, the patient discontinued acemetacin because of epigastric discomfort; at the same time, severe hypokalemia and hyperglycemia developed. Glucagon stimulation and water deprivation tests were performed. Type 2 diabetes mellitus with nephrogenic diabetes insipidus was diagnosed. To avoid further gastrointestinal complications, the patient was treated with celecoxib, a selective cyclooxygenase 2 inhibitor. This case serves as a reminder that Bartter's syndrome is associated with various metabolic derangements including nephrogenic diabetes insipidus, nephrocalcinosis and diabetes mellitus. When treating Bartter's syndrome, it is also prudent to remember that the long-term use of nonsteroidal anti-inflammatory drugs and potassium-sparing diuretics may result in serious adverse reactions.

Congenital chloride diarrhea misdiagnosed as pseudo-Bartter syndrome.

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Saneian, Hossein; Bahraminia, Emad

2013-09-01

Congenital chloride diarrhea (CCD) is a rare autosomal recessive disease which is characterized by intractable diarrhea of infancy, failure to thrive, high fecal chloride, hypochloremia, hypokalemia, hyponatremia and metabolic alkalosis. In this case report, we present the first female and the second official case of CCD in Iran. A 15-month-old girl referred to our hospital due to failure to thrive and poor feeding. She had normal kidneys, liver and spleen. Treating her with Shohl's solution, thiazide and zinc sulfate did not result in weight gain. Consequently, pseudo-Bartter syndrome was suspected, she was treated with intravenous (IV) therapy to which she responded dramatically. In addition, hypokalemia resolved quickly. Since this does not usually happen in patients with the pseudo-Bartter syndrome, stool tests were performed. Abnormal level of chloride in stool suggested CCD and she was thus treated with IV fluid replacement, Total parentral nutrition and high dose of oral omeprazole (3 mg/kg/day). She gained 1 kg of weight and is doing fine until present. CCD is a rare hereditary cause of intractable diarrhea of infancy. It should be considered in infants with unknown severe electrolyte disturbances.

Renal transplantation in a patient with Bartter syndrome and glomerulosclerosis

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Lee, Se Eun; Han, Kyoung Hee; Jung, Yun Hye; Lee, Hyun Kyung; Kang, Hee Gyung; Moon, Kyung Chul; Ha, Il Soo; Choi, Yong

2011-01-01

Bartter syndrome (BS) is a clinically and genetically heterogeneous inherited renal tube disorder characterized by renal salt wasting, hypokalemic metabolic alkalosis and normotensive hyperreninemic hyperaldosteronism. There have been several case reports of BS complicated by focal segmental glomerulosclerosis (FSGS). Here, we have reported the case of a BS patient who developed FSGS and subsequent end-stage renal disease (ESRD) and provided a brief literature review. The patient presented with classic BS at 3 months of age and developed proteinuria at 7 years. Renal biopsy performed at 11 years of age revealed a FSGS perihilar variant. Hemodialysis was initiated at 11 years of age, and kidney transplantation was performed at 16 years of age. The post-transplantation course has been uneventful for more than 3 years with complete disappearance of BS without the recurrence of FSGS. Genetic study revealed a homozygous p.Trp(TGG)610Stop(TGA) mutation in the CLCNKB gene. In summary, BS may be complicated by secondary FSGS due to the adaptive response to chronic salt-losing nephropathy, and FSGS may progress to ESRD in some patients. Renal transplantation in patients with BS and ESRD results in complete remission of BS. PMID:21359059

Unusual Complication of Multidrug Resistant Tuberculosis

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Prerna Sharma

2017-01-01

Full Text Available Introduction. Capreomycin is a second-line drug often used for multidrug-resistant tuberculosis which can result in nephrotoxic effects similar to other aminoglycosides. We describe a case of capreomycin induced Bartter-like syndrome with hypocalcemic tetany. Case Report. 23-year-old female patient presented with carpopedal spasms and tingling sensations in hands. Patient was being treated with capreomycin for two months for tuberculosis. On further investigation, hypocalcemia, hyponatremia, hypomagnesemia, hypokalemia, and hypochloremic metabolic alkalosis were noted. Vitamin D and serum PTH levels were within normal limits. Hypercalciuria was confirmed by urine calcium/creatinine ratio. Calcium, potassium, and magnesium supplementation was given and capreomycin was discontinued. Electrolytes normalized in two days after cessation of capreomycin with no further abnormalities on repeat investigations. Discussion. Aminoglycosides can result in renal tubular dysfunction leading to Fanconi syndrome, Bartter syndrome, and distal tubular acidosis. Impaired mitochondrial function in the tubular cells has been hypothesized as the possible cause of these tubulopathies. Acquired Bartter-like syndrome phenotypically resembles autosomal dominant type 5 Bartter syndrome. Treatment consists of correction of electrolyte abnormalities, indomethacin, and potassium-sparing diuretics. Prompt diagnosis and treatment of severe dyselectrolytemia are warranted in patients on aminoglycoside therapy.

Renal transplantation in a patient with Bartter syndrome and glomerulosclerosis

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Se Eun Lee

2011-01-01

Full Text Available Bartter syndrome (BS is a clinically and genetically heterogeneous inherited renal tube disorder characterized by renal salt wasting, hypokalemic metabolic alkalosis and normotensive hyperreninemic hyperaldosteronism. There have been several case reports of BS complicated by focal segmental glomerulosclerosis (FSGS. Here, we have reported the case of a BS patient who developed FSGS and subsequent end-stage renal disease (ESRD and provided a brief literature review. The patient presented with classic BS at 3 months of age and developed proteinuria at 7 years. Renal biopsy performed at 11 years of age revealed a FSGS perihilar variant. Hemodialysis was initiated at 11 years of age, and kidney transplantation was performed at 16 years of age. The post-transplantation course has been uneventful for more than 3 years with complete disappearance of BS without the recurrence of FSGS. Genetic study revealed a homozygous p.Trp(TGG610Stop(TGA mutation in the CLCNKB gene. In summary, BS may be complicated by secondary FSGS due to the adaptive response to chronic salt-losing nephropathy, and FSGS may progress to ESRD in some patients. Renal transplantation in patients with BS and ESRD results in complete remission of BS.

Proximal duodenoileal anastomosis for treatment of small intestinal obstruction and volvulus in a green iguana (Iguana iguana).

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Wills, Sarah; Beaufrère, Hugues; Watrous, Gwyneth; Oblak, Michelle L; Smith, Dale A

2016-11-01

CASE DESCRIPTION A 13-year-old female green iguana (Iguana iguana) was examined because of a 6-day history of vomiting, anorexia, and lethargy and a 4-day history of decreased fecal and urate output. CLINICAL FINDINGS Physical examination revealed a distended abdomen, signs of depression, pallor, tachycardia, harsh lung sounds, and vomiting. Abdominal radiographs revealed gas distention of the stomach and small intestine with fluid lines evident on the lateral view. Plasma biochemical analysis indicated hypochloremic metabolic alkalosis, hyperglycemia, and hyperuricemia. TREATMENT AND OUTCOME Exploratory laparotomy confirmed a diagnosis of small intestinal entrapment and 170° volvulus involving approximately 80% (20 to 30 cm) of the small intestine. The portion of the small intestine extending from the middle portion of the duodenum to the caudal extent of the ileum was resected, and end-to-end anastomosis of the remaining small intestine was performed. The iguana recovered without apparent complications and was reportedly doing well 1 year after surgery. CLINICAL RELEVANCE Findings suggested that iguanas, as hindgut fermenters, may tolerate > 70% resection of the small intestine with a good outcome and no clinical evidence of residual gastrointestinal dysfunction.

Update in diagnosis and management of primary aldosteronism.

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Dick, Sofia M; Queiroz, Marina; Bernardi, Bárbara L; Dall'Agnol, Angélica; Brondani, Letícia A; Silveiro, Sandra P

2018-02-23

Primary aldosteronism (PA) is a group of disorders in which aldosterone is excessively produced. These disorders can lead to hypertension, hypokalemia, hypervolemia and metabolic alkalosis. The prevalence of PA ranges from 5% to 12% around the globe, and the most common causes are adrenal adenoma and adrenal hyperplasia. The importance of PA recognition arises from the fact that it can have a remarkably adverse cardiovascular and renal impact, which can even result in death. The aldosterone-to-renin ratio (ARR) is the election test for screening PA, and one of the confirmatory tests, such as oral sodium loading (OSL) or saline infusion test (SIT), is in general necessary to confirm the diagnosis. The distinction between adrenal hyperplasia (AH) or aldosterone-producing adenoma (APA) is essential to select the appropriate treatment. Therefore, in order to identify the subtype of PA, imaging exams such as computed tomography or magnetic ressonance imaging, and/or invasive investigation such as adrenal catheterization must be performed. According to the subtype of PA, optimal treatment - surgical for APA or pharmacological for AH, with drugs like spironolactone and amiloride - must be offered.

Determinação de eletrólitos, gases sanguíneos, osmolalidade, hematócrito, hemoglobina, base titulável e anion gap no sangue venoso de equinos destreinados submetidos a exercício máximo e submáximo em esteira rolante Determination of electrolytes, hemogasometry, osmalility, hematocrit, hemoglobin, base concentration, and anion gap in detrained equines submitted a maximum and submaximum exercise on treadmill

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M.A.G. Silva

2009-10-01

Base, SatvO2, and PvO2. So, maximum exercises can lead equines to present metabolic acidosis with respiratory alkalosis as response, hypercalemia and increase in hematocrit and hemoglobin, values. Submaximum exercises can present hypochloremic metabolic alkalosis but no alterations in the hydroelectrolitic balance.

Neurologic complications of electrolyte disturbances and acid-base balance.

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Espay, Alberto J

2014-01-01

Electrolyte and acid-base disturbances are common occurrences in daily clinical practice. Although these abnormalities can be readily ascertained from routine laboratory findings, only specific clinical correlates may attest as to their significance. Among a wide phenotypic spectrum, acute electrolyte and acid-base disturbances may affect the peripheral nervous system as arreflexic weakness (hypermagnesemia, hyperkalemia, and hypophosphatemia), the central nervous system as epileptic encephalopathies (hypomagnesemia, dysnatremias, and hypocalcemia), or both as a mixture of encephalopathy and weakness or paresthesias (hypocalcemia, alkalosis). Disabling complications may develop not only when these derangements are overlooked and left untreated (e.g., visual loss from intracranial hypertension in respiratory or metabolic acidosis; quadriplegia with respiratory insufficiency in hypermagnesemia) but also when they are inappropriately managed (e.g., central pontine myelinolisis when rapidly correcting hyponatremia; cardiac arrhythmias when aggressively correcting hypo- or hyperkalemia). Therefore prompt identification of the specific neurometabolic syndromes is critical to correct the causative electrolyte or acid-base disturbances and prevent permanent central or peripheral nervous system injury. This chapter reviews the pathophysiology, clinical investigations, clinical phenotypes, and current management strategies in disorders resulting from alterations in the plasma concentration of sodium, potassium, calcium, magnesium, and phosphorus as well as from acidemia and alkalemia. © 2014 Elsevier B.V. All rights reserved.

The Importance of the Ionic Product for Water to Understand the Physiology of the Acid-Base Balance in Humans

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María M. Adeva-Andany

2014-01-01

Full Text Available Human plasma is an aqueous solution that has to abide by chemical rules such as the principle of electrical neutrality and the constancy of the ionic product for water. These rules define the acid-base balance in the human body. According to the electroneutrality principle, plasma has to be electrically neutral and the sum of its cations equals the sum of its anions. In addition, the ionic product for water has to be constant. Therefore, the plasma concentration of hydrogen ions depends on the plasma ionic composition. Variations in the concentration of plasma ions that alter the relative proportion of anions and cations predictably lead to a change in the plasma concentration of hydrogen ions by driving adaptive adjustments in water ionization that allow plasma electroneutrality while maintaining constant the ionic product for water. The accumulation of plasma anions out of proportion of cations induces an electrical imbalance compensated by a fall of hydroxide ions that brings about a rise in hydrogen ions (acidosis. By contrast, the deficiency of chloride relative to sodium generates plasma alkalosis by increasing hydroxide ions. The adjustment of plasma bicarbonate concentration to these changes is an important compensatory mechanism that protects plasma pH from severe deviations.

Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

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Adeva-Andany, María M.; Fernández-Fernández, Carlos; Mouriño-Bayolo, David; Castro-Quintela, Elvira; Domínguez-Montero, Alberto

2014-01-01

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated. PMID:25405229

Analisis Gas Darah pada Kucing yang Mengalami Laparohisterotomi dengan Anestesi Xylazin-Ketamin dan Xylazin-Propofol (BLOOD GAS ANALYSIS OF XYLAZIN- KETAMIN AND XYLAZIN-PROPOFOL FOR ANESTHESIA TO LAPARO-HISTEROTOMY SURGERY IN CAT

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Ira Sari Yudaniayanti

2012-03-01

Full Text Available The aim of this research was to study the safety application of xylazine-ketamine and xylazinepropofolrecurrent dosage combination as anesthesia for laparo-histerotomy surgery in cat. Thisresearch used 10 female cats, 12-18 months of age, followed randomly divided into two groups, P1:atropine 0,04 mg/kgBW/SC + xylazine 2 mg/kg BW/IM + ketamine 20 mg/kg BW/IM; P2 : atropine0,04mg/kg BW/SC + xylazine 2 mg/kg BW/IM + Propofol 20 mg/kg BW/IV. The blood of the allgroups was taken from vena femuralis at 0 minute (before treatment, 15, 30, 45 and 60 minutesduring anesthesia for measurement of blood gas value pH, pCO2 and HCO3. After all animals wereanesthetized, the animals were treated laparo-histerotomy surgery. The data were analyzed byusing Randomized Complete Block Design (RCBD. The result showed both of groups were notsignificantly difference (p>0,05 to blood gas values for pH, pCO2 dan HCO3. Besides, both groupsanaesthetic agent perfectly caused metabolic acidosis with respiratory alkalosis compensationperfectly, therefore it is relatively safe to use as anaesthetic agent for surgery that needs long timeprocedure, as laparo-histerotomy.

Dysfunctional breathing: a review of the literature and proposal for classification

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Richard Boulding

2016-09-01

Full Text Available Dysfunctional breathing is a term describing breathing disorders where chronic changes in breathing pattern result in dyspnoea and other symptoms in the absence or in excess of the magnitude of physiological respiratory or cardiac disease. We reviewed the literature and propose a classification system for the common dysfunctional breathing patterns described. The literature was searched using the terms: dysfunctional breathing, hyperventilation, Nijmegen questionnaire and thoraco-abdominal asynchrony. We have summarised the presentation, assessment and treatment of dysfunctional breathing, and propose that the following system be used for classification. 1 Hyperventilation syndrome: associated with symptoms both related to respiratory alkalosis and independent of hypocapnia. 2 Periodic deep sighing: frequent sighing with an irregular breathing pattern. 3 Thoracic dominant breathing: can often manifest in somatic disease, if occurring without disease it may be considered dysfunctional and results in dyspnoea. 4 Forced abdominal expiration: these patients utilise inappropriate and excessive abdominal muscle contraction to aid expiration. 5 Thoraco-abdominal asynchrony: where there is delay between rib cage and abdominal contraction resulting in ineffective breathing mechanics. This review highlights the common abnormalities, current diagnostic methods and therapeutic implications in dysfunctional breathing. Future work should aim to further investigate the prevalence, clinical associations and treatment of these presentations.

Cerebral circulation, metabolism, and blood-brain barrier of rats in hypocapnic hypoxia

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Beck, T.; Krieglstein, J.

1987-01-01

The effects of hypoxic hypoxia on physiological variables, cerebral circulation, cerebral metabolism, and blood-brain barrier were investigated in conscious, spontaneously breathing rats by exposing them to an atmosphere containing 7% O 2 . Hypoxia affected a marked hypotension, hypocapnia and alkalosis. Cortical tissue high-energy phosphates and glucose content were not affected by hypoxia, glucose 6-phosphate lactate, and pyruvate levels were significantly increased. Blood-brain barrier permeability, regional brain glucose content and lumped constant were not changed by hypoxia. Local cerebral glucose utilization (LCGU) rose by 40-70% of control values in gray matter and by 80-90% in white matter. Under hypoxia, columns of increased and decreased LCGU and were detectable in cortical gray matter. Color-coded [ 14 C]2-deoxy-D-glucose autoradiograms of rat brain are shown. Local cerebral blood flow (LCBF) increased by 50-90% in gray matter and by up to 180% in white matter. Coupling between LCGU and LCBF in hypoxia remained unchanged. The data suggests a stimulation of glycolysis, increased glucose transport into the cell, and increased hexokinase activity. The physiological response of gray and white matter to hypoxia obviously differs. Uncoupling of the relation between LCGU and LCBF does not occur

Po2 temperature blood factor for blood gas apparatus.

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Teisseire, B P; Hérigault, R A; Teisseire, L J; Laurent, D N

1984-01-01

PO2 temperature formulae supplied by manufacturers on automatic blood gas apparatus, PO2 corr. = PO2 37 degrees C X 10F X delta T were studied and compared to the experimental determination of the delta log PO2/delta T ratio (Hérigault et al. [10]). Acid-base status at 37 degrees C appeared to have a measurable influence on the PO2 temperature factor; alkalosis increased the delta log PO2/delta T ratio, and the contrary was found for acidosis in comparison with normal acid-base status at 37 degrees C. For the same PO2, measured at 37 degrees C, all the proposed formulae of commercial blood gas automatic apparatus did not give the same temperature corrected PO2. The observed difference between the corrected PO2 may be important and greater than the precision of the initial measurement. To correct the measured PO2 for temperature, a relationship between delta log PO2/delta T and PO2 is proposed, between PO2 zero and PO2 180 mmHg, which takes into account measured pH and PO2 values at 37 degrees C:delta log PO2/delta T = [(-0.35 pH + 0.658) X 10(-4) X PO2] + 0.035.

The Measurement of Maximal (Anaerobic Power Output on a Cycle Ergometer: A Critical Review

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Tarak Driss

2013-01-01

Full Text Available The interests and limits of the different methods and protocols of maximal (anaerobic power ( assessment are reviewed: single all-out tests versus force-velocity tests, isokinetic ergometers versus friction-loaded ergometers, measure of during the acceleration phase or at peak velocity. The effects of training, athletic practice, diet and pharmacological substances upon the production of maximal mechanical power are not discussed in this review mainly focused on the technical (ergometer, crank length, toe clips, methodological (protocols and biological factors (muscle volume, muscle fiber type, age, gender, growth, temperature, chronobiology and fatigue limiting in cycling. Although the validity of the Wingate test is questionable, a large part of the review is dedicated to this test which is currently the all-out cycling test the most often used. The biomechanical characteristics specific of maximal and high speed cycling, the bioenergetics of the all-out cycling exercises and the influence of biochemical factors (acidosis and alkalosis, phosphate ions… are recalled at the beginning of the paper. The basic knowledge concerning the consequences of the force-velocity relationship upon power output, the biomechanics of sub-maximal cycling exercises and the study on the force-velocity relationship in cycling by Dickinson in 1928 are presented in Appendices.

Bartter syndrome presenting as poor weight gain and abdominal mass in an infant.

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Heffernan, Annie; Steffensen, Thora S; Gilbert-Barness, Enid; Perlman, Sharon

2008-01-01

Bartter syndrome, a group of disorders that encompasses multiple genetic defects with similar clinical presentation, has been divided into six different genotypes, according to different genetic defects, and into three main clinical variants (or phenotypes). Classic laboratory findings in all variants include hypochloremia, hypokalemia, and metabolic alkalosis with excessive excretion of chloride and potassium. Classic Bartter syndrome, neonatal Bartter syndrome, and Gitelman syndrome are the three main clinical variants. Classic Bartter syndrome and neonatal Bartter syndrome have defects in genes that affect transport channels in the ascending loop of Henle, where as in Gitleman syndrome the defect occurs in the transport channels of the distal convoluted tubule. Classic Bartter syndrome and neonatal Bartter syndrome have similar presenting symptoms, potential outcomes, and treatment, but different ages at presentation. Gitelman syndrome, a more benign condition than the other clinical variants, has the classic hallmark finding of hypomagnesemia and low to normal excretion of calcium. This differentiates it from the classic and neonatal variants of the disease. With early diagnosis and proper treatment, Bartter syndrome has a good prognosis. But failure to identify it can lead to tubulointerstitial nephritis and renal failure. We present a case of a 6-month-old boy with Bartter syndrome who presented with poor weight gain and an abdominal mass.

ClC-K chloride channels: emerging pathophysiology of Bartter syndrome type 3.

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Andrini, Olga; Keck, Mathilde; Briones, Rodolfo; Lourdel, Stéphane; Vargas-Poussou, Rosa; Teulon, Jacques

2015-06-15

The mutations in the CLCNKB gene encoding the ClC-Kb chloride channel are responsible for Bartter syndrome type 3, one of the four variants of Bartter syndrome in the genetically based nomenclature. All forms of Bartter syndrome are characterized by hypokalemia, metabolic alkalosis, and secondary hyperaldosteronism, but Bartter syndrome type 3 has the most heterogeneous presentation, extending from severe to very mild. A relatively large number of CLCNKB mutations have been reported, including gene deletions and nonsense or missense mutations. However, only 20 CLCNKB mutations have been functionally analyzed, due to technical difficulties regarding ClC-Kb functional expression in heterologous systems. This review provides an overview of recent progress in the functional consequences of CLCNKB mutations on ClC-Kb chloride channel activity. It has been observed that 1) all ClC-Kb mutants have an impaired expression at the membrane; and 2) a minority of the mutants combines reduced membrane expression with altered pH-dependent channel gating. Although further investigation is needed to fully characterize disease pathogenesis, Bartter syndrome type 3 probably belongs to the large family of conformational diseases, in which the mutations destabilize channel structure, inducing ClC-Kb retention in the endoplasmic reticulum and accelerated channel degradation. Copyright © 2015 the American Physiological Society.

Aldosterone hypersecretion in “non-salt-losing” congenital adrenal hyperplasia

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Bartter, Frederic C.; Henkin, Robert I.; Bryan, George T.

1968-01-01

Patients with the “non-salt-losing” form of the adrenogenital syndrome were studied before and after suppression of adrenal cortical activity with carbohydrate-active steroids. The response of aldosterone secretion to sodium deprivation was measured; in some patients response to adrenocorticotropic hormone (ACTH) was measured as well. The aldosterone secretion was normal and responded normally to sodium deprivation in all patients studied during suppression with carbohydrate-active steroids. This finding suggests that 21-hydroxylation of progesterone is normal in this syndrome. The sole abnormality in the production of aldosterone in these patients was found to be excessive secretion of aldosterone while they were not receiving suppressive doses of carbohydrate-active steroids. This finding strongly supports the view that the biogenetic pathways through which aldosterone is produced from progesterone are intact in this syndrome. No patient showed hypertension or hypokalemic alkalosis despite very high aldosterone secretion rates. This observation suggests that the hyper-aldosteronism is secondary to a tendency to sodium loss in the patient whose ACTH production is not suppressed. These studies provide additional evidence in support of the hypothesis that the salt-losing and “non-salt-losing” forms of adrenogenital syndrome are genetically and biochemically distinct. PMID:4299011

Pseudo-Bartter syndrome as the sole manifestation of cystic fibrosis in a child with 711+G>T/IVS8-5T mutation: a new face of an old disease.

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Tinsa, Faten; Hadj Fredj, Sondes; Bel Hadj, Imen; Khalsi, Fatma; Abdelhak, Sonia; Boussetta, Khadija; Messaoud, Taieb

2017-08-01

Pseudo-Bartter syndrome (PBS) describes an uncommon complication of cystic fibrosis leading to hypochloraemic, hypokalaemic metabolic alkalosis. PBS as the sole manifestation of cystic fibrosis in children is extremely rare and has never been described in patients carrying 5T variant. We report a clinical, biochemical and genetic study of a four year-old boy presenting a pseudo-Bartter syndrome as the sole manifestation of cystic fibrosis. All 27 exons and the flanking intron regions of the CFTR gene were analysed by PCR and direct sequencing. Direct sequencing was also used to analyse TG m T n and M470V polymorphisms in the patient and his parents. Two sweat tests were abnormal with elevated chloride levels at 78 and 88 mmol/L. DNA sequencing revealed a heterozygous mutation 711+1 G>T and an IVS8-T5 allele. The mutation 711+1 G>T is in trans with the IVS8-T5-TG11 allele and the child carried M470/V470 genotype. To the best of our knowledge, the genotype 711+1 G>T /IVS8-5T found in our patient is described for the first time. The role of TG11-5T-V470 allele in cases of cystic fibrosis with PB syndrome remains to be determined.

