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Sample records for kidney disease pkd

  1. Proliferative kidney disease (PKD) agent Tetracapsuloides bryosalmonae in brown trout populations in Estonia.

    Science.gov (United States)

    Dash, Megha; Vasemägi, Anti

    2014-05-13

    Proliferative kidney disease (PKD) caused by the myxozoan parasite Tetracapsuloides bryosalmonae is a serious parasitic disease threatening both farmed and wild salmonid populations, but very little is currently known about the distribution of the parasite in the Baltic Sea region. In this study we (1) report the development of a novel multiplex PCR method for fast and reliable screening of T. bryosalmonae; (2) use this multiplex PCR method to show that the PKD agent T. bryosalmonae is widespread in natural brown trout Salmo trutta L. populations in Estonia; (3) evaluate monthly and yearly variation of T. bryosalmonae prevalence in juvenile trout; (4) assess T. bryosalmonae prevalence in different age-classes of fish (0+ vs. 1+ and older) and report the presence of the PKD agent in the kidneys of returning sea trout spawners; and (5) suggest the freshwater bryozoan Plumatella fungosa as a putative invertebrate host of T. bryosalmonae in Estonia. Our results demonstrate a highly heterogeneous distribution of T. bryosalmonae at the micro-geographic scale, indicating that PKD could have an important negative effect on recruitment in Estonian brown trout populations.

  2. Mutational analysis in patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD): Identification of five mutations in the PKD1 gene.

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    Abdelwahed, Mayssa; Hilbert, Pascale; Ahmed, Asma; Mahfoudh, Hichem; Bouomrani, Salem; Dey, Mouna; Hachicha, Jamil; Kamoun, Hassen; Keskes-Ammar, Leila; Belguith, Neïla

    2018-05-31

    Autosomal Dominant Polycystic Kidney Disease (ADPKD), the most frequent genetic disorder of the kidneys, is characterized by a typical presenting symptoms include cysts development in different organs and a non-cysts manifestations. ADPKD is caused by mutations in PKD1 or PKD2 genes. In this study, we aimed to search for molecular causative defects among PKD1 and PKD2 genes. Eighteen patients were diagnosed based on renal ultrasonography and renal/extra-renal manifestations. Then, Sanger sequencing was performed for PKD1 and PKD2 genes. Multiplex Ligation dependent Probe Amplification method (MLPA) methods was performed for both PKD genes. Mutational analysis of the PKD2 gene revealed the absence of variants and no deletions or duplications of both PKD genes were detected. But three novels mutations i.e. p.S463C exon 7; c. c.11156+2T>C IVS38 and c.8161-1G>A IVS22 and two previously reported c.1522T>C exon 7 and c.412C>T exon 4 mutations in the PKD1 gene were detected. Bioinformatics tools predicted that the novel variants have a pathogenic effects on splicing machinery, pre-mRNA secondary structure and stability and protein stability. Our results highlighted molecular features of Tunisian patients with ADPKD and revealed novel variations that can be utilized in clinical diagnosis and in the evaluation of living kidney donor. To the best of our knowledge, this is the first report of Autosomal Polycystic Kidney Disease in Tunisia. Copyright © 2017. Published by Elsevier B.V.

  3. Exon sequencing of PKD1 gene in an Iranian patient with autosomal-dominant polycystic kidney disease.

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    Hafizi, Atousa; Khatami, Saeid Reza; Galehdari, Hamid; Shariati, Gholamreza; Saberi, Ali Hossein; Hamid, Mohammad

    2014-07-01

    Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic kidney disorders with the incidence of 1 in 1,000 births. ADPKD is genetically heterogeneous with two genes identified: PKD1 (16p13.3, 46 exons) and PKD2 (4q21, 15 exons). Eighty five percent of the patients with ADPKD have at least one mutation in the PKD1 gene. Genetic studies have demonstrated an important allelic variability among patients, but very few data are known about the genetic variation among Iranian populations. In this study, exon direct sequencing of PKD1 was performed in a seven-year old boy with ADPKD and in his parents. The patient's father was ADPKD who was affected without any kidney dysfunction, and the patient's mother was congenitally missing one kidney. Molecular genetic testing found a mutation in all three members of this family. It was a missense mutation GTG>ATG at position 3057 in exon 25 of PKD1. On the other hand, two novel missense mutations were reported just in the 7-year-old boy: ACA>GCA found in exon 15 at codon 2241 and CAC>AAC found in exon 38 at codon 3710. For checking the pathogenicity of these mutations, exons 15, 25, and 38 of 50 unrelated normal cases were sequenced. our findings suggested that GTG>ATG is a polymorphism with high frequency (60%) as well as ACA>GCA and CAC>AAC are polymorphisms with frequencies of 14% and 22%, respectively in the population of Southwest Iran.

  4. PKD

    African Journals Online (AJOL)

    Yomi

    2012-03-27

    Mar 27, 2012 ... PKD1 and PKD2 are the two genes responsible for the development of autosomal dominant ... disease, requiring dialysis or renal transplantation. ... which mutations are present is a challenge. ... MATERIALS AND METHODS.

  5. Novel mTORC1 and 2 Signaling Pathways in Polycystic Kidney Disease (PKD)

    Science.gov (United States)

    2017-09-01

    30 27 32 2K (g) 0.35 0.53 0.36 * 2K/TBW (%) 1.1 2.0 1.2 * Cyst volume (%) 0 40.1 14.6 * No of cysts/kidney 0 5.3 0.8 * Heart wt (g) 0.3 0.15 0.17...some delay in the project. There were no other delays in the project Changes that had a significant impact on expenditures Delays in hiring PRA... Heart wt (g) 0.3 0.15 0.17 15 BUN (mg/dL) 24 29 25 SCr (mg/dL) 0.22 0.33 0.2* 2K/TBW (%) Two kidney/total body weight, *pɘ.05 vs. Pkd1

  6. Cryo-EM structure of the polycystic kidney disease-like channel PKD2L1.

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    Su, Qiang; Hu, Feizhuo; Liu, Yuxia; Ge, Xiaofei; Mei, Changlin; Yu, Shengqiang; Shen, Aiwen; Zhou, Qiang; Yan, Chuangye; Lei, Jianlin; Zhang, Yanqing; Liu, Xiaodong; Wang, Tingliang

    2018-03-22

    PKD2L1, also termed TRPP3 from the TRPP subfamily (polycystic TRP channels), is involved in the sour sensation and other pH-dependent processes. PKD2L1 is believed to be a nonselective cation channel that can be regulated by voltage, protons, and calcium. Despite its considerable importance, the molecular mechanisms underlying PKD2L1 regulations are largely unknown. Here, we determine the PKD2L1 atomic structure at 3.38 Å resolution by cryo-electron microscopy, whereby side chains of nearly all residues are assigned. Unlike its ortholog PKD2, the pore helix (PH) and transmembrane segment 6 (S6) of PKD2L1, which are involved in upper and lower-gate opening, adopt an open conformation. Structural comparisons of PKD2L1 with a PKD2-based homologous model indicate that the pore domain dilation is coupled to conformational changes of voltage-sensing domains (VSDs) via a series of π-π interactions, suggesting a potential PKD2L1 gating mechanism.

  7. Technical Evaluation: Identification of Pathogenic Mutations in PKD1 and PKD2 in Patients with Autosomal Dominant Polycystic Kidney Disease by Next-Generation Sequencing and Use of a Comprehensive New Classification System.

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    Kinoshita, Moritoshi; Higashihara, Eiji; Kawano, Haruna; Higashiyama, Ryo; Koga, Daisuke; Fukui, Takafumi; Gondo, Nobuhisa; Oka, Takehiko; Kawahara, Kozo; Rigo, Krisztina; Hague, Tim; Katsuragi, Kiyonori; Sudo, Kimiyoshi; Takeshi, Masahiko; Horie, Shigeo; Nutahara, Kikuo

    2016-01-01

    Genetic testing of PKD1 and PKD2 is expected to play an increasingly important role in determining allelic influences in autosomal dominant polycystic kidney disease (ADPKD) in the near future. However, to date, genetic testing is not commonly employed because it is expensive, complicated because of genetic heterogeneity, and does not easily identify pathogenic variants. In this study, we developed a genetic testing system based on next-generation sequencing (NGS), long-range polymerase chain reaction, and a new software package. The new software package integrated seven databases and provided access to five cloud-based computing systems. The database integrated 241 polymorphic nonpathogenic variants detected in 140 healthy Japanese volunteers aged >35 years, who were confirmed by ultrasonography as having no cysts in either kidney. Using this system, we identified 60 novel and 30 known pathogenic mutations in 101 Japanese patients with ADPKD, with an overall detection rate of 89.1% (90/101) [95% confidence interval (CI), 83.0%-95.2%]. The sensitivity of the system increased to 93.1% (94/101) (95% CI, 88.1%-98.0%) when combined with multiplex ligation-dependent probe amplification analysis, making it sufficient for use in a clinical setting. In 82 (87.2%) of the patients, pathogenic mutations were detected in PKD1 (95% CI, 79.0%-92.5%), whereas in 12 (12.8%) patients pathogenic mutations were detected in PKD2 (95% CI, 7.5%-21.0%); this is consistent with previously reported findings. In addition, we were able to reconfirm our pathogenic mutation identification results using Sanger sequencing. In conclusion, we developed a high-sensitivity NGS-based system and successfully employed it to identify pathogenic mutations in PKD1 and PKD2 in Japanese patients with ADPKD.