Hereditary Hypokalemic salt-losing tubular disorders

International Nuclear Information System (INIS)

Peters, M.; Konard, M.; Seyberth, H.W.

2003-01-01

The inherited hypokalemic tubular disorders are frequently summarized under the heading Bartter Syndrome since they share several clinical and biochemical findings such as renal salt wasting, hypokalemic metabolic alkalosis, normal blood pressure despite hypereninemic hyperaldosteronism and hyperplasia of the juxtaglomerular apparatus. However, careful characterization of the clinical phenotype and correlation with the clinical phenotype and the correlation with the underlying molecular basis justifies the differentiation into at least four distinct disease entities: (i) the hyperprostaglandin E syndrome or antenatal variant of Bartter syndrome (HPS/aBS), which is caused by mutations in either the Na-K-2Cl cotransporter or the potassium channel of the medullary thick ascending limb of Henle's loop; (ii) the HPS/aBS with sensorineural deafness which results from inactivating mutation in the Barttin beta-subunit of the renal chloride channels; (iii) the classic Bartter syndrome caused by mutations in the chloride channel of the distal nephron; and (iv)Gitelman's variant of Bartter syndrome which is caused by mutations of the Na-Cl cotransporter of the distal convoluted tubule. This review will summarize the clinical characteristics of these diseases and progress recently made in the identification of the underlying molecular defects that will hopefully add to the current knowledge of the pathogenesis of these diseases. (author)

Nephrocalcinosis and Placental Findings in Neonatal Bartter Syndrome

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Maruyama, Hidehiko; Shinno, Yoko; Fujiwara, Kaori; Nakamura, Akie; Tajima, Toshihiro; Nakamura, Makoto; Kageyama, Misao

2012-01-01

Neonatal Bartter syndrome (NBS) is an inherited renal tubular disorder associated with hypokalemic alkalosis. Here we report a case of genetically diagnosed NBS. Polyhydramnios was noted at 26 weeks. A boy was born at 31 weeks and 1 day, weighed 1344 g, and had an Apgar score of 8/8. We initiated indomethacin (IND) at a dose of 0.2 mg/kg/d on day 31, and increased it to approximately 3 mg/kg/d. However, his urinary calcium (Ca) levels remained unchanged. At 4 months of age, nephrocalcinosis was detected by ultrasound. The placenta weighed 700 g (+2.7 standard deviations). Although the proportion of terminal villi was consistent with the gestational age, many of them exhibited poorly dilated capillaries. Hemosiderin pigment was seen throughout the amniochorionic connective tissue and along about 50% of the trophoblast basement membrane (TBM). Von Kossa stain revealed the corresponding area of mineralization along the TBM. In our opinion, urinary Ca levels were high and did not change after IND initiation, indicating that nephrocalcinosis may be inevitable. Enhanced inflow of maternal plasma through the basement membrane would cause Ca deposition, given that the same finding was obtained in the case with polyhydramnios. The same mechanism would also explain the hemosiderin pigment distribution. PMID:23943704

Nephrocalcinosis and Placental Findings in Neonatal Bartter Syndrome

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Hidehiko Maruyama

2013-05-01

Full Text Available Neonatal Bartter syndrome (NBS is an inherited renal tubular disorder associated with hypokalemic alkalosis. Here we report a case of genetically diagnosed NBS. Polyhydramnios was noted at 26 weeks. A boy was born at 31 weeks and 1 day, weighed 1344 g, and had an Apgar score of 8/8. We initiated indomethacin (IND at a dose of 0.2 mg/kg/d on day 31, and increased it to approximately 3 mg/kg/d. However, his urinary calcium (Ca levels remained unchanged. At 4 months of age, nephrocalcinosis was detected by ultrasound. The placenta weighed 700 g (+2.7 standard deviations. Although the proportion of terminal villi was consistent with the gestational age, many of them exhibited poorly dilated capillaries. Hemosiderin pigment was seen throughout the amniochorionic connective tissue and along about 50% of the trophoblast basement membrane (TBM. Von Kossa stain revealed the corresponding area of mineralization along the TBM. In our opinion, urinary Ca levels were high and did not change after IND initiation, indicating that nephrocalcinosis may be inevitable. Enhanced inflow of maternal plasma through the basement membrane would cause Ca deposition, given that the same finding was obtained in the case with polyhydramnios. The same mechanism would also explain the hemosiderin pigment distribution.

Renal dysfunction and barttin expression in Bartter syndrome Type IV associated with a G47R mutation in BSND in a family.

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Park, C W; Lim, J H; Youn, D-Y; Chung, S; Lim, M-H; Kim, Y K; Chang, Y S; Lee, J-H

2011-02-01

Bartter syndrome (BS) Type IV, associated with a G47R mutation in the BSND gene, is known to result in a mild renal phenotype. However, we report here on three brothers with varying degrees of renal dysfunction from mild to end-stage renal disease associated with renal barttin and ClC-K expression. The brothers had histories of polyhydramnios, prematurity, polyuria, deafness, and small body size. Laboratory findings showed hypokalemic metabolic alkalosis, normotensive hyperreninemic hyperaldosteronism, and an increased urinary excretion of sodium, potassium and chloride, consistent with BS Type IV. Microscopic examination of renal tissue showed hyperplasia of cells at the juxtaglomerular apparatus with dilated atrophic tubules and tubulointerstitial fibrosis. A weak barttin signal related to CIC-K expression in the cytoplasm of tubule cells, but not the basement membrane, was noted. A sequence analysis of the BSND gene showed that the affected males were homozygous for a missense G47R mutation in exon 1 of BSND. These findings suggest that the G47R mutation results in a dramatic decrease in barttin expression, which appears to be related to the location of CIC-K being changed from the basement membrane to the cytoplasm in the tubule and might have varying effects on renal function associated with factors other than this gene.

Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

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María M. Adeva-Andany

2014-01-01

Full Text Available Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.

Effect of continuous hemofiltration on internal environment and survival rate of severe heatstroke dogs with shock

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Guang-ming CHEN

2011-08-01

Full Text Available Objective To explore the effect of continuous hemofiltration(CHF on internal environment and survival rate of severe heatstroke dogs with shock.Methods Sixteen healthy male dogs were randomly divided into heatshock group(HS group,n=8 and continuous hemofiltration group(CHF group,n=8.Severe heatstroke model was established by applying high temperature to whole body,and then the animals were removed from the heating cabin as soon as they presented manifestations of shock.Dogs of HS group were put into an ordinary environment,while dogs of CHF group received CHF treatment.The core temperature(Tc,mean arterial pressure(MAP,blood gas analysis,serum electrolytes and survival rate of dogs in two groups were observed.Results The time from heat exposure to shock was 107.0±28.5min and 111.4±22.2min in HS group and CHF group respectively(t=-0.354,P=0.729.The Tc in CHF group declined to normal level 15 to 30 minitues after CHF treatment,while the Tc in HS group remained at a level higher than that before heat exposure at 90min after shock.The Tc of two groups showed significant difference at each time point after shock(P < 0.01.The MAP of both groups was obviously lowered than that before heatstroke.The MAP of CHF group raised gradually 30 min after treatment,while the MAP of HS group rose very slowly,and it was significantly lower than that of CHF group at each time point after 45min(P < 0.05,P < 0.01.All the dogs in both groups manifested hyperventilation and respiratory alkalosis when shock appeared.After shock,respiratory alkalosis in HS group gradually became metabolic acidosis,with some animals manifested combined metabolic and respiratory acidosis because of respiratory decompensation,while the blood gas levels in CHF group recovered to normal gradually.The blood gas levels of two groups showed significant difference at each time point after shock(P < 0.05,P < 0.01.Hypernatremia,hyperchloraemia and hyperpotassaemia were found in all animals of both

Citrate Anticoagulation for CRRT in Children: Comparison with Heparin

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Sara Nicole Fernández

2014-01-01

Full Text Available Regional anticoagulation with citrate is an alternative to heparin in continuous renal replacement therapies, which may prolong circuit lifetime and decrease hemorrhagic complications. A retrospective comparative cohort study based on a prospective observational registry was conducted including critically ill children undergoing CRRT. Efficacy, measured as circuit survival, and secondary effects of heparin and citrate were compared. 12 patients on CRRT with citrate anticoagulation and 24 patients with heparin anticoagulation were analyzed. Median citrate dose was 2.6 mmol/L. Median calcium dose was 0.16 mEq/kg/h. Median heparin dose was 15 UI/kg/h. Median circuit survival was 48 hours with citrate and 31 hours with heparin (P=0.028. 66.6% of patients treated with citrate developed mild metabolic alkalosis, which was directly related to citrate dose. There were no cases of citrate intoxication: median total calcium/ionic calcium index (CaT/I of 2.16 and a maximum CaT/I of 2.33, without metabolic acidosis. In the citrate group, 45.5% of patients developed hypochloremia and 27.3% hypomagnesemia. In the heparin group, 27.8% developed hypophosphatemia. Three patients were moved from heparin to citrate to control postoperatory bleeding. In conclusion citrate is a safe and effective anticoagulation method for CRRT in children and it achieves longer circuit survival than heparin.

The alkaline tide goes out and the nitrogen stays in after feeding in the dogfish shark, Squalus acanthias.

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Wood, Chris M; Bucking, Carol; Fitzpatrick, John; Nadella, Sunita

2007-11-15

In light of previous work showing a marked metabolic alkalosis ("alkaline tide") in the bloodstream after feeding in the dogfish shark (Squalus acanthias), we evaluated whether there was a corresponding net base excretion to the water at this time. In the 48 h after a natural voluntary meal (teleost tissue, averaging 5.5% of body weight), dogfish excreted 10,470 micromol kg(-1) more base (i.e. HCO3- equivalents) than the fasted control animals (which exhibited a negative base excretion of -2160 micromol kg(-1)). This large activation of branchial base excretion after feeding thereby prevented a potentially fatal alkalinization of the body fluids by the alkaline tide. The rate peaked at 330 micromol kg(-1) h(-1) at 12.5-24 h after the meal. Despite a prolonged 1.7-fold elevation in MO2 after feeding ("specific dynamic action"), urea-N excretion decreased by 39% in the same 48 h period relative to fasted controls. In contrast, ammonia-N excretion did not change appreciably. The N/O2 ratio declined from 0.51 in fasted animals to 0.19 in fed sharks, indicating a stimulation of N-anabolic processes at this time. These results, which differ greatly from those in teleost fish, are interpreted in terms of the fundamentally different ureotelic osmoregulatory strategy of elasmobranchs, and recent discoveries on base excretion and urea-retention mechanisms in elasmobranch gills.

Recovery by the Norway lobster Nephrops norvegicus (L.) from the physiological stresses of trawling: Influence of season and live-storage position

DEFF Research Database (Denmark)

Lund, H. S.; Wang, T.; Chang, E. S.

2009-01-01

Live Norway lobsters (Nephrops norvegicus L.) were trawled at depths of 30 to 55 m off the coast of Jutland (Denmark) in late winter (March) and in summer (August) in 2006. Water temperatures at the bottom and surface of the sea were 7 °C and 2 °C during the winter, and 12 °C and 21 °C in the sum......Live Norway lobsters (Nephrops norvegicus L.) were trawled at depths of 30 to 55 m off the coast of Jutland (Denmark) in late winter (March) and in summer (August) in 2006. Water temperatures at the bottom and surface of the sea were 7 °C and 2 °C during the winter, and 12 °C and 21 °C...... in the summer, respectively. The recovery of specific physiological and metabolic variables from the intense stresses associated with capture (trawling and air-exposure during sorting) was followed in seawater at 5 °C in winter or 18 °C in summer. Recovery was compared in lobsters held individually in two......-base status. In winter, a potential metabolic lactic acidosis was compensated by a marked respiratory alkalosis, with significantly increased haemolymph pH and decreased CO2 total content and partial pressure. These effects disappeared gradually over 96 h. Summer lobsters showed combined metabolic...

EFEITOS DA SUPLEMENTAÇÃO DE BICARBONATO DE SÓDIO EM UM TESTE ERGOMÉTRICO DE ESFORÇO CRESCENTE EM HOMENS RECREACIONALMENTE ATIVOS

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Everton Marcio Derisso

2014-02-01

Full Text Available The supplementation of sodium bicarbonate (NaHCO3 is being used as a way to induce blood alkalosis and increase the buffering chemical capacity. The literature shows a need for studies that use supplemental NaHCO3 at high intensities lasting more than 5 minutes. This study compares the effect of supplementation of NaHCO3 in speed corresponding to maximum working speed (vMAX and the respiratory compensation point (vRCP during an incremental treadmill test. We evaluate six recreationally active males (22.00 ± 2.00 years, 81.80 ± 9.90 kg, 1.81 ± 0.06 m and BMI 25 ± 2 kg/m2 and previously trained. The volunteers presented to the laboratory on two different days. They ingested 0.1 g/kg body weight of NaHCO3 (Group B or placebo with calcium carbonate (CaCO3 (Group P and performed an incremental test on a treadmill with 1km/h increments every 2 minutes until volitional exhaustion maximum. There was no significant difference in the velocities corresponding to vPCR and vMAX with supplementation of NaHCO3 and in any respiratory parameter. The ingestion of NaHCO3 at a concentration of 0.1 g/kg body weight does not improve performance in an incremental test on a treadmill.

Intracellular pH and inorganic phosphate content of heart in vivo: A 31P-NMR study

International Nuclear Information System (INIS)

Katz, L.A.; Swain, J.A.; Portman, M.A.; Balaban, R.S.

1988-01-01

Studies were performed to determine the contribution of red blood cells to the 31 P-nuclear magnetic resonance (NMR) spectrum of the canine heart in vivo and the feasibility of measuring myocardial intracellular phosphate and pH. This was accomplished by replacing whole blood with a perfluorochemical perfusion emulsion blood substitute, Oxypherol, and noting the difference in the 31 P-NMR spectrum of the heart. NMR data were collected with a NMR transmitter-receiver coil on the surface of the distal portion of the left ventricle. These studies demonstrated that a small contribution from 2,3-diphosphoglycerate (2,3-DPG) and phosphodiesters in the blood could be detected. The magnitude and shift of these blood-borne signals permitted the relative quantification of intracellular inorganic phosphate (P i ) content as well as intracellular pH. Under resting conditions, the intracellular ATP/P i was 7.0 ± 0.08. This corresponds to a free intracellular P 1 content of ∼ 0.8 μmol./g wet wt. The intracellular pH was 7.10 ± 0.01. Acute respiratory alkalosis and acidosis, with the arterial pH ranging from ∼7.0 to 7.7, resulted in only small changes in the intracellular pH. These latter results demonstrate an effective myocardial intracellular proton-buffering mechanism in vivo

Hypoxyradiotherapy: lack of experimental evidence for a preferential radioprotective effect on normal versus tumor tissue as shown by direct oxygenation measurements in experimental sarcomas

International Nuclear Information System (INIS)

Kelleher, Debra K.; Thews, Oliver; Vaupel, Peter

1997-01-01

Aim: In order to investigate possible pathophysiological mechanisms underlying the postulated preferential protective effect of hypoxia on normal tissue during radiotherapy, the impact of acute respiratory hypoxia (8.2% O 2 + 91.8% N 2 ) on tissue oxygenation was assessed. Methods: Tumor and normal tissue oxygenation was directly determined using O 2 -sensitive electrodes in two experimental rat tumors (DS and Yoshida sarcomas) and in the normal subcutis of the hind foot dorsum. Results: During respiratory hypoxia, arterial blood O 2 tension (pO 2 ), oxyhemoglobin saturation and mean arterial blood pressure decreased. Changes in the arterial blood gas status were accompanied by a reflex hyperventilation leading to hypocapnia and respiratory alkalosis. In the subcutis, tissue oxygenation worsened during acute hypoxia, with decreases in the mean and median pO 2 . Significant increases in the hypoxic fractions were, however, not seen. In tumor tissues, oxygenation also worsened upon hypoxic hypoxia with significant decreases in the mean and median pO 2 and increases in the size of the hypoxic fractions for both sarcomas. Conclusion: These results suggest that during respiratory hypoxia, radiobiologically relevant reductions in the oxygenation (and a subsequent selective radioprotection) of normal tissue may not be achieved. In addition, in the tumor models studied, a worsening of tumor oxygenation was seen which could result in an increased radioresistance

A novel variant in the SLC12A1 gene in two families with antenatal Bartter syndrome.

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Breinbjerg, Anders; Siggaard Rittig, Charlotte; Gregersen, Niels; Rittig, Søren; Hvarregaard Christensen, Jane

2017-01-01

Bartter syndrome is an autosomal-recessive inherited disease in which patients present with hypokalaemia and metabolic alkalosis. We present two apparently nonrelated cases with antenatal Bartter syndrome type I, due to a novel variant in the SLC12A1 gene encoding the bumetanide-sensitive sodium-(potassium)-chloride cotransporter 2 in the thick ascending limb of the loop of Henle. Blood samples were received from the two cases and 19 of their relatives, and deoxyribonucleic acid was extracted. The coding regions of the SLC12A1 gene were amplified using polymerase chain reaction, followed by bidirectional direct deoxyribonucleic acid sequencing. Each affected child in the two families was homozygous for a novel inherited variant in the SLC12A1gene, c.1614T>A. The variant predicts a change from a tyrosine codon to a stop codon (p.Tyr538Ter). The two cases presented antenatally and at six months of age, respectively. The two cases were homozygous for the same variant in the SLC12A1 gene, but presented clinically at different ages. This could eventually be explained by the presence of other gene variants or environmental factors modifying the phenotypes. The phenotypes of the patients were similar to other patients with antenatal Bartter syndrome. ©2016 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.

The physiological challenges of the 1952 Copenhagen poliomyelitis epidemic and a renaissance in clinical respiratory physiology

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West, John B.

2005-01-01

The 1952 Copenhagen poliomyelitis epidemic provided extraordinary challenges in applied physiology. Over 300 patients developed respiratory paralysis within a few weeks, and the ventilator facilities at the infectious disease hospital were completely overwhelmed. The heroic solution was to call upon 200 medical students to provide round-the-clock manual ventilation using a rubber bag attached to a tracheostomy tube. Some patients were ventilated in this way for several weeks. A second challenge was to understand the gas exchange and acid-base status of these patients. At the onset of the epidemic, the only measurement routinely available in the hospital was the carbon dioxide concentration in the blood, and the high values were initially misinterpreted as a mysterious “alkalosis.” However, pH measurements were quickly instituted, the PCO2 was shown to be high, and modern clinical respiratory acid-base physiology was born. Taking a broader view, the problems highlighted by the epidemic underscored the gap between recent advances made by physiologists and their application to the clinical environment. However, the 1950s ushered in a renaissance in clinical respiratory physiology. In 1950 the coverage of respiratory physiology in textbooks was often woefully inadequate, but the decade saw major advances in topics such as mechanics and gas exchange. An important development was the translation of the new knowledge from departments of physiology to the clinical setting. In many respects, this period was therefore the beginning of modern clinical respiratory physiology. PMID:16020437

Renal intercalated cells and blood pressure regulation

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Susan M. Wall

2017-12-01

Full Text Available Type B and non-A, non-B intercalated cells are found within the connecting tubule and the cortical collecting duct. Of these cell types, type B intercalated cells are known to mediate Cl⁻ absorption and HCO₃⁻ secretion largely through pendrin-dependent Cl⁻/HCO₃⁻ exchange. This exchange is stimulated by angiotensin II administration and is also stimulated in models of metabolic alkalosis, for instance after aldosterone or NaHCO₃ administration. In some rodent models, pendrin-mediated HCO₃⁻ secretion modulates acid-base balance. However, the role of pendrin in blood pressure regulation is likely of more physiological or clinical significance. Pendrin regulates blood pressure not only by mediating aldosterone-sensitive Cl⁻ absorption, but also by modulating the aldosterone response for epithelial Na⁺ channel (ENaC-mediated Na⁺ absorption. Pendrin regulates ENaC through changes in open channel of probability, channel surface density, and channels subunit total protein abundance. Thus, aldosterone stimulates ENaC activity through both direct and indirect effects, the latter occurring through its stimulation of pendrin expression and function. Therefore, pendrin contributes to the aldosterone pressor response. Pendrin may also modulate blood pressure in part through its action in the adrenal medulla, where it modulates the release of catecholamines, or through an indirect effect on vascular contractile force. This review describes how aldosterone and angiotensin II-induced signaling regulate pendrin and the contributory role of pendrin in distal nephron function and blood pressure.

Differences in Hematological Traits between High- and Low-Altitude Lizards (Genus Phrynocephalus.

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Songsong Lu

Full Text Available Phrynocephalus erythrurus (Lacertilia: Agamidae is considered to be the highest living reptile in the world (about 4500-5000 m above sea level, whereas Phrynocephalus przewalskii inhabits low altitudes (about 1000-1500 m above sea level. Here, we report the differences in hematological traits between these two different Phrynocephalus species. Compared with P. przewalskii, the results indicated that P. erythrurus own higher oxygen carrying capacity by increasing red blood cell count (RBC, hemoglobin concentration ([Hb] and hematocrit (Hct and these elevations could promote oxygen carrying capacity without disadvantage of high viscosity. The lower partial pressure of oxygen in arterial blood (PaO2 of P. erythrurus did not cause the secondary alkalosis, which may be attributed to an efficient pulmonary system for oxygen (O2 loading. The elevated blood-O2 affinity in P. erythrurus may be achieved by increasing intrinsic O2 affinity of isoHbs and balancing the independent effects of potential heterotropic ligands. We detected one α-globin gene and three β-globin genes with 1 and 33 amino acid substitutions between these two species, respectively. Molecular dynamics simulation results showed that amino acids substitutions in β-globin chains could lead to the elimination of hydrogen bonds in T-state Hb models of P. erythrurus. Based on the present data, we suggest that P. erythrurus have evolved an efficient oxygen transport system under the unremitting hypobaric hypoxia.

Is CO2 gas unsufflator necessary for laparoscopic training in animals?

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Tiraboshi Ricardo Brianezi

2003-01-01

Full Text Available OBJECTIVE: To verify the efficacy and safety of compressed air to produce pneumoperitoneum for laparoscopic surgery in pigs for a training program of residence. METHODS: Dalland pigs weighing 15-17kg underwent general anethesia and mechanical ventilation. They were divided in 3 groups: A - (38 the pneumoperitnoneum was established with an automatic CO2 insufflator, B - (7 as in A except the CO2 gas was changed by compressed air, and C - (11 abdomen insufflation was obtained with compressed air directly from hospital pipe network system. Intra-abdominal pressure in all groups was kept between 12 and 15 mmHg. The laparoscopic procedures performed were distributed proportionally among groups: 20 bilateral nephrectomy, 20 dismembered pyeloplasty and 16 partial nephrectomy. Arterial blood sampling for gasometry was obtained before and 2h after establishment of pneumoperitoneum in 5 pigs of group C. RESULTS: The cost of 25 4,5kg CO2 container used in group A was R$ 3,150.00 (U$ 1,050.00. The mean length time of surgeries in groups A, B and C were respectively: 181±30min, 196±39min e 210±47min (p>0.05. Respiratory alkalosis occurred in 3 out of 5 pigs of group C. No animal exhibited signs of gas embolism or died during surgery. CONCLUSION: The use of compressed air for laparoscopy in pigs was safe, reduced costs and did not require the use of an automatic gas insufflator.

Hypersensitivity Reaction and Acute Respiratory Distress Syndrome in Pyrethroid Poisoning and Role of Steroid Therapy

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Jisa George

2015-06-01

Full Text Available Background: Pyrethroids are generally of low toxicity to humans, but in suicidal poisonings which are usually associated with ingestion of high doses, they lead to severe systemic effects. Case Report: A 30-year old woman presented to emergency department with a history of intentional ingestion of about 15 mL of prallethrin around 3 days earlier. She complained of shortness of breath along with chest pain for the last 2 days. She reported no vomiting or stomach pain prior to presentation to hospital. On chest auscultation, breath sounds were mildly decreased in bilateral infrascapular areas with generalized crepitation. Arterial blood gas analysis revealed respiratory alkalosis. Chest X ray and computed tomography of thorax revealed widespread confluent areas of consolidation with interlobular septal thickening involving bilateral parahilar regions suggestive of acute respiratory distress syndrome (ARDS. The patient did not respond to broad spectrum antibiotic coverage, diuretics and oxygen inhalation. Intravenous methylprednisolone (2 mg/kg/day divided 6 hourly was started and slowly tapered off during the next days. The patient discharged after 3 weeks in good health. Discussion: As pyrethroids can affect sodium channels, the osmotic gradient of alveolar epithelium probably disrupts and therefore, alveolar infiltrations gradually spread over lungs. In addition, there is a possibility of hypersensitivity reactions to pyrethroids, which can cause progressive inflammation and involve respiratory tract in severe cases. Conclusion: Pyrethroid poisoning can lead to ARDS. Steroid therapy may help such patients tide over the pulmonary crisis.

Mineralocorticoid hypertension

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Vishal Gupta

2011-01-01

Full Text Available Hypertension affects about 10 - 25% of the population and is an important risk factor for cardiovascular and renal disease. The renin-angiotensin system is frequently implicated in the pathophysiology of hypertension, be it primary or secondary. The prevalence of primary aldosteronism increases with the severity of hypertension, from 2% in patients with grade 1 hypertension to 20% among resistant hypertensives. Mineralcorticoid hypertension includes a spectrum of disorders ranging from renin-producing pathologies (renin-secreting tumors, malignant hypertension, coarctation of aorta, aldosterone-producing pathologies (primary aldosteronism - Conns syndrome, familial hyperaldosteronism 1, 2, and 3, non-aldosterone mineralocorticoid producing pathologies (apparent mineralocorticoid excess syndrome, Liddle syndrome, deoxycorticosterone-secreting tumors, ectopic adrenocorticotropic hormones (ACTH syndrome, congenitalvadrenal hyperplasia, and drugs with mineraocorticoid activity (locorice, carbenoxole therapy to glucocorticoid receptor resistance syndromes. Clinical presentation includes hypertension with varying severity, hypokalemia, and alkalosis. Ratio of plasma aldosterone concentraion to plasma renin activity remains the best screening tool. Bilateral adrenal venous sampling is the best diagnostic test coupled with a CT scan. Treatment is either surgical (adrenelectomy for unilateral adrenal disease versus medical therapy for idiopathic, ambiguous, or bilateral disease. Medical therapy focuses on blood pressure control and correction of hypokalemia using a combination of anti-hypertensives (calcium channel blockers, angiotensin converting enzyme inhibitors, or angiotensin receptor blockers and potassium-raising therapies (mineralcorticoid receptor antagonist or potassium sparing diuretics. Direct aldosterone synthetase antagonists represent a promising future therapy.

Late-onset Bartter syndrome type II.

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Gollasch, Benjamin; Anistan, Yoland-Marie; Canaan-Kühl, Sima; Gollasch, Maik

2017-10-01

Mutations in the ROMK1 potassium channel gene ( KCNJ1 ) cause antenatal/neonatal Bartter syndrome type II (aBS II), a renal disorder that begins in utero , accounting for the polyhydramnios and premature delivery that is typical in affected infants, who develop massive renal salt wasting, hypokalaemic metabolic alkalosis, secondary hyperreninaemic hyperaldosteronism, hypercalciuria and nephrocalcinosis. This BS type is believed to represent a disorder of the infancy, but not in adulthood. We herein describe a female patient with a remarkably late-onset and mild clinical manifestation of BS II with compound heterozygous KCNJ1 missense mutations, consisting of a novel c.197T > A (p.I66N) and a previously reported c.875G > A (p.R292Q) KCNJ1 mutation. We implemented and evaluated the performance of two different bioinformatics-based approaches of targeted massively parallel sequencing [next generation sequencing (NGS)] in defining the molecular diagnosis. Our results demonstrate that aBS II may be suspected in patients with a late-onset phenotype. Our experimental approach of NGS-based mutation screening combined with Sanger sequencing proved to be a reliable molecular approach for defining the clinical diagnosis in our patient, and results in important differential diagnostic and therapeutic implications for patients with BS. Our results could have a significant impact on the diagnosis and methodological approaches of genetic testing in other patients with clinical unclassified phenotypes of nephrocalcinosis and congenital renal electrolyte abnormalities.

Mixed Bartter-Gitelman syndrome: an inbred family with a heterogeneous phenotype expression of a novel variant in the CLCNKB gene.

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Al-Shibli, Amar; Yusuf, Madinah; Abounajab, Issam; Willems, Patrick J

2014-01-01

Patients with renal diseases associated with salt-losing tubulopathies categorized as Gitelman and classic form of Bartter syndrome have undergone genetic screening for possible mutation capture in two different genes: SLC12A3 and CLCNKB. Clinical symptoms of these two diseases may overlap. Bartter syndrome and Gitelman syndrome are autosomal recessive salt-losing tubulopathies with hypokalemia, metabolic alkalosis, hyperreninemia, hyperplasia of the juxtaglomerular apparatus, hyperaldosteronism, and, in some patients, hypomagnesemia. Here we describe four patients from an inbred family with a novel missense variant in the CLCNKB gene. All of patients are asymptomatic; yet they have the typical metabolic abnormality of salt losing tubulopathies. One of those patients had hypomagnesaemia while others not. Clinical and laboratory data of all patients was described. All 4 patients have a homozygous c.490G > T missense variant in exon 5 of the CLCNKB gene. This variant alters a glycine into a cysteine on amino acid position 164 of the resulting protein (p.Gly164Cys). The c.490G > T variant is a novel variant not previously described in other patients nor controls. Polyphen analysis predicts the variation to be possibly damaging. Analysis of SLC12A3 was normal. Here in we are describing a novel homozygous c.490G > T missense variation was identified in exon 5 of the CLCNKB gene was identified in an Emirati patients with a mild manifestation of Bartter - Gitelman syndrome.

Novel Compound Heterozygous CLCNKB Gene Mutations (c.1755A>G/ c.848_850delTCT) Cause Classic Bartter Syndrome.

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Wang, Chunli; Chen, Ying; Zheng, Bixia; Zhu, Mengshu; Fan, Jia; Wang, Juejin; Jia, Zhanjun; Huang, Songming; Zhang, Aihua

2018-02-14

Inactivated variants in CLCNKB gene encoding the basolateral chloride channel ClC-Kb cause classic Bartter syndrome characterized by hypokalemic metabolic alkalosis and hyperreninemic hyperaldosteronism. Here we identified two cBS siblings presenting hypokalemia in a Chinese family due to novel compound heterozygous CLCNKB mutations (c.848_850delTCT/c.1755A>G). Compound heterozygosity was confirmed by amplifying and sequencing the patient's genomic DNA. The synonymous mutation c.1755A>G (Thr585Thr) was located at +2bp from the 5' splice donor site in exon 15, further transcript analysis demonstrated that this single nucleotide mutation causes exclusion of exon 15 in the cDNA from the proband and his mother. Furthermore, we investigated the expression and protein trafficking change of c.848_850delTCT (TCT) and exon 15 deletion（E15）mutation in vitro. The E15 mutation markedly decreased the expression of ClC-Kb and resulted in a low-molecular-weight band (~55kD) trapping in the endoplasmic reticulum, while the TCT mutant only decreased the total and plasma membrane ClC-Kb protein expression but did not affect the subcellular localization. Finally, we studied the physiological functions of mutations by using whole-cell patch clamp and found that E15 or TCT mutation decreased the current of ClC-Kb/barttin channel. These results suggested that the compound defective mutations of CLCNKB gene are the molecular mechanism of the two cBS siblings.

Glucose concentration and blood acid-basis status in high-yielding dairy cows during heat stress

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Vujanac Ivan

2011-01-01

Full Text Available The objective of this work was to examine the effect of heat stress on glucose and pH values in blood of high-yielding dairy cows in the early stage of lactation, as well as to determine whether the changes in these parameters are interdependent under such conditions. An experiment was performed on high-yielding dairy cows during the summer and the spring periods. Forty cows were selected, twenty each for the two periods under investigation. In the course of the experiment, the temperature humidity index (THI was determined for the entire period of investigations, and then also the average daily THI, nightmorning THI (average value of hourly THI measured from 22h on the previous day until 10h of the current day, as well as the day-night THI (average value of hourly THI measured during the period from 10h to 22h of the current day. The pH and glucose concentration were determined in blood samples taken in the morning and afternoon of days 30, 60, and 90 of lactation during the spring and summer periods of the investigations. Based on the results for the THI, it was established that the animals were not exposed to the effect of extreme heat stress during the spring period of investigations, while they were periodically exposed to moderate but also extreme heat stress during the summer, in particular in the afternoon hours. It can be concluded from the results obtained for the blood pH that the cows were in respiratory alkalosis during the summer in the morning and afternoon hours on day 30, in the afternoon hours of days 60 and 90 of lactation, as well as in the afternoon on day 90 of lactation during the spring period of investigations. During the summer period, there were no statistically significant differences between the pH value determined in the morning and afternoon hours on day 30 of lactation, while the pH value was significantly higher in the afternoon hours than in the morning hours on days 60 and 90 of lactation. There were no

Hemogasometria de eqüinos submetidos à obstrução experimental do duodeno, íleo e cólon maior Blood gas analysis of horses submitted to experimental obstruction of duodenum, ileum and large colon

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Paula Alessandra Di Filippo

2009-02-01

HCO-3(vP and cBase(v which, added to the increase of pCO2(v and ctCO2(v, characterized the metabolic alkalosis with respiratory compensation. At T90ob and T120ob, in GII animals, and at T180ob, in GIII animals the pO2(v and sO2(v had similar response. Low values presented by GII animals were associated to hypercapnia or hypoventilation triggered for metabolic alkalosis correction. However, a hypoxemia presented by GIII animals was associated to hypovolemia at that period. There were light and temporary acid-base alterations that are not capable to predict specific intestinal obstruction diagnosis in equines with colic. However they help in prognosis since both have a direct relation with the precociousness of gastrointestinal disturbance.

The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder O papel da hiperventilação: a hipocapnia no patomecanismo do distúrbio de pânico

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Andras Sikter

2007-12-01

Full Text Available OBJECTIVE: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. METHOD: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. DISCUSSION: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO2 when the latent (metabolic acidosis manifests as hypercapnic acidosis. The acidotic condition induces catecholamine release. Sympathicotonia cannot arise during the hypercapnic phase, since low pH decreases catecholamine sensitivity. Catecholamines can provoke panic when hyperventilation causes the hypercapnia to switch to hypocapnic alkalosis (overcompensation and catecholamine sensitivity begins to increase. CONCLUSION: Therapeutic approaches should address long-term regulation of the respiratory pattern and elimination of metabolic acidosis.OBJETIVO: Os autores apresentam um modelo de transtorno do pânico que se baseia nos efeitos da hiperventilação aguda e crônica, característicos do subtipo respiratório de transtorno do pânico. O modelo é generalizado a partir desses efeitos. Ele integra três características da hiperventilação: a hiperventilação é uma resposta fisiológica à hipercapnia; a hiperventilação pode induzir ataques de pânico; a hiperventila

The nutritional limitations of plant-based beverages in infancy and childhood.

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Vitoria, Isidro

2017-10-24

Breastfeeding, infant formula and cow's milk are basic foods in infant nutrition. However, they are being increasingly replaced either totally or partially by plant-based beverages.The composition of 164 plant-based beverages available in Spain was reviewed based on the nutritional labeling of the package and the manufacturers' webpages. This was compared to the composition of cow's milk and infant formula. In addition, the nutritional disease associated with consumption of plant-based beverages in infants and children was reviewed by means of a literature search in Medline and Embase since 1990 based on the key words "plant-based beverages" or "rice beverages" or "almond beverages" or "soy beverages" and "infant" or "child".The nutritional composition of 54 soy beverages, 24 rice beverages, 22 almond beverages, 31 oat beverages, 6 coconut beverages, 12 miscellaneous beverages and 15 mixed beverages was described. At least 30 cases of nutritional disease in children associated with nearly exclusive consumption of plant-based beverages have been published. A characteristic association has been observed between soy beverage and rickets, rice beverage and kwashiorkor, and almond-based beverage and metabolic alkalosis.The nutritional quality of plant-based beverages is lower than that of cow's milk and infant formula, therefore they are not a nutritional alternative. Predominant or exclusive use of these beverages in infant feeding can lead to serious nutritional risks. In the case of nonexclusive feeding with these beverages, the pediatrician should be aware of the nutritional risks and limitations of these beverages in order to complement their deficiencies with other foods.

Insulin receptor-related receptor as an extracellular pH sensor involved in the regulation of acid-base balance.

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Petrenko, Alexander G; Zozulya, Sergey A; Deyev, Igor E; Eladari, Dominique

2013-10-01

Recent studies of insulin receptor-related receptor (IRR) revealed its unusual property to activate upon extracellular application of mildly alkaline media, pH>7.9. The activation of IRR with hydroxyl anion has typical features of ligand-receptor interaction; it is specific, dose-dependent, involves the IRR extracellular domain and is accompanied by a major conformational change. IRR is a member of the insulin receptor minifamily and has been long viewed as an orphan receptor tyrosine kinase since no peptide or protein agonist of IRR was found. In the evolution, IRR is highly conserved since its divergence from the insulin and insulin-like growth factor receptors in amphibia. The latter two cannot be activated by alkali. Another major difference between them is that unlike ubiquitously expressed insulin and insulin-like growth factor receptors, IRR is found in specific sets of cells of only some tissues, most of them being exposed to extracorporeal liquids of extreme pH. In particular, largest concentrations of IRR are in beta-intercalated cells of the kidneys. The primary physiological function of these cells is to excrete excessive alkali as bicarbonate into urine. When IRR is removed genetically, animals loose the property to excrete bicarbonate upon experimentally induced alkalosis. In this review, we will discuss the available in vitro and in vivo data that support the hypothesis of IRR role as a physiological alkali sensor that regulates acid-base balance. This article is part of a Special Issue entitled: Emerging recognition and activation mechanisms of receptor tyrosine kinases. Copyright © 2012 Elsevier B.V. All rights reserved.

Gitelman syndrome in a South African family presenting with hypokalaemia and unusual food cravings.

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van der Merwe, Pieter Du Toit; Rensburg, Megan A; Haylett, William L; Bardien, Soraya; Davids, M Razeen

2017-01-26

Gitelman syndrome (GS) is an autosomal recessive renal tubular disorder characterised by renal salt wasting with hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria. It is caused by mutations in SLC12A3 encoding the sodium-chloride cotransporter on the apical membrane of the distal convoluted tubule. We report a South African family with five affected individuals presenting with hypokalaemia and unusual food cravings. The affected individuals and two unaffected first degree relatives were enrolled into the study. Phenotypes were evaluated through history, physical examination and biochemical analysis of blood and urine. Mutation screening was performed by sequencing of SLC12A3, and determining the allele frequencies of the sequence variants found in this family in 117 ethnically matched controls. The index patient, her sister, father and two aunts had a history of severe salt cravings, fatigue and tetanic episodes, leading to consumption of large quantities of salt and vinegar. All affected individuals demonstrated hypokalaemia with renal potassium wasting. Genetic analysis revealed that the pseudo-dominant pattern of inheritance was due to compound heterozygosity with two novel mutations: a S546G substitution in exon 13, and insertion of AGCCCC at c.1930 in exon 16. These variants were present in the five affected individuals, but only one variant each in the unaffected family members. Neither variant was found in any of the controls. The diagnosis of GS was established in five members of a South African family through clinical assessment, biochemical analysis and mutation screening of the SLC12A3 gene, which identified two novel putative pathogenic mutations.

The ClC-K2 Chloride Channel Is Critical for Salt Handling in the Distal Nephron.

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Hennings, J Christopher; Andrini, Olga; Picard, Nicolas; Paulais, Marc; Huebner, Antje K; Cayuqueo, Irma Karen Lopez; Bignon, Yohan; Keck, Mathilde; Cornière, Nicolas; Böhm, David; Jentsch, Thomas J; Chambrey, Régine; Teulon, Jacques; Hübner, Christian A; Eladari, Dominique

2017-01-01

Chloride transport by the renal tubule is critical for blood pressure (BP), acid-base, and potassium homeostasis. Chloride uptake from the urinary fluid is mediated by various apical transporters, whereas basolateral chloride exit is thought to be mediated by ClC-Ka/K1 and ClC-Kb/K2, two chloride channels from the ClC family, or by KCl cotransporters from the SLC12 gene family. Nevertheless, the localization and role of ClC-K channels is not fully resolved. Because inactivating mutations in ClC-Kb/K2 cause Bartter syndrome, a disease that mimics the effects of the loop diuretic furosemide, ClC-Kb/K2 is assumed to have a critical role in salt handling by the thick ascending limb. To dissect the role of this channel in detail, we generated a mouse model with a targeted disruption of the murine ortholog ClC-K2. Mutant mice developed a Bartter syndrome phenotype, characterized by renal salt loss, marked hypokalemia, and metabolic alkalosis. Patch-clamp analysis of tubules isolated from knockout (KO) mice suggested that ClC-K2 is the main basolateral chloride channel in the thick ascending limb and in the aldosterone-sensitive distal nephron. Accordingly, ClC-K2 KO mice did not exhibit the natriuretic response to furosemide and exhibited a severely blunted response to thiazide. We conclude that ClC-Kb/K2 is critical for salt absorption not only by the thick ascending limb, but also by the distal convoluted tubule. Copyright © 2016 by the American Society of Nephrology.

Exogenous sphingosine-1-phosphate boosts acclimatization in rats exposed to acute hypobaric hypoxia: assessment of haematological and metabolic effects.

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Sonam Chawla

Full Text Available The physiological challenges posed by hypobaric hypoxia warrant exploration of pharmacological entities to improve acclimatization to hypoxia. The present study investigates the preclinical efficacy of sphingosine-1-phosphate (S1P to improve acclimatization to simulated hypobaric hypoxia.Efficacy of intravenously administered S1P in improving haematological and metabolic acclimatization was evaluated in rats exposed to simulated acute hypobaric hypoxia (7620 m for 6 hours following S1P pre-treatment for three days.Altitude exposure of the control rats caused systemic hypoxia, hypocapnia (plausible sign of hyperventilation and respiratory alkalosis due to suboptimal renal compensation indicated by an overt alkaline pH of the mixed venous blood. This was associated with pronounced energy deficit in the hepatic tissue along with systemic oxidative stress and inflammation. S1P pre-treatment improved blood oxygen-carrying-capacity by increasing haemoglobin, haematocrit, and RBC count, probably as an outcome of hypoxia inducible factor-1α mediated erythropoiesis and renal S1P receptor 1 mediated haemoconcentation. The improved partial pressure of oxygen in the blood could further restore aerobic respiration and increase ATP content in the hepatic tissue of S1P treated animals. S1P could also protect the animals from hypoxia mediated oxidative stress and inflammation.The study findings highlight S1P's merits as a preconditioning agent for improving acclimatization to acute hypobaric hypoxia exposure. The results may have long term clinical application for improving physiological acclimatization of subjects venturing into high altitude for occupational or recreational purposes.

Surfactant secretion is stimulated by decreased alveolar CO2

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Chander, A.; Dodia, C.R.; Gullo, J.; Fisher, A.B.

1986-01-01

The authors investigated the hypothesis that altered intracellular pH may modulate lung surfactant secretion. They have used isolated perfused lung preparation to investigate release of [ 3 H]choline labeled phosphatidylcholine (PC) in the alveolar space of rat lungs ventilated with 5%, 2.5%, or 0% CO 2 in air. Adult rats were injected i.p. 40uCi of [ 3 H-methyl] choline and lungs removed after 45 min. Lungs were perfused for 15 or 60 min. with KRB plus 25 mM HEPES. At the end of perfusion lungs were lavaged five times with 7 ml of ice cold saline. Lavage fluid, was centrifuged, lyophilized, and both lung and lavage fluid extracted for lipids. Lipid choline label in lavage fluid, expressed as percent of that in lung lipids, from control lungs (5% CO 2 ) showed 0.6 +/- 0.1 % at 15 min and 1.1 +/- 0.3% (mean +/- SE, n=6) label at 60 min. When perfused with 50 μM 1-isoproterenol, the label after 60 min perfusion increased to 2.76 +/- 0.33 (n=3). Ventilation with air containing 2.5% CO 2 and 0% CO 2 showed 6.1 +/- 2.1 % (n=4) and 6.4 +/- 1.8% (n=4) label in lavage fluid. Addition of 25mM sodium acetate in the perfusion medium and ventilation with 0% CO 2 in air lowered release of label to 4.2 +/- 1.4% (n=4). These results show that low pCO 2 increases surfactant PC secretion in lung and suggest that intracellular alkalosis triggers surfactant release

Hypophosphatemia. From retrospective analysis to the analysis of the potential role of phosphatemia in panic disorders

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Alessandro Riccardi

2010-09-01

Full Text Available The detection of a low serum phosphate level is not unusual in an Emergency Department, especially in clinical conditions linked to hyperventilation and subsequent respiratory alkalosis, asthma, sepsis, severe pain, anxiety. Symptoms of hypophosphatemia are typically not specific when the imbalance is not particularly severe, but if hyphophosphatemia does not resolve rhabdomyolisis, hemolysis, decreased tissue oxygenation and respiratory failure can be observed. Only recently some authors have pointed out that the level of serum phosphate in patient with anxiety and panic disorders can give information on the severity of the attacks as well on the clinical course of the disease. In a retrospective analysis on 599 case of hypophosphatemia observed in our ED, the percentage of case of panic disorders was particularly high among patients with lower phosphatemia. Therefore, we decided to examine this aspect closely, assessing if the determination of serum phosphate could be useful in the management of panic attacks at first approach in emergency room. Our observation are consistent with the statement that hypophosphatemia is one of the main clinical aspect of panic attack, and strongly support the hypothesis that hypophosphatemia correlates with the most severe symptoms of panic attack and should be itself considered as one of the most important aspect of this syndrome. Serum phosphate levels appear to mirror its clinical course, and can be used in the clinical setting of an Emergency Department, for the confirmation of a diagnosis of anxiety-panic disorder and as marker of the response to therapy

Emergency department management of children with acute isoniazid poisoning.

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Parish, R A; Brownstein, D

1986-06-01

We suggest that the following therapeutic regimen be followed in cases of isoniazid poisoning in children. In cases of intractable seizure activity in a child which remains unexplained, consider isoniazid poisoning. Give pyridoxine as an intravenous bolus to all children in whom isoniazid toxicity is suspected, who exhibit seizure activity and are known to have been exposed to isoniazid, or who have a history of ingesting one gram or more of isoniazid. It should be given on a gram-for-gram basis, and the clinician need not await serum isoniazid levels before administering pyridoxine. It can be safely given at a rate of five grams per three minutes in a 50 ml volume. In fact, serum isoniazid determinations are not available in many emergency departments and have not been shown to correlate closely with symptomatology. When available, serum isoniazid levels at best are subject to variability owing to sampling procedures (serum protein must be removed within two hours of sampling). The result is that serum isoniazid levels play only a minor role in the emergency department management of isoniazid poisoning. To potentiate the antidotal effects of pyridoxine, diazepam (0.1 mg/kg) may be given intravenously, preferably at a second intravenous site. Because the lactic acidosis seen after seizures resolves spontaneously, and because metabolic alkalosis may result following excess lactate loading, administration of bicarbonate is usually not necessary, and may be harmful in some cases. After pyridoxine treatment, syrup of ipecac may be given to empty the stomach.(ABSTRACT TRUNCATED AT 250 WORDS)

Mutation of the Na(+)-K(+)-2Cl(-) cotransporter NKCC2 in mice is associated with severe polyuria and a urea-selective concentrating defect without hyperreninemia.