  8. The 10 sea urchin receptor for egg jelly proteins (SpREJ are members of the polycystic kidney disease-1 (PKD1 family

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    Miyata Shinji

    2007-07-01

    Full Text Available Abstract Background Mutations in the human polycystic kidney disease-1 (hPKD1 gene result in ~85% of cases of autosomal dominant polycystic kidney disease, the most frequent human monogenic disease. PKD1 proteins are large multidomain proteins involved in a variety of signal transduction mechanisms. Obtaining more information about members of the PKD1 family will help to clarify their functions. Humans have five hPKD1 proteins, whereas sea urchins have 10. The PKD1 proteins of the sea urchin, Strongylocentrotus purpuratus, are referred to as the Receptor for Egg Jelly, or SpREJ proteins. The SpREJ proteins form a subfamily within the PKD1 family. They frequently contain C-type lectin domains, PKD repeats, a REJ domain, a GPS domain, a PLAT/LH2 domain, 1–11 transmembrane segments and a C-terminal coiled-coil domain. Results The 10 full-length SpREJ cDNA sequences were determined. The secondary structures of their deduced proteins were predicted and compared to the five human hPKD1 proteins. The genomic structures of the 10 SpREJs show low similarity to each other. All 10 SpREJs are transcribed in either embryos or adult tissues. SpREJs show distinct patterns of expression during embryogenesis. Adult tissues show tissue-specific patterns of SpREJ expression. Conclusion Possession of a REJ domain of about 600 residues defines this family. Except for SpREJ1 and 3, that are thought to be associated with the sperm acrosome reaction, the functions of the other SpREJ proteins remain unknown. The sea urchin genome is one-fourth the size of the human genome, but sea urchins have 10 SpREJ proteins, whereas humans have five. Determination of the tissue specific function of each of these proteins will be of interest to those studying echinoderm development. Sea urchins are basal deuterostomes, the line of evolution leading to the vertebrates. The study of individual PKD1 proteins will increase our knowledge of the importance of this gene family.

  9. Standardised Outcomes in Nephrology-Polycystic Kidney Disease (SONG-PKD) : Study protocol for establishing a core outcome set in polycystic kidney disease

    NARCIS (Netherlands)

    Cho, Yeoungjee; Sautenet, Benedicte; Rangan, Gopala; Craig, Jonathan C.; Ong, Albert C. M.; Chapman, Arlene; Ahn, Curie; Chen, Dongping; Coolican, Helen; Kao, Juliana Tze-Wah; Gansevoort, Ron; Perrone, Ronald; Harris, Tess; Torres, Vicente; Pei, York; Kerr, Peter G.; Ryan, Jessica; Gutman, Talia; Howell, Martin; Ju, Angela; Manera, Karine E.; Teixeira-Pinto, Armando; Hamiwka, Lorraine A.; Tong, Allison

    2017-01-01

    Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common potentially life threatening inherited kidney disease and is responsible for 5-10% of cases of end-stage kidney disease (ESKD). Cystic kidneys may enlarge up to 20 times the weight of a normal kidney due to the

  10. Polycystic Kidney Disease (PKD)

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  11. Generation of an induced pluripotent stem cell line, IBMS-iPSC-014-05, from a female autosomal dominant polycystic kidney disease patient carrying a common mutation of R803X in PKD2

    Directory of Open Access Journals (Sweden)

    Ming-Ching Ho

    2017-12-01

    Full Text Available Autosomal dominant polycystic kidney disease (ADPKD is one of the most commonly inherited forms of polycystic kidney disease, and is characterized by the growth of numerous cysts in both kidneys. Here we generated an induced pluripotent stem cell (iPSC line from the peripheral blood mononuclear cells (PBMCs of a 63-year-old female ADPKD patient carrying an R803X mutation in the PKD2 gene using the Sendai-virus delivery system. Downstream characterization of these iPSCs showed that they possessed normal karyotyping, were free of genomic integration, retained the disease-causing PKD2 mutation, expressed pluripotency markers and could differentiate into three germ layers.

  12. RESEARCH ARTICLE Mutational screening of PKD2 gene in north ...

    Indian Academy of Sciences (India)

    2017-01-12

    Jan 12, 2017 ... Background: Polycystic kidney disease (PKD) is a systemic disorder ... in animal models and human kidneys reveals that several proteins are involved in .... for understanding the pathophysiology of PKD in patient cohort from ...

  13. Pkd1 and Pkd2 are required for normal placental development.

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    Miguel A Garcia-Gonzalez

    2010-09-01

    Full Text Available Autosomal dominant polycystic kidney disease (ADPKD is a common cause of inherited renal failure that results from mutations in PKD1 and PKD2. The disorder is characterized by focal cyst formation that involves somatic mutation of the wild type allele in a large fraction of cysts. Consistent with a two-hit mechanism, mice that are homozygous for inactivating mutations of either Pkd1 or Pkd2 develop cystic kidneys, edema and hemorrhage and typically die in midgestation. Cystic kidney disease is unlikely to be the cause of fetal loss since renal function is not required to complete gestation. One hypothesis is that embryonic demise is due to leaky vessels or cardiac pathology.In these studies we used a series of genetically modified Pkd1 and Pkd2 murine models to investigate the cause of embryonic lethality in mutant embryos. Since placental defects are a frequent cause of fetal loss, we conducted histopathologic analyses of placentas from Pkd1 null mice and detected abnormalities of the labyrinth layer beginning at E12.5. We performed placental rescue experiments using tetraploid aggregation and conditional inactivation of Pkd1 with the Meox2 Cre recombinase. We found that both strategies improved the viability of Pkd1 null embryos. Selective inactivation of Pkd1 and Pkd2 in endothelial cells resulted in polyhydramnios and abnormalities similar to those observed in Pkd1(-/- placentas. However, endothelial cell specific deletion of Pkd1 or Pkd2 did not yield the dramatic vascular phenotypes observed in null animals.Placental abnormalities contribute to the fetal demise of Pkd(-/- embryos. Endothelial cell specific deletion of Pkd1 or Pkd2 recapitulates a subset of findings seen in Pkd null animals. Our studies reveal a complex role for polycystins in maintaining vascular integrity.

  14. Novel roles of Pkd2 in male reproductive system development

    OpenAIRE

    Nie, Xuguang; Arend, Lois J

    2014-01-01

    Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common inherited genetic diseases, caused by mutations in PKD1 and/ or PKD2. Infertility and reproductive tract abnormalities in male ADPKD patients are very common and have higher incidence than in the general population. In this work, we reveal novel roles of Pkd2 for male reproductive system development. Disruption of Pkd2 caused dilation of mesonephric tubules/efferent ducts, failure of epididymal coiling, and defecti...

  15. Polycystic kidney disease and cancer after renal transplantation.

    Science.gov (United States)

    Wetmore, James B; Calvet, James P; Yu, Alan S L; Lynch, Charles F; Wang, Connie J; Kasiske, Bertram L; Engels, Eric A

    2014-10-01

    Autosomal dominant polycystic kidney disease (ADPKD), the most common form of polycystic kidney disease (PKD), is a disorder with characteristics of neoplasia. However, it is not known whether renal transplant recipients with PKD have an increased risk of cancer. Data from the Scientific Registry of Transplant Recipients, which contains information on all solid organ transplant recipients in the United States, were linked to 15 population-based cancer registries in the United States. For PKD recipients, we compared overall cancer risk with that in the general population. We also compared cancer incidence in PKD versus non-PKD renal transplant recipients using Poisson regression, and we determined incidence rate ratios (IRRs) adjusted for age, sex, race/ethnicity, dialysis duration, and time since transplantation. The study included 10,166 kidney recipients with PKD and 107,339 without PKD. Cancer incidence in PKD recipients was 1233.6 per 100,000 person-years, 48% higher than expected in the general population (standardized incidence ratio, 1.48; 95% confidence interval [95% CI], 1.37 to 1.60), whereas cancer incidence in non-PKD recipients was 1119.1 per 100,000 person-years. The unadjusted incidence was higher in PKD than in non-PKD recipients (IRR, 1.10; 95% CI, 1.01 to 1.20). However, PKD recipients were older (median age at transplantation, 51 years versus 45 years for non-PKD recipients), and after multivariable adjustment, cancer incidence was lower in PKD recipients than in others (IRR, 0.84; 95% CI, 0.77 to 0.91). The reason for the lower cancer risk in PKD recipients is not known but may relate to biologic characteristics of ADPKD or to cancer risk behaviors associated with ADPKD. Copyright © 2014 by the American Society of Nephrology.

  16. Kidney Disease

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  17. A novel PKD2L1 C-terminal domain critical for trimerization and channel function.

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    Zheng, Wang; Hussein, Shaimaa; Yang, JungWoo; Huang, Jun; Zhang, Fan; Hernandez-Anzaldo, Samuel; Fernandez-Patron, Carlos; Cao, Ying; Zeng, Hongbo; Tang, Jingfeng; Chen, Xing-Zhen

    2015-03-30

    As a transient receptor potential (TRP) superfamily member, polycystic kidney disease 2-like-1 (PKD2L1) is also called TRPP3 and has similar membrane topology as voltage-gated cation channels. PKD2L1 is involved in hedgehog signaling, intestinal development, and sour tasting. PKD2L1 and PKD1L3 form heterotetramers with 3:1 stoichiometry. C-terminal coiled-coil-2 (CC2) domain (G699-W743) of PKD2L1 was reported to be important for its trimerization but independent studies showed that CC2 does not affect PKD2L1 channel function. It thus remains unclear how PKD2L1 proteins oligomerize into a functional channel. By SDS-PAGE, blue native PAGE and mutagenesis we here identified a novel C-terminal domain called C1 (K575-T622) involved in stronger homotrimerization than the non-overlapping CC2, and found that the PKD2L1 N-terminus is critical for dimerization. By electrophysiology and Xenopus oocyte expression, we found that C1, but not CC2, is critical for PKD2L1 channel function. Our co-immunoprecipitation and dynamic light scattering experiments further supported involvement of C1 in trimerization. Further, C1 acted as a blocking peptide that inhibits PKD2L1 trimerization as well as PKD2L1 and PKD2L1/PKD1L3 channel function. Thus, our study identified C1 as the first PKD2L1 domain essential for both PKD2L1 trimerization and channel function, and suggest that PKD2L1 and PKD2L1/PKD1L3 channels share the PKD2L1 trimerization process.