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Kemter, Elisabeth; Rathkolb, Birgit; Bankir, Lise; Schrewe, Anja; Hans, Wolfgang; Landbrecht, Christina; Klaften, Matthias; Ivandic, Boris; Fuchs, Helmut; Gailus-Durner, Valérie; Hrabé de Angelis, Martin; Wolf, Eckhard; Wanke, Ruediger; Aigner, Bernhard

2010-06-01

The bumetanide-sensitive Na(+)-K(+)-2Cl(-) cotransporter NKCC2, located in the thick ascending limb of Henle's loop, plays a critical role in the kidney's ability to concentrate urine. In humans, loss-of-function mutations of the solute carrier family 12 member 1 gene (SLC12A1), coding for NKCC2, cause type I Bartter syndrome, which is characterized by prenatal onset of a severe polyuria, salt-wasting tubulopathy, and hyperreninemia. In this study, we describe a novel chemically induced, recessive mutant mouse line termed Slc12a1(I299F) exhibiting late-onset manifestation of type I Bartter syndrome. Homozygous mutant mice are viable and exhibit severe polyuria, metabolic alkalosis, marked increase in plasma urea but close to normal creatininemia, hypermagnesemia, hyperprostaglandinuria, hypotension,, and osteopenia. Fractional excretion of urea is markedly decreased. In addition, calcium and magnesium excretions are more than doubled compared with wild-type mice, while uric acid excretion is twofold lower. In contrast to hyperreninemia present in human disease, plasma renin concentration in homozygotes is not increased. The polyuria observed in homozygotes may be due to the combination of two additive factors, a decrease in activity of mutant NKCC2 and an increase in medullary blood flow, due to prostaglandin-induced vasodilation, that impairs countercurrent exchange of urea in the medulla. In conclusion, this novel viable mouse line with a missense Slc12a1 mutation exhibits most of the features of type I Bartter syndrome and may represent a new model for the study of this human disease.

Roles of renal ammonia metabolism other than in acid-base homeostasis.

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Weiner, I David

2017-06-01

The importance of renal ammonia metabolism in acid-base homeostasis is well known. However, the effects of renal ammonia metabolism other than in acid-base homeostasis are not as widely recognized. First, ammonia differs from almost all other solutes in the urine in that it does not result from arterial delivery. Instead, ammonia is produced by the kidney, and only a portion of the ammonia produced is excreted in the urine, with the remainder returned to the systemic circulation through the renal veins. In normal individuals, systemic ammonia addition is metabolized efficiently by the liver, but in patients with either acute or chronic liver disease, conditions that increase the addition of ammonia of renal origin to the systemic circulation can result in precipitation and/or worsening of hyperammonemia. Second, ammonia appears to serve as an intrarenal paracrine signaling molecule. Hypokalemia increases proximal tubule ammonia production and secretion as well as reabsorption in the thick ascending limb of the loop of Henle, thereby increasing delivery to the renal interstitium and the collecting duct. In the collecting duct, ammonia decreases potassium secretion and stimulates potassium reabsorption, thereby decreasing urinary potassium excretion and enabling feedback correction of the initiating hypokalemia. Finally, the stimulation of renal ammonia metabolism by hypokalemia may contribute to the development of metabolic alkalosis, which in turn can stimulate NaCl reabsorption and contribute to the intravascular volume expansion, increased blood pressure and diuretic resistance that can develop with hypokalemia. The evidence supporting these novel non-acid-base roles of renal ammonia metabolism is discussed in this review.

Effects of intravenous solutions on acid-base equilibrium: from crystalloids to colloids and blood components.

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Langer, Thomas; Ferrari, Michele; Zazzeron, Luca; Gattinoni, Luciano; Caironi, Pietro

2014-01-01

Intravenous fluid administration is a medical intervention performed worldwide on a daily basis. Nevertheless, only a few physicians are aware of the characteristics of intravenous fluids and their possible effects on plasma acid-base equilibrium. According to Stewart's theory, pH is independently regulated by three variables: partial pressure of carbon dioxide, strong ion difference (SID), and total amount of weak acids (ATOT). When fluids are infused, plasma SID and ATOT tend toward the SID and ATOT of the administered fluid. Depending on their composition, fluids can therefore lower, increase, or leave pH unchanged. As a general rule, crystalloids having a SID greater than plasma bicarbonate concentration (HCO₃-) cause an increase in plasma pH (alkalosis), those having a SID lower than HCO₃- cause a decrease in plasma pH (acidosis), while crystalloids with a SID equal to HCO₃- leave pH unchanged, regardless of the extent of the dilution. Colloids and blood components are composed of a crystalloid solution as solvent, and the abovementioned rules partially hold true also for these fluids. The scenario is however complicated by the possible presence of weak anions (albumin, phosphates and gelatins) and their effect on plasma pH. The present manuscript summarises the characteristics of crystalloids, colloids, buffer solutions and blood components and reviews their effect on acid-base equilibrium. Understanding the composition of intravenous fluids, along with the application of simple physicochemical rules best described by Stewart's approach, are pivotal steps to fully elucidate and predict alterations of plasma acid-base equilibrium induced by fluid therapy.

Hibernation and gas exchange.

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Milsom, William K; Jackson, Donald C

2011-01-01

Hibernation in endotherms and ectotherms is characterized by an energy-conserving metabolic depression due to low body temperatures and poorly understood temperature-independent mechanisms. Rates of gas exchange are correspondly reduced. In hibernating mammals, ventilation falls even more than metabolic rate leading to a relative respiratory acidosis that may contribute to metabolic depression. Breathing in some mammals becomes episodic and in some small mammals significant apneic gas exchange may occur by passive diffusion via airways or skin. In ectothermic vertebrates, extrapulmonary gas exchange predominates and in reptiles and amphibians hibernating underwater accounts for all gas exchange. In aerated water diffusive exchange permits amphibians and many species of turtles to remain fully aerobic, but hypoxic conditions can challenge many of these animals. Oxygen uptake into blood in both endotherms and ectotherms is enhanced by increased affinity of hemoglobin for O₂ at low temperature. Regulation of gas exchange in hibernating mammals is predominately linked to CO₂/pH, and in episodic breathers, control is principally directed at the duration of the apneic period. Control in submerged hibernating ectotherms is poorly understood, although skin-diffusing capacity may increase under hypoxic conditions. In aerated water blood pH of frogs and turtles either adheres to alphastat regulation (pH ∼8.0) or may even exhibit respiratory alkalosis. Arousal in hibernating mammals leads to restoration of euthermic temperature, metabolic rate, and gas exchange and occurs periodically even as ambient temperatures remain low, whereas body temperature, metabolic rate, and gas exchange of hibernating ectotherms are tightly linked to ambient temperature. © 2011 American Physiological Society.

Clinical, genetic, and structural basis of apparent mineralocorticoid excess due to 11β-hydroxysteroid dehydrogenase type 2 deficiency.

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Yau, Mabel; Haider, Shozeb; Khattab, Ahmed; Ling, Chen; Mathew, Mehr; Zaidi, Samir; Bloch, Madison; Patel, Monica; Ewert, Sinead; Abdullah, Wafa; Toygar, Aysenur; Mudryi, Vitalii; Al Badi, Maryam; Alzubdi, Mouch; Wilson, Robert C; Al Azkawi, Hanan Said; Ozdemir, Hatice Nur; Abu-Amer, Wahid; Hertecant, Jozef; Razzaghy-Azar, Maryam; Funder, John W; Al Senani, Aisha; Sun, Li; Kim, Se-Min; Yuen, Tony; Zaidi, Mone; New, Maria I

2017-12-26

Mutations in 11β-hydroxysteroid dehydrogenase type 2 gene ( HSD11B2 ) cause an extraordinarily rare autosomal recessive disorder, apparent mineralocorticoid excess (AME). AME is a form of low renin hypertension that is potentially fatal if untreated. Mutations in the HSD11B2 gene result either in severe AME or a milder phenotype (type 2 AME). To date, ∼40 causative mutations have been identified. As part of the International Consortium for Rare Steroid Disorders, we have diagnosed and followed the largest single worldwide cohort of 36 AME patients. Here, we present the genotype and clinical phenotype of these patients, prominently from consanguineous marriages in the Middle East, who display profound hypertension and hypokalemic alkalosis. To correlate mutations with phenotypic severity, we constructed a computational model of the HSD11B2 protein. Having used a similar strategy for the in silico evaluation of 150 mutations of CYP21A2 , the disease-causing gene in congenital adrenal hyperplasia, we now provide a full structural explanation for the clinical severity of AME resulting from each known HSD11B2 missense mutation. We find that mutations that allow the formation of an inactive dimer, alter substrate/coenzyme binding, or impair structural stability of HSD11B2 yield severe AME. In contrast, mutations that cause an indirect disruption of substrate binding or mildly alter intramolecular interactions result in type 2 AME. A simple in silico evaluation of novel missense mutations could help predict the often-diverse phenotypes of an extremely rare monogenic disorder.

Baking soda misuse as a home remedy: case experience of the California Poison Control System.

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Al-Abri, S A; Kearney, T

2014-02-01

Baking soda is a common household product promoted by the manufacturer as an antacid. It contains sodium bicarbonate and has the potential for significant toxicity when ingested in excessive amounts. Characterizing the patterns and outcomes from the misuse of baking soda as a home remedy can guide the clinical assessment and preventative counselling of patients at risk for use of this product. We conducted a retrospective review of all symptomatic cases involving ingestion and misuse of a baking soda powder product that were reported to the California Poison Control System between the years 2000 and 2012. Of the 192 cases we identified, 55·8% were female, ages ranged 2 months to 79 years, and the most common reasons for misuse included antacid (60·4%), 'beat a urine drug test' (11·5%) and treat a UTI (4·7%). Most cases (55·2%) had significant symptoms warranting a medical evaluation, whereas 12 patients required hospital admission developed either electrolyte imbalances, metabolic alkalosis or respiratory depression. Misuse of baking soda can result in serious electrolyte and acid/base imbalances. Patients at highest risk of toxicity may include those who chronically use an antacid, those who use the method to 'beat' urine drug screens, pregnant women and young children. Self-treatment with baking soda as a home remedy may also mask or delay medical care thereby complicating or exacerbating an existing medical problem. We suggest that healthcare providers counsel high-risk patients about the potential complications of misuse of baking soda as a home remedy. © 2013 John Wiley & Sons Ltd.

Effect of sodium bicarbonate on [HCO3-], pH, and gastrointestinal symptoms.

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Carr, Amelia J; Slater, Gary J; Gore, Christopher J; Dawson, Brian; Burke, Louise M

2011-06-01

Sodium bicarbonate (NaHCO₃) is often ingested at a dose of 0.3 g/kg body mass (BM), but ingestion protocols are inconsistent in terms of using solution or capsules, ingestion period, combining NaHCO₃ with sodium citrate (Na₃C₆H₅O₇), and coingested food and fluid. To quantify the effect of ingesting 0.3 g/kg NaHCO₃ on blood pH, [HCO₃-], and gastrointestinal (GI) symptoms over the subsequent 3 hr using a range of ingestion protocols and, thus, to determine an optimal protocol. In a crossover design, 13 physically active subjects undertook 8 NaHCO₃ experimental ingestion protocols and 1 placebo protocol. Capillary blood was taken every 30 min and analyzed for pH and [HCO₃-]. GI symptoms were quantified every 30 min via questionnaire. Statistics used were pairwise comparisons between protocols; differences were interpreted in relation to smallest worthwhile changes for each variable. A likelihood of >75% was a substantial change. [HCO₃-] and pH were substantially greater than in placebo for all other ingestion protocols at almost all time points. When NaHCO3 was coingested with food, the greatest [HCO₃-] (30.9 mmol/kg) and pH (7.49) and lowest incidence of GI symptoms were observed. The greatest incidence of GI side effects was observed 90 min after ingestion of 0.3 g/kg NaHCO₃ solution. The changes in pH and [HCO₃-] for the 8 NaHCO₃-ingestion protocols were similar, so an optimal protocol cannot be recommended. However, the results suggest that NaHCO₃ coingested with a high-carbohydrate meal should be taken 120-150 min before exercise to induce substantial blood alkalosis and reduce GI symptoms.

Alterations of proteins in MDCK cells during acute potassium deficiency.

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Peerapen, Paleerath; Ausakunpipat, Nardtaya; Chanchaem, Prangwalai; Thongboonkerd, Visith

2016-06-01

Chronic K(+) deficiency can cause hypokalemic nephropathy associated with metabolic alkalosis, polyuria, tubular dilatation, and tubulointerstitial injury. However, effects of acute K(+) deficiency on the kidney remained unclear. This study aimed to explore such effects by evaluating changes in levels of proteins in renal tubular cells during acute K(+) deficiency. MDCK cells were cultivated in normal K(+) (NK) (K(+)=5.3 mM), low K(+) (LK) (K(+)=2.5 mM), or K(+) depleted (KD) (K(+)=0 mM) medium for 24 h and then harvested. Cellular proteins were resolved by two-dimensional gel electrophoresis (2-DE) and visualized by SYPRO Ruby staining (5 gels per group). Spot matching and quantitative intensity analysis revealed a total 48 protein spots that had significantly differential levels among the three groups. Among these, 46 and 30 protein spots had differential levels in KD group compared to NK and LK groups, respectively. Comparison between LK and NK groups revealed only 10 protein spots that were differentially expressed. All of these differentially expressed proteins were successfully identified by Q-TOF MS and/or MS/MS analyses. The altered levels of heat shock protein 90 (HSP90), ezrin, lamin A/C, tubulin, chaperonin-containing TCP1 (CCT1), and calpain 1 were confirmed by Western blot analysis. Global protein network analysis showed three main functional networks, including 1) cell growth and proliferation, 2) cell morphology, cellular assembly and organization, and 3) protein folding in which the altered proteins were involved. Further investigations on these networks may lead to better understanding of pathogenic mechanisms of low K(+)-induced renal injury. Copyright © 2016 Elsevier B.V. All rights reserved.

Acid-base and ionic fluxes in rainbow trout (Oncorhynchus mykiss) during exposure to chloramine-T

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Powell, M.D.; Perry, S.F. [Department of Biology, University of Ottawa, 30 Marie Curie Ottawa, Ontario, K1N 6N5 (Canada)

1998-09-01

The effects of chloramine-T and its degradation products, sodium hypochlorite (NaOCl) and para-toluenesulphonamide (pTSA), on whole body acid-base and branchial and renal ion (Na{sup +}and Cl{sup -}) fluxes were examined in rainbow trout (Oncorhynchus mykiss). Exposure to chloramine-T (3.5 h, 18 mg l{sup -1}) resulted in increases in plasma total CO{sub 2} but no coincident rise in P{sub a}CO{sub 2} or reduction in blood pH. Exposure of fish to 2, 9 or 18 mg l{sup -1} chloramine-T (3.5 h duration) resulted in a reduction in net acid uptake suggesting the development of a metabolic alkalosis. Exposure to the chloramine-T breakdown product pTSA (dissolved in DMSO) resulted in increased net acid uptake (decreased acid excretion) suggesting a metabolic acidosis. Whole body ion fluxes demonstrated increases in the losses of both Na{sup +}and Cl{sup -} with chloramine-T, NaOCl and pTSA. However, the effect of DMSO alone could not be isolated. Confirmatory studies using fish in which the urinary bladder (to allow collection of urine) and dorsal aorta (to allow injection of [{sup 14}C]polyethylene glycol 4000 ([{sup 14}C]PEG), an extracellular fluid marker) were catheterised, revealed that changes in whole body ion fluxes during chloramine-T exposure could not be explained by increased renal efflux through urine flow, glomerular filtration or renal clearance. Branchial effluxes of [{sup 14}C]PEG were not significantly affected by chloramine-T exposure suggesting that the changes in whole body ionic fluxes were caused by transcellular rather than paracellular processes. (Copyright (c) 1998 Elsevier Science B.V., Amsterdam. All rights reserved.)

Acid-base and ionic fluxes in rainbow trout (Oncorhynchus mykiss) during exposure to chloramine-T

International Nuclear Information System (INIS)

Powell, M.D.; Perry, S.F.

1998-01-01

The effects of chloramine-T and its degradation products, sodium hypochlorite (NaOCl) and para-toluenesulphonamide (pTSA), on whole body acid-base and branchial and renal ion (Na + and Cl - ) fluxes were examined in rainbow trout (Oncorhynchus mykiss). Exposure to chloramine-T (3.5 h, 18 mg l -1 ) resulted in increases in plasma total CO 2 but no coincident rise in P a CO 2 or reduction in blood pH. Exposure of fish to 2, 9 or 18 mg l -1 chloramine-T (3.5 h duration) resulted in a reduction in net acid uptake suggesting the development of a metabolic alkalosis. Exposure to the chloramine-T breakdown product pTSA (dissolved in DMSO) resulted in increased net acid uptake (decreased acid excretion) suggesting a metabolic acidosis. Whole body ion fluxes demonstrated increases in the losses of both Na + and Cl - with chloramine-T, NaOCl and pTSA. However, the effect of DMSO alone could not be isolated. Confirmatory studies using fish in which the urinary bladder (to allow collection of urine) and dorsal aorta (to allow injection of [ 14 C]polyethylene glycol 4000 ([ 14 C]PEG), an extracellular fluid marker) were catheterised, revealed that changes in whole body ion fluxes during chloramine-T exposure could not be explained by increased renal efflux through urine flow, glomerular filtration or renal clearance. Branchial effluxes of [ 14 C]PEG were not significantly affected by chloramine-T exposure suggesting that the changes in whole body ionic fluxes were caused by transcellular rather than paracellular processes. (Copyright (c) 1998 Elsevier Science B.V., Amsterdam. All rights reserved.)

Molecular detection and immunological localization of gill Na+/H+ exchanger in the dogfish (Squalus acanthias).

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Claiborne, James B; Choe, Keith P; Morrison-Shetlar, Alison I; Weakley, Jill C; Havird, Justin; Freiji, Abe; Evans, David H; Edwards, Susan L

2008-03-01

The dogfish (Squalus acanthias) can make rapid adjustments to gill acid-base transfers to compensate for internal acidosis/alkalosis. Branchial Na+/H+ exchange (NHE) has been postulated as one mechanism driving the excretion of H+ following acidosis. We have cloned gill cDNA that includes an open reading frame coding for a 770-residue protein most homologous (approximately 71%) to mammalian NHE2. RT-PCR revealed NHE2 transcripts predominantly in gill, stomach, rectal gland, intestine, and kidney. In situ hybridization with an antisense probe against NHE2 in gill sections revealed a strong mRNA signal from a subset of interlamellar and lamellae cells. We developed dogfish-specific polyclonal antibodies against NHE2 that detected a approximately 70-kDa protein in Western blots and immunologically recognized branchial cells having two patterns of protein expression. Cytoplasmic and apical NHE2 immunoreactivity were observed in cells coexpressing basolateral Na+-K+-ATPase. Other large ovoid cells more generally staining for NHE2 also were strongly positive for basolateral H+-ATPase. Gill mRNA levels for NHE2 and H+-ATPase did not change following systemic acidosis (as measured by quantitative PCR 2 h after a 1- or 2-meq/kg acid infusion). These data indicate that posttranslational adjustments of NHE2 and other transport systems (e.g., NHE3) following acidosis may be of importance in the short-term pH adjustment and net branchial H+ efflux observed in vivo. NHE2 may play multiple roles in the gills, involved with H+ efflux from acid-secreting cells, basolateral H+ reabsorption for pHi regulation, and in parallel with H+-ATPase for the generation of HCO3(-) in base-secreting cells.

NEUMOCISTOSIS EN EL SERVICIO DE MEDICINA INTERNA, COMPLEJO HOSPITALARIO UNIVERSITARIO “DR. LUIS RAZETTI”, BARCELONA, VENEZUELA, 2011-2012 I PNEUMOCYSTOSIS IN THE INTERNAL MEDICINE SERVICE, UNIVERSITY HOSPITAL COMPLEX “DR. LUIS RAZETTI”, BARCELONA, VENEZUELA, 2011-2012

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Fadi Wahab-El-Fatairi

2015-07-01

Full Text Available In Venezuela and in the state Anzoátegui, the pneumocystosis, is little studied. To weigh that it is an infection opportunist caused by Pneumocystis jirovecii, it causes pneumonia of high morbility and mortality. The inmunocompromised patient is those that present bigger risks of acquiring this infection. The objectives of this investigation were to determine the infection frequency for P. jirovecii in patient with breathing symptoms and immunocompromised hospitalized in the Service of Internal Medicine of the Complex Hospital University “Dr. Luis Razetti", and to describe the clinical parameters, of laboratory, radiological and epidemic. To increase the sensibility of the diagnosis etiologic of the pneumocystosis you employment the combination of microscopic methods (Giemsa and direct immunofluorescence technique. 52 samples of spontaneous sputum were studied, which were processed by fluidification -concentration. Results: 8 patients (15.38% they were positive. The most frequent clinical manifestations among the patients with pneumocystosis were the dyspnea (75%, cough (62% and bullous (50% they were the most common signs among those infected, the one infiltrated alveolar (62.5% and the spill pleural (37.5% they prevailed as radiological signs. Was the LDH presented in values 300 UI/L in 5 of the positive patients. Other common discoveries were: moderate anemia and breathing alkalosis. The evaluated epidemic aspects were the gender, occupation, smoking, accumulation and comorbidities, in this last aspect, the diabetes, hypertension and infection for the VIH was opposing comorbidities among these patients. The confirmation of the infection in the state Anzoátegui, demonstrates that in this hospital the agent exists and probably you this underdiagnosticated the pneumocystosis.

Capsiate supplementation reduces oxidative cost of contraction in exercising mouse skeletal muscle in vivo.

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Yashiro, Kazuya; Tonson, Anne; Pecchi, Émilie; Vilmen, Christophe; Le Fur, Yann; Bernard, Monique; Bendahan, David; Giannesini, Benoît

2015-01-01

Chronic administration of capsiate is known to accelerate whole-body basal energy metabolism, but the consequences in exercising skeletal muscle remain very poorly documented. In order to clarify this issue, the effect of 2-week daily administration of either vehicle (control) or purified capsiate (at 10- or 100-mg/kg body weight) on skeletal muscle function and energetics were investigated throughout a multidisciplinary approach combining in vivo and in vitro measurements in mice. Mechanical performance and energy metabolism were assessed strictly non-invasively in contracting gastrocnemius muscle using magnetic resonance (MR) imaging and 31-phosphorus MR spectroscopy (31P-MRS). Regardless of the dose, capsiate treatments markedly disturbed basal bioenergetics in vivo including intracellular pH alkalosis and decreased phosphocreatine content. Besides, capsiate administration did affect neither mitochondrial uncoupling protein-3 gene expression nor both basal and maximal oxygen consumption in isolated saponin-permeabilized fibers, but decreased by about twofold the Km of mitochondrial respiration for ADP. During a standardized in vivo fatiguing protocol (6-min of repeated maximal isometric contractions electrically induced at a frequency of 1.7 Hz), both capsiate treatments reduced oxidative cost of contraction by 30-40%, whereas force-generating capacity and fatigability were not changed. Moreover, the rate of phosphocreatine resynthesis during the post-electrostimulation recovery period remained unaffected by capsiate. Both capsiate treatments further promoted muscle mass gain, and the higher dose also reduced body weight gain and abdominal fat content. These findings demonstrate that, in addition to its anti-obesity effect, capsiate supplementation improves oxidative metabolism in exercising muscle, which strengthen this compound as a natural compound for improving health.

Hyponatremic hypochloremic dehydration in children with cystic fibrosis in Slovenia; the incidence and recommendations for prevention and treatment

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Marina Praprotnik

2015-05-01

Full Text Available Background: Young children and rarely adolescents with cystic fibrosis can develop hyponatremic hypochloremic dehydration with metabolic alkalosis. The purpose of this article was to review the incidence of this metabolic disorder in our CF patients.Methods: We investigated the medical records of all children diagnosed with cystic fibrosis who are under follow-up in the CF center at the University Childrenʹs Hospital Ljubljana, and were hospitalised or treated on an outpatient basis due to hyponatremic, hypochloremic dehydration in the period from 2007–2012. Data analysis included clinical and laboratory findings.Results: A total of 4 children (7.2 % from Ljubljana CF center (55 patients under the age of 19 years were enrolled in the study. We observed 5 episodes of hyponatremic hypochloremic dehydration in 4 patients (one boy had two episodes. All were homozigous for ΔF 508 mutation. Two had episodes in summer and two in autumn, so that no season prevalence of its occurence was found. Median age at admission to the hospital due to hyponatremic hypochloremic dehydration was 7 months (range 4–34. One boy had a hypovolemic shock at the time of admission to the hospital.Conclusions: The results of our study show that dehydration with hypoelectrolytaemia is a rare complication in children with CF in Slovenia, but due to the severity of clinical signs it is an important disorder. Vomiting and fatigue are the warning signs that should alert parents and physicians to consider the possibility of this complication which can be prevented by proper hydration and salt replacement. If left untreated, it can cause seizures, arrhythmias and even death.

Effects of xylazine on acid-base balance and arterial blood-gas tensions in goats under different environmental temperature and humidity conditions

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E.G.M. Mogoa

2000-07-01

Full Text Available The effects of acute exposure to 3 different temperature and humidity conditions on arterial blood-gas and acid-base balance in goats were investigated after intravenous bolus administration of xylazine at a dose of 0.1 mg/kg. Significant (P < 0.05 changes in the variables occurred under all 3 environmental conditions. Decreases in pH, partial pressure of oxygen and oxyhaemoglobin saturation were observed, and the minimum values for oxygen tension and oxyhaemoglobin saturation were observed within 5 min of xylazine administration. The pH decreased to its minimum values between 5 and 15 min. Thereafter, the variables started to return towards baseline, but did not reach baseline values at the end of the 60 min observation period. Increases in the partial pressure of carbon dioxide, total carbon dioxide content, bicarbonate ion concentration, and the actual base excess were observed. The maximum increase in the carbon dioxide tension occurred within 5 min of xylazine administration. The increase in the actual base excess only became significant after 30 min in all 3 environments, and maximal increases were observed at 60 min. There were no significant differences between the variables in the 3 different environments. It was concluded that intravenous xylazine administration in goats resulted in significant changes in arterial blood-gas and acid-base balance that were associated with hypoxaemia and respiratory acidosis, followed by metabolic alkalosis that continued for the duration of the observation period. Acute exposure to different environmental temperature and humidity conditions after xylazine administration did not influence the changes in arterial blood-gas and acid-base balance.

Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer

International Nuclear Information System (INIS)

Robey, Ian F; Martin, Natasha K

2011-01-01

The glycolytic nature of malignant tumors contributes to high levels of extracellular acidity in the tumor microenvironment. Tumor acidity is a driving force in invasion and metastases. Recently, it has been shown that buffering of extracellular acidity through systemic administration of oral bicarbonate can inhibit the spread of metastases in a mouse model for metastatic breast cancer. While these findings are compelling, recent assessments into the use of oral bicarbonate as a cancer intervention reveal limitations. We posited that safety and efficacy of bicarbonate could be enhanced by dichloroacetate (DCA), a drug that selectively targets tumor cells and reduces extracellular acidity through inhibition of glycolysis. Using our mouse model for metastatic breast cancer (MDA-MB-231), we designed an interventional survival study where tumor bearing mice received bicarbonate, DCA, or DCA-bicarbonate (DB) therapies chronically. Dichloroacetate alone or in combination with bicarbonate did not increase systemic alkalosis in mice. Survival was longest in mice administered bicarbonate-based therapies. Primary tumor re-occurrence after surgeries is associated with survival rates. Although DB therapy did not significantly enhance oral bicarbonate, we did observe reduced pulmonary lesion diameters in this cohort. The DCA monotherapy was not effective in reducing tumor size or metastases or improving survival time. We provide in vitro evidence to suggest this outcome may be a function of hypoxia in the tumor microenvironment. DB combination therapy did not appear to enhance the effect of chronic oral bicarbonate. The anti-tumor effect of DCA may be dependent on the cancer model. Our studies suggest DCA efficacy is unpredictable as a cancer therapy and further studies are necessary to determine the role of this agent in the tumor microenvironment

Pseudo-Bartter syndrome in an infant with congenital chloride diarrhoea.

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Igrutinović, Zoran; Peco-Antić, Amira; Radlović, Nedeljko; Vuletić, Biljana; Marković, Slavica; Vujić, Ana; Rasković, Zorica

2011-01-01

Pseudo-Bartter syndrome encompasses a heterogenous group of disorders similar to Bartter syndrome. We are presenting an infant with pseudo-Bartter syndrome caused by congenital chloride diarrhoea. A male newborn born in the 37th gestational week (GW) to young healthy and non-consanguineous parents. In the 35th GW a polyhydramnios with bowel dilatation was verified by ultrasonography. After birth he manifested several episodes of hyponatremic dehydration with hypochloraemia, hypokalaemia and metabolic alkalosis, so as Bartter syndrome was suspected treatment with indomethacin, spironolactone and additional intake of NaCl was initiated. However, this therapy gave no results, so that at age six months he was rehospitalized under the features of persistent watery diarrhoea, vomiting, dehydration and acute renal failure (serum creatinine 123 micromol/L). The laboratory results showed hyponatraemia (123 mmol/L), hypokalaemia (3.1 mmol/L), severe hypochloraemia (43 mmol/L), alcalosis (blood pH 7.64, bicarbonate 50.6 mmol/L), high plasma renin (20.6 ng/ml) and aldosterone (232.9 ng/ml), but a low urinary chloride concentration (2.1 mmol/L). Based on these findings, as well as the stool chloride concentration of 110 mmol/L, the patient was diagnosed congenital chloride diarrhoea. In further course, the patient was treated by intensive fluid, sodium and potassium supplementation which resulted in the normalization of serum electrolytes, renal function, as well as his mental and physical development during 10 months of follow-up. Persistent watery diarrhoea with a high concentration of chloride in stool is the key finding in the differentiation of congenital chloride diarrhoea from Bartter syndrome. The treatment of congenital chloride diarrhoea consists primarily of adequate water and electrolytes replacement.

Voluntary activation of the sympathetic nervous system and attenuation of the innate immune response in humans.

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Kox, Matthijs; van Eijk, Lucas T; Zwaag, Jelle; van den Wildenberg, Joanne; Sweep, Fred C G J; van der Hoeven, Johannes G; Pickkers, Peter

2014-05-20

Excessive or persistent proinflammatory cytokine production plays a central role in autoimmune diseases. Acute activation of the sympathetic nervous system attenuates the innate immune response. However, both the autonomic nervous system and innate immune system are regarded as systems that cannot be voluntarily influenced. Herein, we evaluated the effects of a training program on the autonomic nervous system and innate immune response. Healthy volunteers were randomized to either the intervention (n = 12) or control group (n = 12). Subjects in the intervention group were trained for 10 d in meditation (third eye meditation), breathing techniques (i.a., cyclic hyperventilation followed by breath retention), and exposure to cold (i.a., immersions in ice cold water). The control group was not trained. Subsequently, all subjects underwent experimental endotoxemia (i.v. administration of 2 ng/kg Escherichia coli endotoxin). In the intervention group, practicing the learned techniques resulted in intermittent respiratory alkalosis and hypoxia resulting in profoundly increased plasma epinephrine levels. In the intervention group, plasma levels of the anti-inflammatory cytokine IL-10 increased more rapidly after endotoxin administration, correlated strongly with preceding epinephrine levels, and were higher. Levels of proinflammatory mediators TNF-α, IL-6, and IL-8 were lower in the intervention group and correlated negatively with IL-10 levels. Finally, flu-like symptoms were lower in the intervention group. In conclusion, we demonstrate that voluntary activation of the sympathetic nervous system results in epinephrine release and subsequent suppression of the innate immune response in humans in vivo. These results could have important implications for the treatment of conditions associated with excessive or persistent inflammation, such as autoimmune diseases.

Clinical and diagnostic methods for evaluation of sharp foreign body syndrome in buffaloes

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Nasr-Eldin M. Aref

2013-06-01

Full Text Available Aim: The present study was designed to evaluate clinically and under laboratory condition the sharp foreign body syndrome (SFBS in buffaloes with special emphasis on the diagnostic value of radiography, ultrasonography and blood gases and acidbase balance. Materials and Methods: 196 buffaloes with a history of anorexia, reduction of milk production and no response to previous medical treatment were included in the present study. These animals were subjected to clinical and radiographical examinations. Positive cases for SFBS were further evaluated by sonography, hemato-biochemical and blood gas and acid base balance analysis.Results: Out of 196 admitted cases, 49 (25% cases were confirmed as SFBS by clinical and radiographical examination. Positive cases were subsequently divided into two main categories (complicated and non complicated according to radiographical and sonographical findings. SFBS with no complication was diagnosed in 16 cases while 33 cases showed various degrees of complication including reticular adhesion (abdominal and diaphragmatic, n= 23, diaphragmatic hernia (n = 6 and traumatic pericarditis (n = 4. Leukocytosis, hyperprotenemia and increased activity of AST and ALT were of additional values in the diagnosis of SFBS. A consistent finding of primary metabolic alkalosis was recorded in all cases except one with advanced traumatic pericarditis that showed metabolic acidosis. Conclusion: While there is no substitution for clinical examination, using of ultrasonography and radiography simultaneously are essential for proper evaluation and differentiation between various sequelae of SFBS in buffaloes. Radiography is an efficient tool for visualization of metallic foreign body while ultrasonography is an excellent device in assessing fibrinous deposits. Hemato-biochemical and blood gases and acid base balance are of additional values in discriminating between various outcomes of SFBS.

Acid-Base and Plasma Biochemical Changes Using Crystalloid Fluids in Stranded Juvenile Loggerhead Sea Turtles (Caretta caretta).

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Camacho, María; Quintana, María Del Pino; Calabuig, Pascual; Luzardo, Octavio P; Boada, Luis D; Zumbado, Manuel; Orós, Jorge

2015-01-01

The aim of this study was to compare the efficacy and effects on acid-base and electrolyte status of several crystalloid fluids in 57 stranded juvenile loggerhead turtles. Within a rehabilitation program four different crystalloid fluids were administered (0.9% Na Cl solution; 5% dextrose + 0.9% Na Cl solutions 1:1; 0.9% Na Cl + lactated Ringer's solutions 1:1; lactated Ringer's solution). Crystalloid fluids were intracoelomically administered during three days (20 ml/kg/day). Animals were sampled at three different moments: Upon admission for evaluating the type of acid-base or biochemical disorder, post-fluid therapy treatment for controlling the evolution of the disorder, and post-recovery period for obtaining the baseline values for rehabilitated loggerhead turtles. Each sample was analyzed with a portable electronic blood analyzer for pH, pO2, pCO2, lactate, sodium, potassium, chloride, glucose, and BUN concentration. Admission and post-fluid therapy treatment values were compared with those obtained for each turtle immediately before release. The highest percentage of acid-base recovery and electrolyte balance was observed in turtles treated with mixed saline-lactated Ringer's solution (63.6%), followed by turtles treated with physiological saline solution (55%), lactated Ringer's solution (33.3%), and dextrose-saline solutions (10%). Most turtles treated with lactated Ringer's solution had lower lactate concentrations compared with their initial values; however, 66.6% of turtles treated with lactated Ringer's solution had metabolic alkalosis after therapy. Significant higher concentrations of glucose were detected after saline-dextrose administration compared with all the remaining fluids. This is the first study evaluating the effects of several crystalloid fluids on the acid-base status and plasma biochemical values in stranded loggerhead sea turtles. Reference convalescent venous blood gas, acid-base, and plasma biochemical values, useful for veterinary

Theorethical principles of fluid managment according to physicochemical Stewart approach.

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Smuszkiewicz, Piotr; Szrama, Jakub

2013-01-01

Interpreting acid base disturbances according to the physicochemical Stewart approach allows the cause of such abnormalities to be discovered. This method is based on three independent variables: SID (strong ion difference), mainly sodium and chloride; weak acids concentration - Atot, mainly albumins and phosphate; and carbon dioxide tension - pCO₂. These three independent variables are responsible for the change of water dissociation and for the change in H+ concentration and, consequently, the change in serum pH value. The SID value of the fluids administered to a patient is responsible for the change of serum SID value and therefore causes a change in the patient's acid base status. During the infusion of a given fluid, the SID value of the serum becomes closer to the SID value of that fluid; on the other hand, the infusion causes a decrease in Atot concentration. In order to avoid acid base disturbances connected with fluid administration, the SID value of fluids being administered should be greater than 0 and lower then the serum SID. It has been suggested that fluids should be given of which the SID value is as close as possible to the actual serum HCO₃ concentration. Knowing the SID value of the fluid administered, and the serum HCO₃ concentration, one can expect a change of serum pH after a fluid infusion. Administering a fluid with a SID greater than the HCO₃ concentration causes a pH increase towards alkalosis. Likewise, administering a a fluid with a SID lower than the HCO₃ concentration causes a pH decrease towards acidosis. It seems that knowledge of the electrolyte concentration and the SID value of an administered fluid is an important factor regarding acid base disturbances.

High Antifouling Property of Ion-Selective Membrane: toward In Vivo Monitoring of pH Change in Live Brain of Rats with Membrane-Coated Carbon Fiber Electrodes.

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Hao, Jie; Xiao, Tongfang; Wu, Fei; Yu, Ping; Mao, Lanqun

2016-11-15

In vivo monitoring of pH in live brain remains very essential to understanding acid-base chemistry in various physiological processes. This study demonstrates a potentiometric method for in vivo monitoring of pH in the central nervous system with carbon fiber-based proton-selective electrodes (CF-H + ISEs) with high antifouling property. The CF-H + ISEs are prepared by formation of a H + -selective membrane (H + ISM) with polyvinyl chloride polymeric matrixes containing plasticizer bis(2-ethylhexyl)sebacate, H + ionophore tridodecylamine, and ion exchanger potassium tetrakis(4-chlorophenyl)borate onto carbon fiber electrodes (CFEs). Both in vitro and in vivo studies demonstrate that the H + ISM exhibits strong antifouling property against proteins, which enables the CF-H + ISEs to well maintain the sensitivity and reversibility for pH sensing after in vivo measurements. Moreover, the CF-H + ISEs exhibit a good response to pH changes within a narrow physiological pH range from 6.0 to 8.0 in quick response time with high reversibility and selectivity against species endogenously existing in the central nervous system. The applicability of the CF-H + ISEs is illustrated by real-time monitoring of pH changes during acid-base disturbances, in which the brain acidosis is induced by CO 2 inhalation and brain alkalosis is induced by bicarbonate injections. The results demonstrate that brain pH value rapidly decreases in the amygdaloid nucleus by ca. 0.14 ± 0.01 (n = 5) when the rats breath in pure CO 2 gas, while increases in the cortex by about 0.77 ± 0.12 (n = 3) following intraperitoneal injection of 5 mmol/kg NaHCO 3 . This study demonstrates a new potentiometric method for in vivo measurement of pH change in the live brain of rats with high reliability.

Sensitivity of the spiny dogfish (Squalus acanthias) to waterborne silver exposure.

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De Boeck, G; Grosell, M; Wood, C

2001-10-01

The physiological effects of waterborne silver exposure (added as AgNO(3)) on spiny dogfish, Squalus acanthias, were evaluated at 30, 200 and 685 microg silver per l in 30 per thousand seawater. These concentrations cover the toxic range observed for freshwater teleosts, where silver is extremely toxic, to seawater teleosts which tolerate higher silver concentrations. However, these levels are considerably higher than those that occur in the normal environment. At 685 microg l(-1), dogfish died within 24 h. Causes of death were respiratory as well as osmoregulatory failure. Arterial P(a)O(2) rapidly declined below 20 Torr, and blood acidosis (both respiratory and metabolic) occurred. Urea excretion increased dramatically and plasma urea dropped from 340 to 225 mM. There were pronounced increases in plasma Na(+), Cl(-), and Mg(2+), indicative of ionoregulatory failure due to increased diffusive permeability as well as inhibited NaCl excretion. At 200 microg l(-1), fish died between 24 and 72 h of silver exposure. The same physiological events occurred with a small time delay. At 30 microg l(-1), effects were much less severe, although slight mortality (12.5%) still occurred. Respiratory alkalosis occurred, together with moderate elevations in plasma Na(+) and Cl(-) levels. Silver accumulated to the highest concentrations on gills, with only low levels in the intestine, in accord with the virtual absence of drinking. Na(+)/K(+)-ATP-ase activities of gill and rectal gland tissue were impaired at the highest silver concentration. Normal gill function was impaired due to swelling and fusion of lamellae, lamellar aneurism and lifting of the lamellar epithelium. Our results clearly indicate that this elasmobranch is much more sensitive (about 10-fold) to silver than marine teleosts, with silver's toxic action exerted on the gill rather than on the intestine, in contrast to the latter.

Nitrogen metabolism, acid-base regulation, and molecular responses to ammonia and acid infusions in the spiny dogfish shark (Squalus acanthias).

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Nawata, C Michele; Walsh, Patrick J; Wood, Chris M

2015-07-01

Although they are ureotelic, marine elasmobranchs express Rh glycoproteins, putative ammonia channels. To address questions raised by a recent study on high environmental ammonia (HEA) exposure, dogfish were intravascularly infused for 24 h at 3 ml kg(-1) h(-1) with isosmotic NaCl (500 mmol l(-1), control), NH4HCO3 (500 mmol l(-1)), NH4Cl (500 mmol l(-1)), or HCl (as 125 mmol l(-1) HCl + 375 mmol l(-1) NaCl). While NaCl had no effect on arterial acid-base status, NH4HCO3 caused mild alkalosis, NH4Cl caused strong acidosis, and HCl caused lesser acidosis, all predominantly metabolic in nature. Total plasma ammonia (T(Amm)) and excretion rates of ammonia (J(Amm)) and urea-N (J(Urea-N)) were unaffected by NaCl or HCl. However, despite equal loading rates, plasma T(Amm) increased to a greater extent with NH4Cl, while J(Amm) increased to a greater extent with NH4HCO3 due to much greater increases in blood-to-water PNH3 gradients. As with HEA, both treatments caused large (90%) elevations of J(Urea-N), indicating that urea-N synthesis by the ornithine-urea cycle (OUC) is driven primarily by ammonia rather than HCO3(-). Branchial mRNA expressions of Rhbg and Rhp2 were unaffected by NH4HCO3 or NH4Cl, but v-type H(+)-ATPase was down-regulated by both treatments, and Rhbg and Na(+)/H(+) exchanger NHE2 were up-regulated by HCl. In the kidney, Rhbg was unresponsive to all treatments, but Rhp2 was up-regulated by HCl, and the urea transporter UT was up-regulated by HCl and NH4Cl. These responses are discussed in the context of current ideas about branchial, renal, and OUC function in this nitrogen-limited predator.

Predicting the safety and efficacy of buffer therapy to raise tumour pHe: an integrative modelling study

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Martin, N K; Robey, I F; Gaffney, E A; Gillies, R J; Gatenby, R A; Maini, P K

2012-01-01

Background: Clinical positron emission tomography imaging has demonstrated the vast majority of human cancers exhibit significantly increased glucose metabolism when compared with adjacent normal tissue, resulting in an acidic tumour microenvironment. Recent studies demonstrated reducing this acidity through systemic buffers significantly inhibits development and growth of metastases in mouse xenografts. Methods: We apply and extend a previously developed mathematical model of blood and tumour buffering to examine the impact of oral administration of bicarbonate buffer in mice, and the potential impact in humans. We recapitulate the experimentally observed tumour pHe effect of buffer therapy, testing a model prediction in vivo in mice. We parameterise the model to humans to determine the translational safety and efficacy, and predict patient subgroups who could have enhanced treatment response, and the most promising combination or alternative buffer therapies. Results: The model predicts a previously unseen potentially dangerous elevation in blood pHe resulting from bicarbonate therapy in mice, which is confirmed by our in vivo experiments. Simulations predict limited efficacy of bicarbonate, especially in humans with more aggressive cancers. We predict buffer therapy would be most effectual: in elderly patients or individuals with renal impairments; in combination with proton production inhibitors (such as dichloroacetate), renal glomular filtration rate inhibitors (such as non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors), or with an alternative buffer reagent possessing an optimal pK of 7.1–7.2. Conclusion: Our mathematical model confirms bicarbonate acts as an effective agent to raise tumour pHe, but potentially induces metabolic alkalosis at the high doses necessary for tumour pHe normalisation. We predict use in elderly patients or in combination with proton production inhibitors or buffers with a pK of 7.1–7.2 is most

Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer

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Martin Natasha K

2011-06-01

Full Text Available Abstract Background The glycolytic nature of malignant tumors contributes to high levels of extracellular acidity in the tumor microenvironment. Tumor acidity is a driving force in invasion and metastases. Recently, it has been shown that buffering of extracellular acidity through systemic administration of oral bicarbonate can inhibit the spread of metastases in a mouse model for metastatic breast cancer. While these findings are compelling, recent assessments into the use of oral bicarbonate as a cancer intervention reveal limitations. Methods We posited that safety and efficacy of bicarbonate could be enhanced by dichloroacetate (DCA, a drug that selectively targets tumor cells and reduces extracellular acidity through inhibition of glycolysis. Using our mouse model for metastatic breast cancer (MDA-MB-231, we designed an interventional survival study where tumor bearing mice received bicarbonate, DCA, or DCA-bicarbonate (DB therapies chronically. Results Dichloroacetate alone or in combination with bicarbonate did not increase systemic alkalosis in mice. Survival was longest in mice administered bicarbonate-based therapies. Primary tumor re-occurrence after surgeries is associated with survival rates. Although DB therapy did not significantly enhance oral bicarbonate, we did observe reduced pulmonary lesion diameters in this cohort. The DCA monotherapy was not effective in reducing tumor size or metastases or improving survival time. We provide in vitro evidence to suggest this outcome may be a function of hypoxia in the tumor microenvironment. Conclusions DB combination therapy did not appear to enhance the effect of chronic oral bicarbonate. The anti-tumor effect of DCA may be dependent on the cancer model. Our studies suggest DCA efficacy is unpredictable as a cancer therapy and further studies are necessary to determine the role of this agent in the tumor microenvironment.

Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer

Science.gov (United States)

2011-01-01

Background The glycolytic nature of malignant tumors contributes to high levels of extracellular acidity in the tumor microenvironment. Tumor acidity is a driving force in invasion and metastases. Recently, it has been shown that buffering of extracellular acidity through systemic administration of oral bicarbonate can inhibit the spread of metastases in a mouse model for metastatic breast cancer. While these findings are compelling, recent assessments into the use of oral bicarbonate as a cancer intervention reveal limitations. Methods We posited that safety and efficacy of bicarbonate could be enhanced by dichloroacetate (DCA), a drug that selectively targets tumor cells and reduces extracellular acidity through inhibition of glycolysis. Using our mouse model for metastatic breast cancer (MDA-MB-231), we designed an interventional survival study where tumor bearing mice received bicarbonate, DCA, or DCA-bicarbonate (DB) therapies chronically. Results Dichloroacetate alone or in combination with bicarbonate did not increase systemic alkalosis in mice. Survival was longest in mice administered bicarbonate-based therapies. Primary tumor re-occurrence after surgeries is associated with survival rates. Although DB therapy did not significantly enhance oral bicarbonate, we did observe reduced pulmonary lesion diameters in this cohort. The DCA monotherapy was not effective in reducing tumor size or metastases or improving survival time. We provide in vitro evidence to suggest this outcome may be a function of hypoxia in the tumor microenvironment. Conclusions DB combination therapy did not appear to enhance the effect of chronic oral bicarbonate. The anti-tumor effect of DCA may be dependent on the cancer model. Our studies suggest DCA efficacy is unpredictable as a cancer therapy and further studies are necessary to determine the role of this agent in the tumor microenvironment. PMID:21663677

Pseudo-bartter syndrome, pattern and correlation with other cystic fibrosis features

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Muna M Dahabreh

2013-01-01

Full Text Available Pseudo-Bartter Syndrome (PBS, although quite common in patients with cystic fibrosis (CF, is often missed as simple dehydration or Bartter syndrome. This study was performed in patients with PBS to compare the pattern and course of the disease with those with CF not manifesting with this syndrome. All patients with CF who attended the respiratory clinic at Queen Rania Al-Abdallah Hospital from January 2000 to April 2010 were included in this retrospective case-control study. A specially formulated data sheet was used and those with PBS and those not having the syndrome were identified. A total of 110 patients (51% female with CF with a median age of seven years were followed-up. Eighteen (16.3% of them had one or more episodes of PBS. The median follow-up period was 6.2 years. All the episodes occurred during summer and in infancy. Median age of the initial episode of PBS was three months. One-third of them were initially followed at the nephrology clinic. Three patterns of PBS were identified: single episode in three (16.6% patients, recurrent in 12 (66.6% patients and chronic in three (16.6% patients. Early colonization of Pseudomonas spp before 1 st birthday was seen in 44% patients with PBS compared with 12% in other CF patients (P-value = 0.0075. The total number of colonized patients and other CF features at the time of the study did not differ significantly among patients, although the mean Shwachman-Kulczycki score is significantly lower in those with recurrent PBS (69 compared with 85 in other CF patients. Gene mutation was identified in only 30% of the entire cohort. PBS is common in patients with CF, and it should be kept in mind in any patient with hypotonic dehydration and metabolic alkalosis. Recurrent pattern is associated with earlier Pseudomonas colonization.