  18. Chromosomal evolution of the PKD1 gene family in primates

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    Krawczak Michael

    2008-09-01

    Full Text Available Abstract Background The autosomal dominant polycystic kidney disease (ADPKD is mostly caused by mutations in the PKD1 (polycystic kidney disease 1 gene located in 16p13.3. Moreover, there are six pseudogenes of PKD1 that are located proximal to the master gene in 16p13.1. In contrast, no pseudogene could be detected in the mouse genome, only a single copy gene on chromosome 17. The question arises how the human situation originated phylogenetically. To address this question we applied comparative FISH-mapping of a human PKD1-containing genomic BAC clone and a PKD1-cDNA clone to chromosomes of a variety of primate species and the dog as a non-primate outgroup species. Results Comparative FISH with the PKD1-cDNA clone clearly shows that in all primate species studied distinct single signals map in subtelomeric chromosomal positions orthologous to the short arm of human chromosome 16 harbouring the master PKD1 gene. Only in human and African great apes, but not in orangutan, FISH with both BAC and cDNA clones reveals additional signal clusters located proximal of and clearly separated from the PKD1 master genes indicating the chromosomal position of PKD1 pseudogenes in 16p of these species, respectively. Indeed, this is in accordance with sequencing data in human, chimpanzee and orangutan. Apart from the master PKD1 gene, six pseudogenes are identified in both, human and chimpanzee, while only a single-copy gene is present in the whole-genome sequence of orangutan. The phylogenetic reconstruction of the PKD1-tree reveals that all human pseudogenes are closely related to the human PKD1 gene, and all chimpanzee pseudogenes are closely related to the chimpanzee PKD1 gene. However, our statistical analyses provide strong indication that gene conversion events may have occurred within the PKD1 family members of human and chimpanzee, respectively. Conclusion PKD1 must have undergone amplification very recently in hominid evolution. Duplicative

  19. Cux1 promotes cell proliferation and polycystic kidney disease progression in an ADPKD mouse model.

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    Porath, Binu; Livingston, Safia; Andres, Erica L; Petrie, Alexandra M; Wright, Joshua C; Woo, Anna E; Carlton, Carol G; Baybutt, Richard; Vanden Heuvel, Gregory B

    2017-10-01

    Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common monogenic hereditary disorders in humans characterized by fluid-filled cysts, primarily in the kidneys. Cux1, a cell cycle regulatory gene highly expressed during kidney development, is elevated in the cyst-lining cells of Pkd1 mutant mice, and in human ADPKD cells. However, forced expression of Cux1 is insufficient to induce cystic disease in transgenic mice or to induce rapid cyst formation after cilia disruption in the kidneys of adult mice. Here we report a double mutant mouse model that has a conditional deletion of the Pkd1 gene in the renal collecting ducts together with a targeted mutation in the Cux1 gene (Pkd1 CD ;Cux1 tm2Ejn ). While kidneys isolated from newborn Pkd1 CD mice exhibit cortical and medullary cysts, kidneys isolated from newborn Pkd1 CD ;Cux1 tm2Ejn-/- mice did not show any cysts. Because Cux1 tm2Ejn-/- are perinatal lethal, we evaluated Pkd1 CD mice that were heterozygote for the Cux1 mutation. Similar to the newborn Pkd1 CD ;Cux1 tm2Ejn-/- mice, newborn Pkd1 CD ;Cux1 tm2Ejn+/- mice did not show any cysts. Comparison of Pkd1 CD and Pkd1 CD ;Cux1 tm2Ejn+/- mice at later stages of development showed a reduction in the severity of PKD in the Pkd1 CD ;Cux1 tm2Ejn+/- mice. Moreover, we observed an increase in expression of the cyclin kinase inhibitor p27, a target of Cux1 repression, in the rescued collecting ducts. Taken together, our results suggest that Cux1 expression in PKD is not directly involved in cystogenesis but promotes cell proliferation required for expansion of existing cysts, primarily by repression of p27. Copyright © 2017 the American Physiological Society.