Pseudo-Bartter syndrome in an infant with congenital chloride diarrhoea

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Igrutinović Zoran

2011-01-01

Full Text Available Introduction. Pseudo-Bartter syndrome encompasses a heterogenous group of disorders similar to Bartter syndrome. We are presenting an infant with pseudo-Bartter syndrome caused by congenital chloride diarrhoea. Case Outline. A male newborn born in the 37th gestational week (GW to young healthy and non-consanguineous parents. In the 35th GW a polyhydramnios with bowel dilatation was verified by ultrasonography. After birth he manifested several episodes of hyponatremic dehydration with hypochloraemia, hypokalaemia and metabolic alkalosis, so as Bartter syndrome was suspected treatment with indomethacin, spironolactone and additional intake of NaCl was initiated. However, this therapy gave no results, so that at age six months he was rehospitalized under the features of persistent watery diarrhoea, vomiting, dehydration and acute renal failure (serum creatinine 123 μmol/L. The laboratory results showed hyponatraemia (123 mmol/L, hypokalaemia (3.1 mmol/L, severe hypochloraemia (43 mmol/L, alcalosis (blood pH 7.64, bicarbonate 50.6 mmol/L, high plasma renin (20.6 ng/ml and aldosterone (232.9 ng/ml, but a low urinary chloride concentration (2.1 mmol/L. Based on these findings, as well as the stool chloride concentration of 110 mmol/L, the patient was diagnosed congenital chloride diarrhoea. In further course, the patient was treated by intensive fluid, sodium and potassium supplementation which resulted in the normalization of serum electrolytes, renal function, as well as his mental and physical development during 10 months of follow-up. Conclusion. Persistent watery diarrhoea with a high concentration of chloride in stool is the key finding in the differentiation of congenital chloride diarrhoea from Bartter syndrome. The treatment of congenital chloride diarrhoea consists primarily of adequate water and electrolytes replacement.

Laxative-induced rhabdomyolysis

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Alfonso Merante

2010-03-01

Full Text Available Alfonso Merante1, Pietro Gareri2,3, Norma Maria Marigliano2, Salvatore De Fazio2, Elvira Bonacci1, Carlo Torchia1, Gaetano Russo1, Pasquale Lacroce1, Roberto Lacava3, Alberto Castagna3, Giovambattista De Sarro2, Giovanni Ruotolo11Geriatrist, Geriatric Unit “Pugliese-Ciaccio” Hospital, Catanzaro, Italy; 2Department of Experimental and Clinical Medicine, Faculty of Medicine and Surgery, University Magna Graecia of Catanzaro, Clinical Pharmacology and Pharmacovigilance Unit, Mater Domini University Hospital, Catanzaro, Italy; 3Geriatrist, Operative Unit Elderly Health Care, Catanzaro, ItalyAbstract: The present study describes a case of laxative-induced rhabdomyolysis in an elderly patient. An 87-year-old woman was hospitalized for the onset of confusion, tremors, an inability to walk, and a fever that she had been experiencing for 36 hours. She often took high dosages of lactulose and sorbitol syrup as a laxative (about 70 g/day. During her physical examination, the patient was confused, drowsy, and she presented hyposthenia in her upper and lower limbs, symmetric and diffuse moderate hyporeflexia, and her temperature was 37.8°C. Laboratory tests revealed severe hyponatremia with hypokalemia, hypocalcemia, hypochloremia, and metabolic alkalosis. Moreover, rhabdomyolysis markers were found. The correction of hydroelectrolytic imbalances with saline, potassium and sodium chlorure, calcium gluconate was the first treatment. During her hospitalization the patient presented acute delirium, treated with haloperidol and prometazine chloridrate intramuscularly. She was discharged 12 days later, after resolution of symptoms, and normalized laboratory tests. Over-the-counter drugs such as laxatives are usually not considered dangerous; on the other hand, they may cause serum electrolytic imbalance and rhabdomyolysis. A careful monitoring of all the drugs taken by the elderly is one of the most important duties of a physician since drug interactions and

Pseudo-bartter syndrome, pattern and correlation with other cystic fibrosis features.

Science.gov (United States)

Dahabreh, Muna M; Najada, Abdelhamid S

2013-03-01

Pseudo-Bartter Syndrome (PBS), although quite common in patients with cystic fibrosis (CF), is often missed as simple dehydration or Bartter syndrome. This study was performed in patients with PBS to compare the pattern and course of the disease with those with CF not manifesting with this syndrome. All patients with CF who attended the respiratory clinic at Queen Rania Al-Abdallah Hospital from January 2000 to April 2010 were included in this retrospective case-control study. A specially formulated data sheet was used and those with PBS and those not having the syndrome were identified. A total of 110 patients (51% female) with CF with a median age of seven years were followed-up. Eighteen (16.3%) of them had one or more episodes of PBS. The median follow-up period was 6.2 years. All the episodes occurred during summer and in infancy. Median age of the initial episode of PBS was three months. One-third of them were initially followed at the nephrology clinic. Three patterns of PBS were identified: single episode in three (16.6%) patients, recurrent in 12 (66.6%) patients and chronic in three (16.6%) patients. Early colonization of Pseudomonas spp before 1 st birthday was seen in 44% patients with PBS compared with 12% in other CF patients (P-value = 0.0075). The total number of colonized patients and other CF features at the time of the study did not differ significantly among patients, although the mean Shwachman-Kulczycki score is significantly lower in those with recurrent PBS (69 compared with 85 in other CF patients). Gene mutation was identified in only 30% of the entire cohort. PBS is common in patients with CF, and it should be kept in mind in any patient with hypotonic dehydration and metabolic alkalosis. Recurrent pattern is associated with earlier Pseudomonas colonization.

Secondary elements of blood pH variation can influence the effort effectiveness based on adaptive changes within a group of elite athletes.

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Martin, Ştefan Adrian; Tomescu, Valeriu; Voidăzan, Septimiu

2016-01-01

pH is the direct indicator of the body reaction following the activities performed. Establishing precise correlations between pH and blood biochemical parameters might support the balancing of values during periods of marked physical activity. We conducted a case study in a group of elite rowers. Twelve athletes were included in the study. Monitoring was carried out by collecting biological samples several times a day: in the morning, 80 minutes pre-workout, 12 hours after the last physical effort performed, at two different times, 10 days apart. Determinations were aimed at adapting the reported biochemical parameters depending on the effort performed. The following parameters were monitored: pH, HCO3, pCO2, pO2, BE, SBE, SBC, Ca++, Mg++, LDH, GPT, T-Pro, and Alb. The mean value of pH found in athletes was 7.41±0.024. The value obtained was significantly correlated to biochemical parameters such as BE (2.32±1.79), SBC (1.67±1.45), SBE (2.70±1.75). However, bicarbonate (HCO3) was statistically significantly related with SBE, SBC, SBE, and pO2, but did not present a strong association with the pH value (p=0.094). However, values such as Alb, Ca++, LDH, BE, SBC are related to pH value as a result of variations in the data submitted. The processed data evidence the fact that blood pH, in this case, is significantly influenced by a number of indices that correlate energy system activity, individual adaptation to effort, and the recovery process. The parameters under investigation (SBE, SBC, SBE, CPK, LDH) are associated with pH changes that could confirm the recovery efficiency of the athlete, along with a possible metabolic acidosis/alkalosis.

Modulation of Acid-sensing Ion Channel 1a by Intracellular pH and Its Role in Ischemic Stroke.

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Li, Ming-Hua; Leng, Tian-Dong; Feng, Xue-Chao; Yang, Tao; Simon, Roger P; Xiong, Zhi-Gang

2016-08-26

An important contributor to brain ischemia is known to be extracellular acidosis, which activates acid-sensing ion channels (ASICs), a family of proton-gated sodium channels. Lines of evidence suggest that targeting ASICs may lead to novel therapeutic strategies for stroke. Investigations of the role of ASICs in ischemic brain injury have naturally focused on the role of extracellular pH in ASIC activation. By contrast, intracellular pH (pHi) has received little attention. This is a significant gap in our understanding because the ASIC response to extracellular pH is modulated by pHi, and activation of ASICs by extracellular protons is paradoxically enhanced by intracellular alkalosis. Our previous studies show that acidosis-induced cell injury in in vitro models is attenuated by intracellular acidification. However, whether pHi affects ischemic brain injury in vivo is completely unknown. Furthermore, whereas ASICs in native neurons are composed of different subunits characterized by distinct electrophysiological/pharmacological properties, the subunit-dependent modulation of ASIC activity by pHi has not been investigated. Using a combination of in vitro and in vivo ischemic brain injury models, electrophysiological, biochemical, and molecular biological approaches, we show that the intracellular alkalizing agent quinine potentiates, whereas the intracellular acidifying agent propionate inhibits, oxygen-glucose deprivation-induced cell injury in vitro and brain ischemia-induced infarct volume in vivo Moreover, we find that the potentiation of ASICs by quinine depends on the presence of the ASIC1a, ASIC2a subunits, but not ASIC1b, ASIC3 subunits. Furthermore, we have determined the amino acids in ASIC1a that are involved in the modulation of ASICs by pHi. © 2016 by The American Society for Biochemistry and Molecular Biology, Inc.

Pathophysiologic Changes in Extracellular pH Modulate Parathyroid Calcium-Sensing Receptor Activity and Secretion via a Histidine-Independent Mechanism.

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Campion, Katherine L; McCormick, Wanda D; Warwicker, Jim; Khayat, Mohd Ezuan Bin; Atkinson-Dell, Rebecca; Steward, Martin C; Delbridge, Leigh W; Mun, Hee-Chang; Conigrave, Arthur D; Ward, Donald T

2015-09-01

The calcium-sensing receptor (CaR) modulates renal calcium reabsorption and parathyroid hormone (PTH) secretion and is involved in the etiology of secondary hyperparathyroidism in CKD. Supraphysiologic changes in extracellular pH (pHo) modulate CaR responsiveness in HEK-293 (CaR-HEK) cells. Therefore, because acidosis and alkalosis are associated with altered PTH secretion in vivo, we examined whether pathophysiologic changes in pHo can significantly alter CaR responsiveness in both heterologous and endogenous expression systems and whether this affects PTH secretion. In both CaR-HEK and isolated bovine parathyroid cells, decreasing pHo from 7.4 to 7.2 rapidly inhibited CaR-induced intracellular calcium (Ca(2+)i) mobilization, whereas raising pHo to 7.6 potentiated responsiveness to extracellular calcium (Ca(2+)o). Similar pHo effects were observed for Ca(2+)o-induced extracellular signal-regulated kinase phosphorylation and actin polymerization and for L-Phe-induced Ca(2+)i mobilization. Intracellular pH was unaffected by acute 0.4-unit pHo changes, and the presence of physiologic albumin concentrations failed to attenuate the pHo-mediated effects. None of the individual point mutations created at histidine or cysteine residues in the extracellular domain of CaR attenuated pHo sensitivity. Finally, pathophysiologic pHo elevation reversibly suppressed PTH secretion from perifused human parathyroid cells, and acidosis transiently increased PTH secretion. Therefore, pathophysiologic pHo changes can modulate CaR responsiveness in HEK-293 and parathyroid cells independently of extracellular histidine residues. Specifically, pathophysiologic acidification inhibits CaR activity, thus permitting PTH secretion, whereas alkalinization potentiates CaR activity to suppress PTH secretion. These findings suggest that acid-base disturbances may affect the CaR-mediated control of parathyroid function and calcium metabolism in vivo. Copyright © 2015 by the American Society of

The role of the kidney in compensating the alkaline tide, electrolyte load, and fluid balance disturbance associated with feeding in the freshwater rainbow trout, Oncorhynchus mykiss.

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Bucking, Carol; Landman, Michael J; Wood, Chris M

2010-05-01

The effect in freshwater rainbow trout of digesting a commercial pellet meal on the renal handling of water, ions and acid-base equivalents was investigated through urine collection over a 48 h period following meal ingestion. The glomerular filtration rate (GFR) and urine flow rate (UFR) were reduced in fed fish between 12 and 24h following the meal, likely reflecting a loss of endogenous water across the gastric epithelium as a result of ingesting dry, ion-rich food pellets. The kidney was also responsible for the excretion of some excess dietary Ca(2+), and, to a much lesser extent, Na(+) and Cl(-), while the urinary excretion of K(+) was unaffected. The most dramatic effect of feeding was the elevation of renal Mg(2+) excretion, with the kidney transitioning from net Mg(2+) reabsorption to net Mg(2+) secretion during digestion. The renal handling of dietary ions accounted for 3-27% of the total ions absorbed from the diet, indicating that a majority of the ions are excreted extra-renally or incorporated into growth. However this does highlight the underestimation of renal ion handling when using unfed fish models. The metabolic alkalosis created by digestion (the alkaline tide) resulted in an increase in urine pH as well as a transition from net acidic equivalent excretion in the urine to net basic equivalent excretion. This was due to a decrease in the titratable acidity minus bicarbonate component of urine as well as a decrease in ammonia secretion. Additionally, the experimental separation of the urinary component of acid-base excretion from that of the gills highlighted the substantially larger contribution of the latter. During the alkaline tide, renal excretion accounted for approximately 5% of the total basic equivalent excretion to the external water. Copyright 2009 Elsevier Inc. All rights reserved.

[Development and basics of metabolic monitoring in dairy cows. Focus on research in Eastern Germany and at the University of Leipzig, Germany].

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Fürll, M

2016-01-01

Systematic metabolic monitoring began in German-speaking countries in the late 1960s, early 1970s, due to an increase in metabolic disorders as a cause of infertility and mastitis and aimed at their prevention through early diagnosis. Development of a unified monitoring standard: Initiated by Rossow, Gürtler, Ehrentraut, Seidel and Furcht a standard "metabolic monitoring in cattle production" was developed in the 1970s. It included farm analysis, clinical and biochemical controls, prophylaxis and follow-up controls. Key points were: periodic screenings of heavily loaded, healthy indicator animals 2-4 days post partum (p.  p.), 2-8 weeks p.  p. and 1-2 weeks ante partum, maximal 10 animals/group, pooled samples are useful, optimal are individual samples, use of informative sample substrate and parameters, precise handling of specimens, expert assessment and follow-up. Metabolic controls during 1982-1989 in approximately 242  000 cows revealed means of 32.9% ketoses, 20.0% metabolic acidosis, 21.9% metabolic alkalosis, 34.2% nitrogen-metabolism disorders, 17.3% sodium deficiency and 23.7% liver disorders. Development of a metabolic profile after 1989: Reference values at higher milk yield, early diagnosis of diseases of the fat mobilization syndrome and improved early diagnosis by new indicators, including creatine kinase (CK), alkaline phosphatase (AP) with isoenzymes, acute phase proteins, cytokines, antioxidants, carnitine and lipoprotein fractions, were established. Optimized blood and urine screenings have important advantages over milk analysis. They are an important method of health and performance stabilization by exact analysis of causes and derived prevention. The fertility related parameters free fatty acids, β-hydroxybutyrate, urea, inorganic phosphate, CK, AP, sodium, potassium, selenium, copper, β-carotene and net acid-base excretion proved to be a standard spectrum for screenings. These should be tested once a year/herd, if necessary as

Sedative and cardiorespiratory effects of detomidine constant rate infusion in sheep.

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de Moura, Rauane Sousa; Bittar, Isabela Plazza; da Silva, Luiz Henrique; Villela, Ana Carolina Vasquez; Dos Santos Júnior, Marcelo Borges; Borges, Naida Cristina; Franco, Leandro Guimarães

2018-02-01

The use of sheep in experiments is widespread and is increasing worldwide, and so is the need to develop species-specific anaesthetic techniques to ensure animal safety. Previous studies have mentioned several protocols involving the administration of alpha-2 adrenergic agonists in sheep; however, assessment of the efficacy and safety of these infusion techniques is still relatively new. Thus, the aim of the present study is to assess the effectiveness of detomidine constant rate infusion (CRI) in sheep by measuring the cardiovascular and respiratory parameters, blood gas variables and sedation scores. Eight adult female Santa Inês sheep received 20 µg/kg of detomidine hydrochloride intravenously as a bolus loading dose, followed by an infusion rate of 60 µg/kg/h. The heart rates and respiratory rates changed continuously during the CRI period. No arrhythmias were observed. The reduction in arterial partial pressure of oxygen (PaO 2 ) was not significant, but one animal showed signs of hypoxaemia (minimum PaO 2 of 66.9 mmHg). The arterial partial pressure of carbon dioxide (PaCO 2 ) increased, but the animals did not become hypercapnic. The bicarbonate (HCO 3- ), pH and base excess (BE) tended towards metabolic alkalosis. The cardiac output (CO), stroke volume (SV), cardiac index (CI) and ejection fraction (EF%) showed no significant changes. The fractional shortening (FS%) decreased slightly, starting at T 45min . Sedation scores varied between 3 (0/10) after sedation and during recovery and 7 (0/10) during CRI. We concluded that administering detomidine at an infusion rate of 60 µg/kg/h in Santa Inês sheep is a simple technique that produces satisfactory sedation for minimally invasive procedures.

A comparison of traditional and quantitative analysis of acid-base imbalances in hypoalbuminemic dogs.

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Torrente, Carlos; Manzanilla, Edgar G; de Gopegui, Rafael Ruiz

2014-01-01

To compare the traditional (HH) and quantitative approaches used for the evaluation of the acid-base balance in hypoalbuminemic dogs. Prospective observational study. ICU of a veterinary teaching hospital. One hundred and five client-owned dogs. Jugular venous blood samples were collected from each patient on admission to determine: total plasma protein (TP), albumin (Alb), blood urea nitrogen (BUN), glucose (Glu), hematocrit (HCT), Na(+) , Cl(-) , K(+) , phosphate (Pi ), pH, PvCO2, bicarbonate (HCO3 (-) ), anion gap (AG), adjusted anion gap for albumin (AGalb ) or phosphate (AGalb-phos ), standardized base excess (SBE), strong ion difference (SID), concentration of nonvolatile weak buffers (Atot ), and strong ion gap (SIG). Patients were divided in 2 groups according to the severity of the hypoalbuminemia: mild (Alb = 21-25 g/L) and severe (Alb ≤20 g/L). All parameters were compared among groups. Patients with severe hypoalbuminemia showed significant decrease in TP (P = 0.011), Atot (P = 0.050), and a significant increase in adjusted AG (P = 0.048) and the magnitude of SIG (P = 0.011) compared to animals with mild hypoalbuminemia. According to the HH approach, the most frequent imbalances were simple disorders (51.4%), primarily metabolic acidosis (84.7%) associated with a high AG acidosis. However, when using the quantitative method, 58.1% of patients had complex disorders, with SIG acidosis (74.3%) and Atot alkalosis (33.3%) as the most frequent acid-base imbalances. Agreement between methods only matched in 32 cases (kappa acid-base balance was poor and many imbalances detected using the quantitative approach were missed using the HH approach. Further studies are necessary to confirm the clinical utility of using the quantitative approach in the decision-making process of the severely ill hypoalbuminemic patients. © Veterinary Emergency and Critical Care Society 2014.

Predicting the safety and efficacy of buffer therapy to raise tumour pHe: an integrative modelling study.

Science.gov (United States)

Martin, N K; Robey, I F; Gaffney, E A; Gillies, R J; Gatenby, R A; Maini, P K

2012-03-27

Clinical positron emission tomography imaging has demonstrated the vast majority of human cancers exhibit significantly increased glucose metabolism when compared with adjacent normal tissue, resulting in an acidic tumour microenvironment. Recent studies demonstrated reducing this acidity through systemic buffers significantly inhibits development and growth of metastases in mouse xenografts. We apply and extend a previously developed mathematical model of blood and tumour buffering to examine the impact of oral administration of bicarbonate buffer in mice, and the potential impact in humans. We recapitulate the experimentally observed tumour pHe effect of buffer therapy, testing a model prediction in vivo in mice. We parameterise the model to humans to determine the translational safety and efficacy, and predict patient subgroups who could have enhanced treatment response, and the most promising combination or alternative buffer therapies. The model predicts a previously unseen potentially dangerous elevation in blood pHe resulting from bicarbonate therapy in mice, which is confirmed by our in vivo experiments. Simulations predict limited efficacy of bicarbonate, especially in humans with more aggressive cancers. We predict buffer therapy would be most effectual: in elderly patients or individuals with renal impairments; in combination with proton production inhibitors (such as dichloroacetate), renal glomular filtration rate inhibitors (such as non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors), or with an alternative buffer reagent possessing an optimal pK of 7.1-7.2. Our mathematical model confirms bicarbonate acts as an effective agent to raise tumour pHe, but potentially induces metabolic alkalosis at the high doses necessary for tumour pHe normalisation. We predict use in elderly patients or in combination with proton production inhibitors or buffers with a pK of 7.1-7.2 is most promising.

Bartter syndrome type 3 in an elderly complicated with adrenocorticotropin-deficiency.

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Tamagawa, Eri; Inaba, Hidefumi; Ota, Takayuki; Ariyasu, Hiroyuki; Kawashima, Hiromichi; Wakasaki, Hisao; Furuta, Hiroto; Nishi, Masahiro; Nakao, Taisei; Kaito, Hiroshi; Iijima, Kazumoto; Nakanishi, Koichi; Yoshikawa, Norishige; Akamizu, Takashi

2014-01-01

Bartter syndrome (BS) is a disorder with normotensive hypokalemic alkalosis and hyperreninemic hyperaldosteronemia. BS affects infants or early childhood. Patients with BS type 3 harbor mutation in CLCNKB, Cl channel Kb. Gitelman syndrome (GS) is a disorder in childhood, with mutation in SLC12A3. Isolated adrenocorticotropin deficiency (IAD) causes secondary adrenal insufficiency. Neither elderly cases, nor cases with IAD were previously reported in BS. A 72-year-old man was admitted with acute adrenal crisis. He had been treated for IAD for 19 years. He had no trouble during perinatal period, delivery, and growth. After the recovery from adrenal crisis, laboratory tests revealed hypokalemia; 3.0 mEq/L (normal: 3.5-4.5), impaired renal function: eGFR; 37.6 mL/min/1.73 m2, normomagnesemia; 2.1 mg/dL (1.7-2.3), hyperreninemia; 59.4 ng/mL/h (0.2-2.7), hyperaldosteronemia; 23.5 ng/dL (3.0-15.9), and normal urinary ratio of calcium/creatinine. In diuretic tests, he showed a fine response to furosemide, and a mild response to thiazide. In genetic tests, no mutation of SLC12A3 was found and homozygous mutation: c.1830 G > A in CLCNKB was shown. Thus he was diagnosed as BS type 3. Current case presented with unusual features as BS type 3, 1) his late and mild clinical manifestation suggested GS rather than BS, 2) laboratory data and diuretics tests did not show typical features as BS, and 3) IAD and chronic renal failure altered electrolyte metabolism. In conclusion, current case implies that BS type 3 should be considered even in elderly cases with normotensive hypokalemia, and highlights importance of endocrinological and genetic examinations.

Poor phenotype-genotype association in a large series of patients with Type III Bartter syndrome.