  20. Pathogenic sequence for dissecting aneurysm formation in a hypomorphic polycystic kidney disease 1 mouse model

    NARCIS (Netherlands)

    Hassane, S.; Claij, N.; Lantinga-van Leeuwen, I.S.; Munsteren, J.C. van; Lent, N. van; Hanemaaijer, R.; Breuning, M.H.; Peters, D.J.M.; Ruiter, M.C. de

    2007-01-01

    OBJECTIVE - Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a multi-system disorder characterized by progressive cyst formation in the kidneys. Serious complications of ADPKD are intracranial and aortic aneurysms. The condition is mainly caused by mutations in the PKD1 or PKD2 gene. We have

  1. Advances in cell proliferation and apoptosis signal pathway and therapies of polycystic kidney disease

    Directory of Open Access Journals (Sweden)

    Xiao-ying LIAN

    2016-12-01

    Full Text Available Polycystic kidney disease (PKD is one of the monogenic inherited diseases. In PKD, excessive cell proliferation and fluid secretion, and disruption of the mechanisms controlling tubular diameter may all lead to cyst formation. Current evidence has demonstrated that intracellular calcium ion and cAMP imbalance drive both abnormal cell proliferation and apoptosis signal pathway. The present paper summarized the evidence implicating calcium ion and cAMP as central players in the signaling pathway of cell proliferation and apoptosis in PKD, and considered the potential therapeutic approaches targeted to slow cyst growth in PKD. DOI: 10.11855/j.issn.0577-7402.2016.11.13

  2. Prenatal MRI Findings of Polycystic Kidney Disease Associated with Holoprosencephaly

    International Nuclear Information System (INIS)

    Koplay, Mustafa; Onbas, Omer; Alper, Fatih; Borekci, Bunyamin

    2009-01-01

    Holoprosencephaly (HPE) and polycystic kidney disease (PKD) are genetically heterogeneous anomalies which can make up part of various syndromes or chromosomal anomalies. Due to the rapid lethality prognosis, early and precise prenatal diagnosis would be of great value. This case report describes extensive PKD involvement, already present in utero, in a patient with HPE and subdural effusion visible by MR imaging. The detailed anatomic information obtained by the MR imaging can guide the surgical planning and can aid antenatal counseling

  3. Prenatal MRI Findings of Polycystic Kidney Disease Associated with Holoprosencephaly

    Energy Technology Data Exchange (ETDEWEB)

    Koplay, Mustafa [Ergani Status Hospital, Diyarbakir (Turkmenistan); Onbas, Omer; Alper, Fatih; Borekci, Bunyamin [Ataturk University, Erzurum (Turkmenistan)

    2009-06-15

    Holoprosencephaly (HPE) and polycystic kidney disease (PKD) are genetically heterogeneous anomalies which can make up part of various syndromes or chromosomal anomalies. Due to the rapid lethality prognosis, early and precise prenatal diagnosis would be of great value. This case report describes extensive PKD involvement, already present in utero, in a patient with HPE and subdural effusion visible by MR imaging. The detailed anatomic information obtained by the MR imaging can guide the surgical planning and can aid antenatal counseling.

  4. Pathogenesis and potential therapy of autosomal dominant polycystic kidney disease

    Directory of Open Access Journals (Sweden)

    O.O. Melnyk

    2017-10-01

    Full Text Available Autosomal dominant polycystic kidney disease (ADPKD is a hereditary disease characterized by progressive growth of the cyst and an increase in the total volume of the kidneys which leads to kidney failure. The main causes of ADPKD are mutations in the genes PKD1 and PKD2 which encode the formation of polycystin-1 and polycystin-2 proteins. There is a connection between structural and functional defects in the primary cilia with the ADPKD. The most promising drugs for the treatment of ADPKD today are vasopressin-2 receptor antagonists, m-TOR and c-AMP inhibitors.

  5. Autosomal dominant polycystic kidney disease in a family with mosaicism and hypomorphic allele.

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    Reiterová, Jana; Štekrová, Jitka; Merta, Miroslav; Kotlas, Jaroslav; Elišáková, Veronika; Lněnička, Petr; Korabečná, Marie; Kohoutová, Milada; Tesař, Vladimír

    2013-03-15

    Autosomal dominant polycystic kidney disease (ADPKD) is the most common form of inherited kidney disease that results in renal failure. ADPKD is a systemic disorder with cysts and connective tissue abnormalities involving many organs. ADPKD caused by mutations in PKD1 gene is significantly more severe than the cases caused by PKD2 gene mutations. The large intra-familial variability of ADPKD highlights a role for genetic background. Here we report a case of ADPKD family initially appearing unlinked to the PKD1 or PKD2 loci and the influence of mosaicism and hypomorphic allele on the variability of the clinical course of the disease. A grandmother with the PKD1 gene mutation in mosaicism (p.Val1105ArgfsX4) and with mild clinical course of ADPKD (end stage renal failure at the age of 77) seemed to have ADPKD because of PKD2 gene mutation. On the other hand, her grandson had a severe clinical course (end stage renal disease at the age of 45) in spite of the early treatment of mild hypertension. There was found by mutational analysis of PKD genes that the severe clinical course was caused by PKD1 gene frameshifting mutation inherited from his father and mildly affected grandmother in combination with inherited hypomorphic PKD1 allele with described missense mutation (p.Thr2250Met) from his clinically healthy mother. The sister with two cysts and with PKD1 hypomorphic allele became the kidney donor to her severely affected brother. We present the first case of ADPKD with the influence of mosaicism and hypomorphic allele of the PKD1 gene on clinical course of ADPKD in one family. Moreover, this report illustrates the role of molecular genetic testing in assessing young related kidney donors for patients with ADPKD.