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García Castaño, Alejandro; Pérez de Nanclares, Gustavo; Madariaga, Leire; Aguirre, Mireia; Madrid, Álvaro; Chocrón, Sara; Nadal, Inmaculada; Navarro, Mercedes; Lucas, Elena; Fijo, Julia; Espino, Mar; Espitaletta, Zilac; García Nieto, Víctor; Barajas de Frutos, David; Loza, Reyner; Pintos, Guillem; Castaño, Luis; Ariceta, Gema

2017-01-01

Type III Bartter syndrome (BS) is an autosomal recessive renal tubule disorder caused by loss-of-function mutations in the CLCNKB gene, which encodes the chloride channel protein ClC-Kb. In this study, we carried out a complete clinical and genetic characterization in a cohort of 30 patients, one of the largest series described. By comparing with other published populations, and considering that 80% of our patients presented the p.Ala204Thr Spanish founder mutation presumably associated with a common phenotype, we aimed to test the hypothesis that allelic differences could explain the wide phenotypic variability observed in patients with type III BS. Clinical data were retrieved from the referral centers. The exon regions and flanking intronic sequences of the CLCNKB gene were screened for mutations by polymerase chain reaction (PCR) followed by direct Sanger sequencing. Presence of gross deletions or duplications in the region was checked for by MLPA and QMPSF analyses. Polyuria, polydipsia and dehydration were the main common symptoms. Metabolic alkalosis and hypokalemia of renal origin were detected in all patients at diagnosis. Calciuria levels were variable: hypercalciuria was detected in 31% of patients, while 23% had hypocalciuria. Nephrocalcinosis was diagnosed in 20% of the cohort. Two novel CLCNKB mutations were identified: a small homozygous deletion (c.753delG) in one patient and a small deletion (c.1026delC) in another. The latter was present in compound heterozygosis with the already previously described p.Glu442Gly mutation. No phenotypic association was obtained regarding the genotype. A poor correlation was found between a specific type of mutation in the CLCNKB gene and type III BS phenotype. Importantly, two CLCNKB mutations not previously described were found in our cohort.

Bartter and Gitelman syndromes: Spectrum of clinical manifestations caused by different mutations

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Al Shibli, Amar; Narchi, Hassib

2015-01-01

Bartter and Gitelman syndromes (BS and GS) are inherited disorders resulting in defects in renal tubular handling of sodium, potassium and chloride. Previously considered as genotypic and phenotypic heterogeneous diseases, recent evidence suggests that they constitute a spectrum of disease caused by different genetic mutations with the molecular defects of chloride reabsorption originating at different sites of the nephron in each condition. Although they share some characteristic metabolic abnormalities such as hypokalemia, metabolic alkalosis, hyperplasia of the juxtaglomerular apparatus with hyperreninemia, hyperaldosteronism, the clinical and laboratory manifestations may not always allow distinction between them. Diuretics tests, measuring the changes in urinary fractional excretion of chloride from baseline after administration of either hydrochlorothiazide or furosemide show very little change (< 2.3%) in the fractional excretion of chloride from baseline in GS when compared with BS, except when BS is associated with KCNJ1 mutations where a good response to both diuretics exists. The diuretic test is not recommended for infants or young children with suspected BS because of a higher risk of volume depletion in such children. Clinical symptoms and biochemical markers of GS and classic form of BS (type III) may overlap and thus genetic analysis may specify the real cause of symptoms. However, although genetic analysis is available, its use remains limited because of limited availability, large gene dimensions, lack of hot-spot mutations, heavy workup time and costs involved. Furthermore, considerable overlap exists between the different genotypes and phenotypes. Although BS and GS usually have distinct presentations and are associated with specific gene mutations, there remains considerable overlap between their phenotypes and genotypes. Thus, they are better described as a spectrum of clinical manifestations caused by different gene mutations. PMID:26140272

Poor phenotype-genotype association in a large series of patients with Type III Bartter syndrome.

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Alejandro García Castaño

Full Text Available Type III Bartter syndrome (BS is an autosomal recessive renal tubule disorder caused by loss-of-function mutations in the CLCNKB gene, which encodes the chloride channel protein ClC-Kb. In this study, we carried out a complete clinical and genetic characterization in a cohort of 30 patients, one of the largest series described. By comparing with other published populations, and considering that 80% of our patients presented the p.Ala204Thr Spanish founder mutation presumably associated with a common phenotype, we aimed to test the hypothesis that allelic differences could explain the wide phenotypic variability observed in patients with type III BS.Clinical data were retrieved from the referral centers. The exon regions and flanking intronic sequences of the CLCNKB gene were screened for mutations by polymerase chain reaction (PCR followed by direct Sanger sequencing. Presence of gross deletions or duplications in the region was checked for by MLPA and QMPSF analyses.Polyuria, polydipsia and dehydration were the main common symptoms. Metabolic alkalosis and hypokalemia of renal origin were detected in all patients at diagnosis. Calciuria levels were variable: hypercalciuria was detected in 31% of patients, while 23% had hypocalciuria. Nephrocalcinosis was diagnosed in 20% of the cohort. Two novel CLCNKB mutations were identified: a small homozygous deletion (c.753delG in one patient and a small deletion (c.1026delC in another. The latter was present in compound heterozygosis with the already previously described p.Glu442Gly mutation. No phenotypic association was obtained regarding the genotype.A poor correlation was found between a specific type of mutation in the CLCNKB gene and type III BS phenotype. Importantly, two CLCNKB mutations not previously described were found in our cohort.

Mesenteric microcirculatory dysfunctions and translocation of indigenous bacteria in a rat model of strangulated small bowel obstruction

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Fernando Luiz Zanoni

2009-01-01

Full Text Available PRUPOSE: Bacterial translocation has been shown to occur in critically ill patients after extensive trauma, shock, sepsis, or thermal injury. The present study investigates mesenteric microcirculatory dysfunctions, the bacterial translocation phenomenon, and hemodynamic/metabolic disturbances in a rat model of intestinal obstruction and ischemia. METHODS: Anesthetized (pentobarbital 50 mg/kg, i.p. male Wistar rats (250-350 g were submitted to intestinal obstruction or laparotomy without intestinal obstruction (Sham and were evaluated 24 hours later. Bacterial translocation was assessed by bacterial culture of the mesenteric lymph nodes (MLN, liver, spleen, and blood. Leukocyte-endothelial interactions in the mesenteric microcirculation were assessed by intravital microscopy, and P-selectin and intercellular adhesion molecule (ICAM-1 expressions were quantified by immunohistochemistry. Hematocrit, blood gases, lactate, glucose, white blood cells, serum urea, creatinine, bilirubin, and hepatic enzymes were measured. RESULTS: About 86% of intestinal obstruction rats presented positive cultures for E. coli in samples of the mesenteric lymph nodes, liver, and spleen, and 57% had positive hemocultures. In comparison to the Sham rats, intestinal obstruction induced neutrophilia and increased the number of rolling (~2-fold, adherent (~5-fold, and migrated leukocytes (~11-fold; this increase was accompanied by an increased expression of P-selectin (~2-fold and intercellular adhesion molecule-1 (~2-fold in the mesenteric microcirculation. Intestinal obstruction rats exhibited decreased PaCO2, alkalosis, hyperlactatemia, and hyperglycemia, and increased blood potassium, hepatic enzyme activity, serum urea, creatinine, and bilirubin. A high mortality rate was observed after intestinal obstruction (83% at 72 h vs. 0% in Sham rats. CONCLUSION: Intestinal obstruction and ischemia in rats is a relevant model for the in vivo study of mesenteric microcirculatory

Sodium bicarbonate ingestion and boxing performance.

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Siegler, Jason C; Hirscher, Kristian

2010-01-01

Boxing is a sport that consists of multiple high-intensity bouts separated by minimal recovery time and may benefit from a pre-exercise alkalotic state. The purpose of this study was to observe the ergogenic potential of sodium bicarbonate (NaHCO3) ingestion on boxing performance. Ten amateur boxers volunteered to participate in 2 competitive sparring bouts. The boxers were prematched for weight and boxing ability and consumed either 0.3 g.kg(-1) body weight (BW) of NaHCO3 (BICARB) or 0.045 g.kg(-1) BW of NaCl placebo (PLAC) mixed in diluted low calorie-flavored cordial. The sparring bouts consisted of four 3-minute rounds, each separated by 1-minute seated recovery. Blood acid-base (pH, bicarbonate [HCO3(-)], base excess [BE]), and performance (rates of perceived exertion [RPE], heart rate [HR] [HR(ave) and HR(max)], total punches landed successfully) profiles were analyzed before (where applicable) and after sparring. The results indicated a significant interaction effect for HCO3(-) (p < or = 0.001) and BE (p < 0.001), but not for pH (p = 0.48). Post hoc analysis revealed higher presparring HCO3(-) and BE for the BICARB condition, but no differences between the BICARB and PLAC conditions postsparring. There was a significant increase in punches landed during the BICARB condition (p < 0.001); however, no significant interaction effects for HRave (p = 0.15), HRmax (p = 0.32), or RPE (p = 0.38). The metabolic alkalosis induced by the NaHCO3 loading elevated before and after sparring blood buffering capacity. In practical application, the findings suggest that a standard NaHCO3 loading dose (0.3 g.kg(-1)) improves punch efficacy during 4 rounds of sparring performance.

Effects of chronic waterborne nickel exposure on growth, ion homeostasis, acid-base balance, and nickel uptake in the freshwater pulmonate snail, Lymnaea stagnalis.

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Niyogi, Som; Brix, Kevin V; Grosell, Martin

2014-05-01

The freshwater pulmonate snail, Lymnaea stagnalis, is the most sensitive aquatic organism tested to date for Ni. We undertook a series of experiments to investigate the underlying mechanism(s) for this observed hypersensitivity. Consistent with previous experiments, juvenile snail growth in a 21-day exposure was reduced by 48% relative to the control when exposed to 1.3 μg l(-1) Ni (EC20 less than the lowest concentration tested). Ca(2+) homeostasis was significantly disrupted by Ni exposure as demonstrated by reductions in net Ca(2+) uptake, and reductions in Ca(2+) concentrations in the hemolymph and soft tissues. We also observed reduced soft tissue [Mg(2+)]. Snails underwent a significant alkalosis with hemolymph pH increasing from 8.1 to 8.3 and hemolymph TCO2 increasing from 19 to 22 mM in control versus Ni-exposed snails, respectively. Unlike in previous studies with Co and Pb, snail feeding rates were found to be unaffected by Ni at the end of the exposure. Snails accumulated Ni in the soft tissue in a concentration-dependent manner, and Ni uptake experiments with (63)Ni revealed a biphasic uptake profile - a saturable high affinity component at low exposure concentrations (36-189 nM) and a linear component at the high exposure concentrations (189-1,897 nM). The high affinity transport system had an apparent Km of 89 nM Ni(2+) and Vmax of 2.4 nmol g(-1)h(-1). This equates to a logK of 7.1, significantly higher than logK's (2.6-5.2) for any other aquatic organisms evaluated to date, which will have implications for Biotic Ligand Model development. Finally, pharmacological inhibitors that block Ca(2+) uptake pathways in snails did not inhibit Ni uptake, suggesting that the uptake of Ni does not occur via Ca(2+) uptake pathways. As with Cu and Pb, the exact mechanism for the significant disruption in Ca(2+) homeostasis and reduction in juvenile snail growth remains unknown. Copyright © 2014 Elsevier B.V. All rights reserved.

Analysis and physiological implications of renal 2-oxoglutaramate metabolism.

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Nissim, I; Wehrli, S; States, B; Nissim, I; Yudkoff, M

1991-07-01

The relative significance of the flux through the glutamine aminotransferase (glutaminase II) pathway to renal ammoniagenesis is poorly understood. A basic and unresolved question is whether 2-oxoglutaramate (2-OGM), a product of the glutaminase II reaction, is deamidated to yield 2-oxoglutarate and NH3, or whether 2-OGM accumulates as an unreactive lactam, depending on the environmental pH. In the current studies we utilized 13C n.m.r. as well as 15N n.m.r. as well as 15N n.m.r. to demonstrate that 2-OGM occurs as a lactam, i.e. 5-hydroxypyroglutamate, regardless of the environmental pH. Our additional aims were to determine whether human kidney cells (HK cells) in culture can produce 2-OGM and to ascertain a pH-dependent relationship between NH3 and 2-OGM production from glutamine. We therefore developed an isotope dilution assay for 2-OGM utilizing 5-hydroxy[4-13C,1-15N]pyroglutamate as the labelled species. Incubations of HK cells in minimal essential medium supplemented with 1 mM-[2-15N]glutamine demonstrated significantly higher production of 2-OGM at pH 6.8 and lower production at pH 7.6 compared with pH 7.4. Similarly both 15NH3 and [15N]alanine formation were significantly higher in acute acidosis (pH 6.8) and lower in acute alkalosis (pH 7.6) compared with that at physiological pH. Addition of 1 mM-amino-oxyacetate to the incubation medium at pH 7.4 significantly diminished [15N]alanine and 2-OGM production, but the production of 15NH3 via the glutamate dehydrogenase pathway was significantly stimulated. The current observations indicate that the glutaminase II pathway plays a minor role and that flux through glutamate dehydrogenase is the predominant site for regulation of ammoniagenesis in human kidney.

Response properties of the genetically encoded optical H2O2 sensor HyPer.

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Weller, Jonathan; Kizina, Kathrin M; Can, Karolina; Bao, Guobin; Müller, Michael

2014-11-01

Reactive oxygen species mediate cellular signaling and neuropathologies. Hence, there is tremendous interest in monitoring (sub)cellular redox conditions. We evaluated the genetically engineered redox sensor HyPer in mouse hippocampal cell cultures. Two days after lipofection, neurons and glia showed sufficient expression levels, and H2O2 reversibly and dose-dependently increased the fluorescence ratio of cytosolic HyPer. Yet, repeated H2O2 treatment caused progressively declining responses, and with millimolar doses an apparent recovery started while H2O2 was still present. Although HyPer should be H2O2 specific, it seemingly responded also to other oxidants and altered cell-endogenous superoxide production. Control experiments with the SypHer pH sensor confirmed that the HyPer ratio responds to pH changes, decreasing with acidosis and increasing during alkalosis. Anoxia/reoxygenation evoked biphasic HyPer responses reporting apparent reduction/oxidation; replacing Cl(-) exerted only negligible effects. Mitochondria-targeted HyPer readily responded to H2O2-albeit less intensely than cytosolic HyPer. With ratiometric two-photon excitation, H2O2 increased the cytosolic HyPer ratio. Time-correlated fluorescence-lifetime imaging microscopy (FLIM) revealed a monoexponential decay of HyPer fluorescence, and H2O2 decreased fluorescence lifetimes. Dithiothreitol failed to further reduce HyPer or to induce reasonable FLIM and two-photon responses. By enabling dynamic recordings, HyPer is superior to synthetic redox-sensitive dyes. Its feasibility for two-photon excitation also enables studies in more complex preparations. Based on FLIM, quantitative analyses might be possible independent of switching excitation wavelengths. Yet, because of its pronounced pH sensitivity, adaptation to repeated oxidation, and insensitivity to reducing stimuli, HyPer responses have to be interpreted carefully. For reliable data, side-by-side pH monitoring with SypHer is essential. Copyright �

Small cell carcinoma of the prostate presenting with Cushing Syndrome. A narrative review of an uncommon condition.

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Rueda-Camino, José Antonio; Losada-Vila, Beatriz; De Ancos-Aracil, Cristina Lucía; Rodríguez-Lajusticia, Laura; Tardío, Juan Carlos; Zapatero-Gaviria, Antonio

2016-01-01

Small cell carcinoma (SCC) of the prostate is an uncommon condition; there are very few cases in which presenting symptoms are consistent with Cushing Syndrome (CS). We report a new case in which CS triggers the suspicion of an SCC of the prostate and a review of the published cases of SCC of the prostate presenting with CS. The origin of these neoplasms is still unclear. It may be suspected when laboratory features appear in patients diagnosed with prostatic adenocarcinoma which becomes resistant to specific therapy. SCC usually occurs after the 6th decade. Patients suffering SCC of the prostate presenting with CS usually present symptoms such as hypertension, hyperglycemia, alkalosis or hypokalemia; cushingoid phenotype is less frequent. Cortisol and ACTH levels are often high. Prostatic-specific antigen levels are usually normal. CT scan is the preferred imaging test to localize the lesion, but its performance may be improved by adding other tests, such as FDG-PET scan. All patients have metastatic disease at the time of diagnosis. Lymph nodes, liver and bone are the most frequent metastases sites. Surgery and Ketokonazole are the preferred treatments for CS. The prognosis is very poor: 2- and 5-year survival rates are 27.5 and 14.3%, respectively. Key messages When a patient presents with ectopic Cushing Syndrome but lungs are normal, an atypical localization should be suspected. We should suspect a prostatic origin if Cushing Syndrome is accompanied by obstructive inferior urinary tract symptoms or in the setting of a prostatic adenocarcinoma with rapid clinical and radiological progression with relatively low PSA levels. Although no imaging test is preferred to localize these tumors, FDG-PET-TC can be very useful. Hormone marker scintigraphy (e.g. somatostatin) could be used too. As Cushing Syndrome is a paraneoplastic phenomenon, treatment of the underlying disease may help control hypercortisolism manifestations. These tumors are usually metastatic by the

Branched-chain aminoacids and retraining of patients with chronic obstructive lung disease.

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Menier, R; Talmud, J; Laplaud, D; Bernard, M P

2001-12-01

The aim of this work was to improve the efficacy of rehabilitation by retraining, by oral supply in branched-chain aminoacids (BCAA). Patients with chronic respiratory insufficiency mainly suffer from obstructive bronchitis due to tobacco or asthma. Nutritional assessment is one of the components of respiratory rehabilitation, with retraining. Intense physical training for several days negativates the nitrogen balance, the beginning of a training programme for sedentary patients increases their need in proteins. An additional supply in branched-chain aminoacids increases proteic anabolism, by synthesis increase and catabolism slackening of proteins. Moreover it is known that exposure to high altitude reduces lean mass by inducing a muscular atrophy, which can be avoided by the BCAA provided. This leads to wonder if extra supply of BCAA could play similar role in muscular mass loss induced by pathological chronic hypoxia. The prospective and comparative survey carried out in Toki-Eder (private hospital in Cambo) consisted in supplying (during five weeks or more) 30 retrained patients suffering from chronic obstructive bronchitis, and in matching them with 30 witnesses (obstructive patients retrained without additional supply in BCAA). Their mean hypoxemia amounted to 7 torr for age. Each of them improved their reached maximal power, and their VO2 SL, very highly significantly. Each of them developed a moderate metabolic acidosis (whose possible mechanisms are discussed) and slightly increased their ventilation at rest. On the other hand only the supplied patients improved their PaO2 at rest highly significantly, a result which poses the question of the responsible mechanism, most likely a decrease of pulmonary shunt effect. The hypotheses concerning the acid load due to BCAA ingestion are discussed. Only the supplied patients developed hypocapnia expressing a gaseous alkalosis which might be due to a direct effect of BCAA on the respiratory centers. This observation

Role of tolvaptan in the management of hyponatremia in patients with lung and other cancers: current data and future perspectives

International Nuclear Information System (INIS)

Thajudeen, Bijin; Salahudeen, Abdulla K

2016-01-01

Hyponatremia is the most frequently observed electrolyte abnormality in clinical practice, and its frequency is almost double in hospitalized cancer patients. As a subset of cancer, hyponatremia is quite common in lung cancer patients, and it is often coupled with the diagnosis of syndrome of inappropriate antidiuretic hormone secretion. The presence of hyponatremia is consequential in that its presence adversely affects cancer patients’ prognosis and outcomes. Limited data suggest that correcting hyponatremia in lung cancer patients can increase response to anticancer treatment, may help reduce length of hospital stay and cost, and reduce morbidity and mortality. The type of treatment for hyponatremia depends on several factors; the key factors are the duration and severity of neurological symptoms of hyponatremia and the status of extracellular volume. When hyponatremia is caused by syndrome of inappropriate antidiuretic hormone, hypertonic saline is indicated for acute symptomatic cases, whereas fluid restriction is recommended in chronic asymptomatic hyponatremia. The latter allows a slower rate of correction, thus avoiding the dreaded complication of osmotic demyelination syndrome. Fluid restriction is, however, insufficient or impractical, and often the use of pharmacological therapy such as antidiuretic hormone receptor antagonists becomes necessary. Availability of these antagonists as an effective treatment in the management of hyponatremia has been a major breakthrough, and furthermore, its clinical or investigational use in cancer-related hyponatremia may offer a potential opportunity to gain further insights into the prognostic impact of hyponatremia correction on cancer patients’ outcomes. Tolvaptan is a prototype of ADH receptor antagonists that acts at renal tubular levels to increase free water excretion without inducing major systemic electrolyte abnormalities such as hypokalemia or alkalosis. The aim of this paper is to provide a brief review

Multum in Parvo: Explorations with a Small Bag of Carbon Dioxide

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EJM Campbell

2001-01-01

Full Text Available A collection of 12 papers published between 1957 and 1972 are revisited. The papers had a common theme of the use of rebreathing carbon dioxide and explored a variety of topics in respiratory physiology. The first study established a method for the noninvasive and indirect estimation of arterial carbon dioxide pressure that was suitable for the routine clinical monitoring of respiratory failure and whose clinical utility remains to this day, but which also provided observations that were the stimulus for the studies that followed. The rate of rise in the partial pressure of carbon dioxide (PCO2 during rebreathing led to an analysis of body carbon dioxide storage capacity. Knowledge of carbon dioxide storage led to a method for quantifying lactate production in exercise without the need for blood sampling. The changes in ventilation that accompanied the increase in PCO2 provided the basis for a rapid method for measuring aspects of breathing control (Read's method, which was later modified to measure the ventilatory response to hypoxia. The physiology of breath-holding was explored through observations of the fall in breath-holding time as PCO2 climbed. Rebreathing also allowed increases in voluntary ventilation to be achieved without the development of alkalosis, leading to studies of maximal voluntary ventilation and respiratory muscle fatigue. Equilibration of PCO2 during rebreathing was used to measure mixed venous PCO2 during exercise and develop an integrated approach to the physiology of exercise in health and disease; alveolar-arterial disequilibrium in PCO2 during exercise was uncovered. Equilibration of PCO2, as well as PO2, during rebreathing of carbon dioxide and nitrogen gas mixtures showed different time courses of venous gases at the onset of exercise. Starting with the rebreathing of carbon dioxide in oxygen mixtures in a small rubber bag, an astonishing range of topics in respiratory physiology was explored, with observations

The alkaline tide and ammonia excretion after voluntary feeding in freshwater rainbow trout.

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Bucking, Carol; Wood, Chris M

2008-08-01

We investigated the potential acid-base and nitrogenous waste excretion challenges created by voluntary feeding in freshwater rainbow trout, with particular focus on the possible occurrence of an alkaline tide (a metabolic alkalosis created by gastric HCl secretion during digestion). Plasma metabolites (glucose, urea and ammonia) were measured at various time points before and after voluntary feeding to satiation (approximately 5% body mass meal of dry commercial pellets), as was the net flux of ammonia and titratable alkalinity to the water from unfed and fed fish. Arterial blood, sampled by indwelling catheter, was examined for post-prandial effects on pH, plasma bicarbonate and plasma CO2 tension. There was no significant change in plasma glucose or urea concentrations following feeding, whereas plasma ammonia transiently increased, peaking at threefold above resting values at 12 h after the meal and remaining elevated for 24 h. The increased plasma ammonia was correlated with an increase in net ammonia excretion to the water, with fed fish significantly elevating their net ammonia excretion two- to threefold between 12 and 48 h post feeding. These parameters did not change in unfed control fish. Fed fish likewise increased the net titratable base flux to the water by approximately threefold, which resulted in a transition from a small net acid flux seen in unfed fish to a large net base flux in fed fish. Over 48 h, this resulted in a net excretion of 13 867 micromol kg(-1) more base to the external water than in unfed fish. The arterial blood exhibited a corresponding rise in pH (between 6 and 12 h) and plasma bicarbonate (between 3 and 12 h) following feeding; however, no respiratory compensation was observed, as PaCO2 remained constant. Overall, there was evidence of numerous challenges created by feeding in a freshwater teleost fish, including the occurrence of an alkaline tide, and its compensation by excretion of base to the external water. The possible

Prostaglandin-E2 Mediated Increase in Calcium and Phosphate Excretion in a Mouse Model of Distal Nephron Salt Wasting.

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Manoocher Soleimani

Full Text Available Contribution of salt wasting and volume depletion to the pathogenesis of hypercalciuria and hyperphosphaturia is poorly understood. Pendrin/NCC double KO (pendrin/NCC-dKO mice display severe salt wasting under basal conditions and develop profound volume depletion, prerenal renal failure, and metabolic alkalosis and are growth retarded. Microscopic examination of the kidneys of pendrin/NCC-dKO mice revealed the presence of calcium phosphate deposits in the medullary collecting ducts, along with increased urinary calcium and phosphate excretion. Confirmatory studies revealed decreases in the expression levels of sodium phosphate transporter-2 isoforms a and c, increases in the expression of cytochrome p450 family 4a isotypes 12 a and b, as well as prostaglandin E synthase 1, and cyclooxygenases 1 and 2. Pendrin/NCC-dKO animals also had a significant increase in urinary prostaglandin E2 (PGE-2 and renal content of 20-hydroxyeicosatetraenoic acid (20-HETE levels. Pendrin/NCC-dKO animals exhibit reduced expression levels of the sodium/potassium/2chloride co-transporter 2 (NKCC2 in their medullary thick ascending limb. Further assessment of the renal expression of NKCC2 isoforms by quantitative real time PCR (qRT-PCR reveled that compared to WT mice, the expression of NKCC2 isotype F was significantly reduced in pendrin/NCC-dKO mice. Provision of a high salt diet to rectify volume depletion or inhibition of PGE-2 synthesis by indomethacin, but not inhibition of 20-HETE generation by HET0016, significantly improved hypercalciuria and salt wasting in pendrin/NCC dKO mice. Both high salt diet and indomethacin treatment also corrected the alterations in NKCC2 isotype expression in pendrin/NCC-dKO mice. We propose that severe salt wasting and volume depletion, irrespective of the primary originating nephron segment, can secondarily impair the reabsorption of salt and calcium in the thick ascending limb of Henle and/or proximal tubule, and reabsorption of

Carboxyl-terminal Truncations of ClC-Kb Abolish Channel Activation by Barttin Via Modified Common Gating and Trafficking.

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Stölting, Gabriel; Bungert-Plümke, Stefanie; Franzen, Arne; Fahlke, Christoph

2015-12-18

ClC-K chloride channels are crucial for auditory transduction and urine concentration. Mutations in CLCNKB, the gene encoding the renal chloride channel hClC-Kb, cause Bartter syndrome type III, a human genetic condition characterized by polyuria, hypokalemia, and alkalosis. In recent years, several Bartter syndrome-associated mutations have been described that result in truncations of the intracellular carboxyl terminus of hClC-Kb. We here used a combination of whole-cell patch clamp, confocal imaging, co-immunoprecipitation, and surface biotinylation to study the functional consequences of a frequent CLCNKB mutation that creates a premature stop codon at Trp-610. We found that W610X leaves the association of hClC-Kb and the accessory subunit barttin unaffected, but impairs its regulation by barttin. W610X attenuates hClC-Kb surface membrane insertion. Moreover, W610X results in hClC-Kb channel opening in the absence of barttin and prevents further barttin-mediated activation. To describe how the carboxyl terminus modifies the regulation by barttin we used V166E rClC-K1. V166E rClC-K1 is active without barttin and exhibits prominent, barttin-regulated voltage-dependent gating. Electrophysiological characterization of truncated V166E rClC-K1 demonstrated that the distal carboxyl terminus is necessary for slow cooperative gating. Since barttin modifies this particular gating process, channels lacking the distal carboxyl-terminal domain are no longer regulated by the accessory subunit. Our results demonstrate that the carboxyl terminus of hClC-Kb is not part of the binding site for barttin, but functionally modifies the interplay with barttin. The loss-of-activation of truncated hClC-Kb channels in heterologous expression systems fully explains the reduced basolateral chloride conductance in affected kidneys and the clinical symptoms of Bartter syndrome patients. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc.

Carboxyl-terminal Truncations of ClC-Kb Abolish Channel Activation by Barttin Via Modified Common Gating and Trafficking*

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Stölting, Gabriel; Bungert-Plümke, Stefanie; Franzen, Arne; Fahlke, Christoph

2015-01-01

ClC-K chloride channels are crucial for auditory transduction and urine concentration. Mutations in CLCNKB, the gene encoding the renal chloride channel hClC-Kb, cause Bartter syndrome type III, a human genetic condition characterized by polyuria, hypokalemia, and alkalosis. In recent years, several Bartter syndrome-associated mutations have been described that result in truncations of the intracellular carboxyl terminus of hClC-Kb. We here used a combination of whole-cell patch clamp, confocal imaging, co-immunoprecipitation, and surface biotinylation to study the functional consequences of a frequent CLCNKB mutation that creates a premature stop codon at Trp-610. We found that W610X leaves the association of hClC-Kb and the accessory subunit barttin unaffected, but impairs its regulation by barttin. W610X attenuates hClC-Kb surface membrane insertion. Moreover, W610X results in hClC-Kb channel opening in the absence of barttin and prevents further barttin-mediated activation. To describe how the carboxyl terminus modifies the regulation by barttin we used V166E rClC-K1. V166E rClC-K1 is active without barttin and exhibits prominent, barttin-regulated voltage-dependent gating. Electrophysiological characterization of truncated V166E rClC-K1 demonstrated that the distal carboxyl terminus is necessary for slow cooperative gating. Since barttin modifies this particular gating process, channels lacking the distal carboxyl-terminal domain are no longer regulated by the accessory subunit. Our results demonstrate that the carboxyl terminus of hClC-Kb is not part of the binding site for barttin, but functionally modifies the interplay with barttin. The loss-of-activation of truncated hClC-Kb channels in heterologous expression systems fully explains the reduced basolateral chloride conductance in affected kidneys and the clinical symptoms of Bartter syndrome patients. PMID:26453302

The Reproducibility of 4-km Time Trial (TT) Performance Following Individualised Sodium Bicarbonate Supplementation: a Randomised Controlled Trial in Trained Cyclists.

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Gough, Lewis Anthony; Deb, Sanjoy Kumar; Sparks, Andy; McNaughton, Lars Robert

2017-09-21

Individual time to peak blood bicarbonate (HCO 3 - ) has demonstrated good to excellent reproducibility following ingestion of both 0.2 g kg -1 body mass (BM) and 0.3 g kg -1 BM sodium bicarbonate (NaHCO 3 ), but the consistency of the time trial (TT) performance response using such an individualised NaHCO 3 ingestion strategy remains unknown. This study therefore evaluated the reproducibility of 4-km TT performance following NaHCO 3 ingestion individualised to time to peak blood bicarbonate. Eleven trained male cyclists completed five randomised treatments with prior ingestion of 0.2 g kg -1 (SBC2) or 0.3 g kg -1 BM (SBC3) NaHCO 3 , on two separate occasions each, or a control trial entailing no supplementation. Participants completed a 4-km cycling TT on a Velotron ergometer where time to complete, power and speed were measured, whilst acid-base blood parameters were also recorded (pH and blood bicarbonate concentration HCO 3 - ) and lactate [La - ]. Alkalosis was achieved prior to exercise in both SBC2 and SBC3, as pH and HCO 3 - were greater compared to baseline (p  0.05). The reproducibility of the mean absolute change from baseline to peak in HCO 3 - was good in SBC2 (r = 0.68) and excellent in SBC3 (r = 0.78). The performance responses following both SBC2 and SBC3 displayed excellent reproducibility (r range = 0.97 to 0.99). Results demonstrate excellent reproducibility of exercise performance following individualised NaHCO 3 ingestion, which is due to the high reproducibility of blood acid-base variables with repeat administration of NaHCO 3 . Using a time to peak HCO 3 - strategy seems to cause no dose-dependent effects on performance for exercise of this duration and intensity; therefore, athletes may consider smaller doses of NaHCO 3 to mitigate gastrointestinal (GI) discomfort.

Clorhidrorrea congénita:: primer reporte en Cuba Congenital chlorhydria:: first report in Cuba

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Carlos Ramírez Pérez

2009-12-01

Full Text Available En el presente trabajo se exponen los antecedentes prenatales, perinatales y posnatales de un lactante de 6 meses de edad, del sexo masculino, con clorhidrorrea congénita, así como el cuadro clínico, diagnóstico y tratamiento utilizado. Un elemento significativo lo constituyó la expulsión anal de abundante líquido no meconial desde las primeras horas de nacido, así como alcalosis metabólica grave y la presencia de desnutrición rápidamente progresiva. En los exámenes complementarios se constató hipocloremia de un 50 % con respecto a las cifras de referencia y un pH sanguíneo mayor de 7,50. El diagnóstico confirmatorio se obtuvo al comprobar concentraciones de cloro en heces fecales superiores a las de la suma de sodio y potasio. Se proponen indicadores diagnósticos prenatales entre los que tienen gran valor la consanguinidad, el polihidramnios y los resultados del ultrasonido en el tercer trimestre del embarazo. El diagnóstico precoz permitió establecer el tratamiento y evitó el frecuente desenlace fatal. Es el primer caso de esta enfermedad que se informa en el país.In present paper are showed the prenatal, perinatal and postnatal backgrounds from a male breast-fed baby aged 6 months presenting with congenital chlorhydria, as well as the clinical picture, diagnosis and treatment applied. A significant element was the anal expulsion of non-meconium abundant fluid from the first hours of born, as well as a severe metabolic alkalosis and the presence of a quickly progressive malnutrition. In complementary examinations was confirmed a 50% hypochloremia regarding the reference figures and a blood pH over 7,50. Confirmatory diagnosis was achieved verifying the chlorine concentrations in feces higher to that of the sum of sodium and potassium. Prenatal diagnostic indicators are proposed those with higher value including the consanguinity, polyhydramnios and the US results during the third trimester of pregnancy. Early diagnosis

Role of tolvaptan in the management of hyponatremia in patients with lung and other cancers: current data and future perspectives

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Thajudeen B

2016-08-01

ADH receptor antagonists that acts at renal tubular levels to increase free water excretion without inducing major systemic electrolyte abnormalities such as hypokalemia or alkalosis. The aim of this paper is to provide a brief review while focusing on cancer hyponatremia; (1 of the epidemiology of hyponatremia and its pathophysiology and diagnostic approaches and (2 of the pharmacokinetics of tolvaptan and its clinical efficacy, safety, and compliance. Keywords: treatment, pharmacology, safety, tolerability, efficacy, adherence

Patterns of unexpected in-hospital deaths: a root cause analysis

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Curry J Paul

2011-02-01

Full Text Available Abstract Background Respiratory alarm monitoring and rapid response team alerts on hospital general floors are based on detection of simple numeric threshold breaches. Although some uncontrolled observation trials in select patient populations have been encouraging, randomized controlled trials suggest that this simplistic approach may not reduce the unexpected death rate in this complex environment. The purpose of this review is to examine the history and scientific basis for threshold alarms and to compare thresholds with the actual pathophysiologic patterns of evolving death which must be timely detected. Methods The Pubmed database was searched for articles relating to methods for triggering rapid response teams and respiratory alarms and these were contrasted with the fundamental timed pathophysiologic patterns of death which evolve due to sepsis, congestive heart failure, pulmonary embolism, hypoventilation, narcotic overdose, and sleep apnea. Results In contrast to the simplicity of the numeric threshold breach method of generating alerts, the actual patterns of evolving death are complex and do not share common features until near death. On hospital general floors, unexpected clinical instability leading to death often progresses along three distinct patterns which can be designated as Types I, II and III. Type I is a pattern comprised of hyperventilation compensated respiratory failure typical of congestive heart failure and sepsis. Here, early hyperventilation and respiratory alkalosis can conceal the onset of instability. Type II is the pattern of classic CO2 narcosis. Type III occurs only during sleep and is a pattern of ventilation and SPO2 cycling caused by instability of ventilation and/or upper airway control followed by precipitous and fatal oxygen desaturation if arousal failure is induced by narcotics and/or sedation. Conclusion The traditional threshold breach method of detecting instability on hospital wards was not

Pathophysiological aspects of malignant brain tumors studied with positron emission tomography

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Jarden, J.O.

1994-01-01

To further understand the control of brain tumor fluid balance and pH, the following studies were undertaken. The transport of a water soluble molecule across the brain and tumor capillary endothelium was studied during glucocorticoid and radiation treatment. The brain and brain-tumor acidity (pH) was evaluated as a single measurement in patients receiving a low maintenance dose of glucocorticoid. Transport changes and pH were measured in 61 patients with cerebral tumors using 82 Rubidium ( 82 Rb) and 11 C-Dimethyloxa-zolidindione ( 11 C-DMO), respectively, and Positron Emission Tomography (PET). Supplementary studies of tumor and contralateral brain blood flow and blood volume using the C 15 O 2 /PET and C 15 O/PET technique, respectively, were included to validate the 82 Rb/PET model and obtain further information. A total of 125 PET scans were performed. Supplementary studies were undertaken to estimate delay of blood registration and form distribution of arterial blood isotope activity curves. Blood-to-tumor barrier transport was outlined at baseline and at 6 and 24 hours after the start of glucocorticoid treatment, finding a significant decrease in the transpfort. Radiation treatment (2-6 gray) did not alter the blood-to-tumor barrier transport when restudied within one hour in patients receiving glucocorticoid. The pH in brain tumors was as high as 6.88-7.26, suggesting that tumors are more alkalotic than the normal brain. The permeability surface area product and the permeability coefficient were determined form the 82 Rb/PET transport and C 15 O 2 /PET flow studies. Baseline permeability values were comparable to the literature values both for 82 Rb and potassium. No difference in tissue blood volume was seen between 82 Rb/PET and C 15 O/PET models and was of the same magnitude in the tumor and the contralateral tissue. Aspects of tumor alkalosis, tumor edema production, glucocorticoid edema clearance, and relationship between the anti-edema effect of

Blood oxygen transport in common map turtles during simulated hibernation.

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Maginniss, Leigh A; Ekelund, Summer A; Ultsch, Gordon R

2004-01-01

We assessed the effects of cold and submergence on blood oxygen transport in common map turtles (Graptemys geographica). Winter animals were acclimated for 6-7 wk to one of three conditions at 3 degrees C: air breathing (AB-3 degrees C), normoxic submergence (NS-3 degrees C), and hypoxic (PO2=49 Torr) submergence (HS-3 degrees C). NS-3 degrees C turtles exhibited a respiratory alkalosis (pH 8.07; PCO2=7.9 Torr; [lactate]=2.2 mM) relative to AB-3 degrees C animals (pH 7.89; PCO2=13.4 Torr; [lactate]=1.1 mM). HS-3 degrees C animals experienced a profound metabolic acidosis (pH 7.30; PCO2=7.9 Torr; [lactate]=81 mM). NS-3 degrees C turtles exhibited an increased blood O2 capacity; however, isoelectric focusing revealed no seasonal changes in the isohemoglobin (isoHb) profile. Blood O2 affinity was significantly increased by cold acclimation; half-saturation pressures (P50's) for air-breathing turtles at 3 degrees and 22 degrees C were 6.5 and 18.8 Torr, respectively. P50's for winter animals submerged in normoxic and hypoxic water were 5.2 and 6.5 Torr, respectively. CO2 Bohr slopes (Delta logP50/Delta pH) were -0.15, -0.16, and -0.07 for AB-3 degrees C, NS-3 degrees C, and HS-3 degrees C turtles, respectively; the corresponding value for AB-22 degrees C was -0.37. The O2 equilibrium curve (O2EC) shape was similar for AB-3 degrees C and NS-3 degrees C turtles; Hill plot n coefficients ranged from 1.8 to 2.0. The O2EC shape for HS-3 degrees C turtles was anomalous, exhibiting high O2 affinity below P50 and a right-shifted segment above half-saturation. We suggest that increases in Hb-O2 affinity and O2 capacity enhance extrapulmonary O2 uptake by turtles overwintering in normoxic water. The anomalous O2EC shape and reduced CO2 Bohr effect of HS-3 degrees C turtles may also promote some aerobic metabolism in hypoxic water.

The Reproducibility of Blood Acid Base Responses in Male Collegiate Athletes Following Individualised Doses of Sodium Bicarbonate: A Randomised Controlled Crossover Study.

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Gough, Lewis A; Deb, Sanjoy K; Sparks, Andy S; McNaughton, Lars R

2017-10-01

Current evidence suggests sodium bicarbonate (NaHCO 3 ) should be ingested based upon the individualised alkalotic peak of either blood pH or bicarbonate (HCO 3 - ) because of large inter-individual variations (10-180 min). If such a strategy is to be practical, the blood analyte response needs to be reproducible. This study aimed to evaluate the degree of reproducibility of both time to peak (TTP) and absolute change in blood pH, HCO 3 - and sodium (Na + ) following acute NaHCO 3 ingestion. Male participants (n = 15) with backgrounds in rugby, football or sprinting completed six randomised treatments entailing ingestion of two doses of 0.2 g·kg -1 body mass (BM) NaHCO 3 (SBC2a and b), two doses of 0.3 g·kg -1 BM NaHCO 3 (SBC3a and b) or two control treatments (CON1a and b) on separate days. Blood analysis included pH, HCO 3 - and Na + prior to and at regular time points following NaHCO 3 ingestion over a 3-h period. HCO 3 - displayed greater reproducibility than pH in intraclass correlation coefficient (ICC) analysis for both TTP (HCO 3 - SBC2 r = 0.77, P = 0.003; SBC3 r = 0.94, P < 0.001; pH SBC2 r = 0.62, P = 0.044; SBC3 r = 0.71, P = 0.016) and absolute change (HCO 3 - SBC2 r = 0.89, P < 0.001; SBC3 r = 0.76, P = 0.008; pH SBC2 r = 0.84, P = 0.001; SBC3 r = 0.62, P = 0.041). Our results indicate that both TTP and absolute change in HCO 3 - is more reliable than pH. As such, these data provide support for an individualised NaHCO 3 ingestion strategy to consistently elicit peak alkalosis before exercise. Future work should utilise an individualised NaHCO 3 ingestion strategy based on HCO 3 - responses and evaluate effects on exercise performance.

Effects of feeding on arterial blood gases in the American alligator Alligator mississippiensis.

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Busk, M; Overgaard, J; Hicks, J W; Bennett, A F; Wang, T

2000-10-01

Reptiles habitually ingest large meals at infrequent intervals, leading to changes in acid-base status as the net secretion of acid to the stomach causes a metabolic alkalosis (the alkaline tide). In chronically cannulated and undisturbed amphibians and reptiles, the pH changes in arterial blood are, nevertheless, reduced by a concomitant respiratory acidosis (increased P(CO2) caused by a relative hypoventilation). Alligators (Alligator mississippiensis) have been reported to exhibit exceptionally large increases in plasma [HCO3(-)] following feeding, but these studies were based on blood samples obtained by cardiac puncture, so stress and disturbance may have affected the blood gas levels. Furthermore, crocodilian haemoglobin is characterised by a unique binding of HCO3(-) that act to reduce blood oxygen-affinity, and it has been proposed that this feature safeguards oxygen offloading by counteracting pH effects on blood oxygen-affinity. Therefore, to study acid-base regulation and the interaction between the alkaline tide and oxygen transport in more detail, we describe the arterial blood gas composition of chronically cannulated and undisturbed alligators before and after voluntary feeding (meal size 7.5+/-1% of body mass). Digestion was associated with an approximately fourfold increase in metabolic rate (from 0.63+/-0.04 to 2.32+/-0.24 ml O(2) min(-1)kg(-1)) and was accompanied by a small increase in the respiratory gas exchange ratio. The arterial P(O2) of fasting alligators was 60.3+/-6.8 mmHg (1 mmHg = 0.133 kPa) and reached a maximum of 81.3+/-2.7 mmHg at 96 h following feeding; there was only a small increase in lactate levels, so the increased metabolic rate seems to be entirely aerobic. Plasma [HCO3(-)] increased from 24.4+/-1.1 to 36.9+/-1.7 mmol l(-1) (at 24 h), but since arterial P(CO2) increased from 29.0+/-1.1 to 36.8+/-1.3 mmHg, arterial pH remained virtually unaffected (changing from 7.51+/-0.01 to 7.58+/-0.01 at 24 h). The changes in plasma [HCO

A critical analysis of carbonic anhydrase function, respiratory gas exchange, and the acid-base control of secretion in the rectal gland of Squalus acanthias.

Science.gov (United States)

Shuttleworth, Trevor J; Thompson, Jill; Munger, R Stephen; Wood, Chris M

2006-12-01

We compared in vivo responses of rectal gland secretion to carbonic anhydrase (CA) inhibition (10(-4) mol l(-1) acetazolamide) in volume-loaded dogfish with in vitro responses in an isolated-perfused gland stimulated with 5 x 10(-6) mol l(-1) forskolin and removed from systemic influences. We also measured respiratory gas exchange in the perfused gland, described the acid-base status of the secreted fluid, and determined the relative importance of various extracellular and intracellular acid-base parameters in controlling rectal gland secretion in vitro. In vivo, acetazolamide inhibited Cl(-) secretion and decreased pHi in the rectal gland, but interpretation was confounded by an accompanying systemic respiratory acidosis, which would also have contributed to the inhibition. In the perfused gland, M(CO(2)) and M(O(2)) increased in linear relation to increases in Cl(-) secretion rate. CA inhibition (10(-4) mol l(-1) acetazolamide) had no effect on Cl(-) secretion rate or pHi in the perfused gland, in contrast to in vivo, but caused a transitory 30% inhibition of M(CO(2)) (relative to stable M(O(2))) and elevation in secretion P(CO(2)) effects, which peaked at 2 h and attenuated by 3.5-4 h. Secretion was inhibited by acidosis and stimulated by alkalosis; the relationship between relative Cl(-) secretion rate and pHe was almost identical to that seen in vivo. Experimental manipulations of perfusate pH, P(CO(2)) and HCO(3)(-) concentration, together with measurements of pHi, demonstrated that these responses were most strongly correlated with changes in pHe, and were not related to changes in P(CO(2)), extracellular HCO(3)(-), or intracellular HCO(3)(-) levels, though changes in pHi may also have played a role. The acid-base status of the secreted fluid varied with that of the perfusate, secretion pH remaining about 0.3-0.5 units lower, and changing in concert with pHe rather than pHi; secretion HCO(3)(-) concentrations remained low, even in the face of greatly

Hyperventilation and circadian rhythm of the electrical stability of rat myocardium

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Svorc P

2013-08-01

Full Text Available Pavol Svorc,1,2 Alexander Marossy,1 Pavol Svorc Jr2 1Department of Physiology, Medical Faculty, Safarik University, Kosice, Slovak Republic; 2Department of Physiology, Medical Faculty, Ostrava University, Ostrava, Czech Republic Objective: Respiratory alkalosis is an extremely common and complicated problem affecting virtually every organ system where the etiologies may be related to pulmonary or cardiovascular disorders. However, there are only few works describing daytime experiments or synchronization of animals to the external environmental periodicity. The aim of the study is to describe the circadian rhythm of the electrical stability of the heart under hyperventilatory conditions. Methods: Circadian rhythms of the electrical stability of the heart, measured by ventricular arrhythmia threshold ([VAT] measurement in 3 hour intervals, were followed during normal artificial ventilation (40 breaths/minute, tidal volume = 1 mL/100 g; n = 17 and hyperventilation (80 breaths/minute, tidal volume = 2 mL/100 g; n = 7 in pentobarbital (40 mg/kg administered intraperitoneally anesthetized female Wistar rats, after 4 week adaptation on the light/dark regime of 12 hour light/12 hour dark (40%–60% humidity, room temperature of 24°C in cages, two animals/cage with access to food and water ad libitum, with the dark period from 18.00h to 06.00h for 4 weeks. Results: The 24 hour course of the VAT showed the highest susceptibility of the rat ventricular myocardium to arrhythmias between 12.00h and 15.00h, and highest resistance between 19.20h and 00.28h (acrophase −338° in time at 22.53h with confidence intervals −2,880° to −70°, under normoxic conditions. Mesor was 2.59 ± 0.53 mA and amplitude 0.33 ± 0.11 mA. Hyperventilation increased the VAT at each interval of the measurement, but did not change the character of its circadian rhythm. Acrophase was on −40° (02.40h, mesor was increased (2.91 mA, and amplitude was decreased (0.13 m

Sodium bicarbonate ingestion improves Yo-Yo intermittent recovery test 1 performance: a randomized crossover trial

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Dixon H

2017-04-01

through an increased lactate efflux, demonstrated by increased [BLa]. Keywords: alkalosis, anaerobic, blood lactate, ergogenic aid, performance, repeated sprints