  6. A Case of New Familiar Genetic Variant of Autosomal Dominant Polycystic Kidney Disease-2: A Case Study.

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    Litvinchuk, Tetiana; Tao, Yunxia; Singh, Ruchi; Vasylyeva, Tetyana L

    2015-01-01

    Autosomal dominant polycystic kidney disease (ADPKD) is characterized by renal cyst formation due to mutations in genes coding for polycystin-1 [PKD1 (85-90% of cases), on ch 16p13.3] and polycystin-2 [PKD2 (10-15% of cases), on ch 4q13-23] and PKD3 gene (gene unmapped). It is also associated with TSC2/PKD1 contiguous gene syndrome. ADPKD is usually inherited, but new mutations without a family history occur in approximately 10% of the cases. A 17-year-old boy was followed up for bilateral cystic kidney disease, hypertension, and obesity since he was 13 years old. The diagnosis was an accidental finding during abdominal CT at age 13 to rule out appendicitis. A renal ultrasonogram also demonstrated a multiple bilateral cysts. Because of parental history of bilateral renal cysts, PKD1 and PKD2, genetic testing was ordered. Results showed, PKD2 variant 1:3 bp deletion of TGT; nucleotide position: 1602-1604; codon position: 512-513; mRNA reading frame maintained. The same mutation was later identified in his father. A smaller number of patients have a defect in the PKD2 locus on chromosome 4 (resulting in PKD2 disease). There are no known published cases on this familiar genetic variant of ADPKD-2 cystic kidney disease. In this case, the disease is present unusually early in life.

  7. PKD1 Mono-Allelic Knockout Is Sufficient to Trigger Renal Cystogenesis in a Mini-Pig Model

    OpenAIRE

    He, Jin; Li, Qiuyan; Fang, Suyun; Guo, Ying; Liu, Tongxin; Ye, Jianhua; Yu, Zhengquan; Zhang, Ran; Zhao, Yaofeng; Hu, Xiaoxiang; Bai, Xueyuan; Chen, Xiangmei; Li, Ning

    2015-01-01

    PKD1 and PKD2 mutations could lead to autosomal dominant polycystic kidney disease (ADPKD), which afflicts millions of people worldwide. Due to the marked differences in the lifespan, size, anatomy, and physiology from humans, rodent ADPKD models cannot fully mimic the disease. To obtain a large animal model that recapitulates the disease, we constructed a mini-pig model by mono-allelic knockout (KO) of PKD1 using zinc finger nuclease. The mono-allelic KO pigs had lower PKD1 expression than t...

  8. Organoid cystogenesis reveals a critical role of microenvironment in human polycystic kidney disease

    Science.gov (United States)

    Cruz, Nelly M.; Song, Xuewen; Czerniecki, Stefan M.; Gulieva, Ramila E.; Churchill, Angela J.; Kim, Yong Kyun; Winston, Kosuke; Tran, Linh M.; Diaz, Marco A.; Fu, Hongxia; Finn, Laura S.; Pei, York; Himmelfarb, Jonathan; Freedman, Benjamin S.

    2017-11-01

    Polycystic kidney disease (PKD) is a life-threatening disorder, commonly caused by defects in polycystin-1 (PC1) or polycystin-2 (PC2), in which tubular epithelia form fluid-filled cysts. A major barrier to understanding PKD is the absence of human cellular models that accurately and efficiently recapitulate cystogenesis. Previously, we have generated a genetic model of PKD using human pluripotent stem cells and derived kidney organoids. Here we show that systematic substitution of physical components can dramatically increase or decrease cyst formation, unveiling a critical role for microenvironment in PKD. Removal of adherent cues increases cystogenesis 10-fold, producing cysts phenotypically resembling PKD that expand massively to 1-centimetre diameters. Removal of stroma enables outgrowth of PKD cell lines, which exhibit defects in PC1 expression and collagen compaction. Cyclic adenosine monophosphate (cAMP), when added, induces cysts in both PKD organoids and controls. These biomaterials establish a highly efficient model of PKD cystogenesis that directly implicates the microenvironment at the earliest stages of the disease.

  9. Mammalian target of rapamycin inhibition in polycystic kidney disease: From bench to bedside

    Directory of Open Access Journals (Sweden)

    Hyun-Jung Kim

    2012-09-01

    Full Text Available Autosomal dominant polycystic kidney disease (ADPKD is the most common life-threatening hereditary disease in the USA resulting in chronic kidney disease and the need for dialysis and transplantation. Approximately 85% of cases of ADPKD are caused by a mutation in the Pkd1 gene that encodes polycystin-1, a large membrane receptor. The Pkd1 gene mutation results in abnormal proliferation in tubular epithelial cells, which plays a crucial role in cyst development and/or growth in PKD. Activation of the proliferative mammalian target of rapamycin (mTOR signaling pathway has been demonstrated in polycystic kidneys from rodents and humans. mTOR inhibition with sirolimus or everolimus decreases cysts in most animal models of PKD including Pkd1 and Pkd2 gene deficient orthologous models of human disease. On the basis of animal studies, human studies were undertaken. Two large randomized clinical trials published in the New England Journal of Medicine of everolimus or sirolimus in ADPKD patients were very unimpressive and associated with a high side-effect profile. Possible reasons for the unimpressive nature of the human studies include their short duration, the high drop-out rate, suboptimal dosing, lack of randomization of “fast” and “slow progressors” and the lack of correlation between kidney size and kidney function in ADPKD. The future of mTOR inhibition in ADPKD is discussed.

  10. Aberrant Regulation of Notch3 Signaling Pathway in Polycystic Kidney Disease.

    Science.gov (United States)

    Idowu, Jessica; Home, Trisha; Patel, Nisha; Magenheimer, Brenda; Tran, Pamela V; Maser, Robin L; Ward, Christopher J; Calvet, James P; Wallace, Darren P; Sharma, Madhulika

    2018-02-20

    Polycystic kidney disease (PKD) is a genetic disorder characterized by fluid-filled cysts in the kidney and liver that ultimately leads to end-stage renal disease. Currently there is no globally approved therapy for PKD. The Notch signaling pathway regulates cellular processes such as proliferation and de-differentiation, which are cellular hallmarks of PKD. Thus we hypothesized that the Notch pathway plays a critical role in PKD. Evaluation of protein expression of Notch signaling components in kidneys of Autosomal Recessive PKD (ARPKD) and Autosomal Dominant PKD (ADPKD) mouse models and of ADPKD patients revealed that Notch pathway members, particularly Notch3, were consistently upregulated or activated in cyst-lining epithelial cells. Notch3 expression correlated with rapidly growing cysts and co-localized with the proliferation marker, PCNA. Importantly, Notch inhibition significantly decreased forskolin-induced Notch3 activation and proliferation of primary human ADPKD cells, and significantly reduced cyst formation and growth of human ADPKD cells cultured in collagen gels. Thus our data indicate that Notch3 is aberrantly activated and facilitates epithelial cell proliferation in PKD, and that inhibition of Notch signaling may prevent cyst formation and growth.

  11. Chronic Kidney Diseases

    Science.gov (United States)

    ... Safe Videos for Educators Search English Español Chronic Kidney Diseases KidsHealth / For Kids / Chronic Kidney Diseases What's ... re talking about your kidneys. What Are the Kidneys? Your kidneys are tucked under your lower ribs ...

  12. Tear drops of kidney: a historical overview of Polycystic Kidney Disease.

    Science.gov (United States)

    Balat, Ayse

    2016-02-01

    Polycystic kidneydisease (PKD) is one of the most common inheritedkidneydiseases causing end stage renal disease. Although it has been in existence with humanity, it was defined in 18th century. The most detailed observations on PKD have been written after the disease of Stephen Bathory, the King of Poland. He had fatigue and chest pain accompanied by unconsciousness within a few days after a hunting trip, and died within 9 days, at the age of 53 years in 1586. Surgeon Jan Zigulitz described the cysts in his kidneys as large like those of a bull, with an uneven and bumpy surface during the mummification. Based on available information, 347 years later, a group of physicians and historians in Krakow concluded that the probable cause of Kings death was PKD and uremia. Unfortunately, PKD did not attracted the interest of physicians until the 18th century. In late 18th century, Matthew Baillie noted that these vesicular cysts in kidney were different from hydatid cysts, and described them as "false hydatids of kidney". In 1888, Flix Lejars used the term of "polycystic kidney" for the first time, and stressed that these cysts were bilateral, and causing clinically identifiable symptoms. At the end of 19th century, the basic clinical signs, and genetic basis of the disease have been better defined. However, the inheritance pattern could only be understood long years later. In this study, the history of PKD, i.e., the tear drops (cysts) of kidney will try to be explained by the light of old and current knowledge.

  13. PKD signaling and pancreatitis

    Science.gov (United States)

    Yuan, Jingzhen; Pandol, Stephen J.

    2016-01-01

    Background Acute pancreatitis is a serious medical disorder with no current therapies directed to the molecular pathogenesis of the disorder. Inflammation, inappropriate intracellular activation of digestive enzymes, and parenchymal acinar cell death by necrosis are the critical pathophysiologic processes of acute pancreatitis. Thus, it is necessary to elucidate the key molecular signals that mediate these pathobiologic processes and develop new therapeutic strategies to attenuate the appropriate signaling pathways in order to improve outcomes for this disease. A novel serine/threonine protein kinase D (PKD) family has emerged as key participants in signal transduction, and this family is increasingly being implicated in the regulation of multiple cellular functions and diseases. Methods This review summarizes recent findings of our group and others regarding the signaling pathway and the biological roles of the PKD family in pancreatic acinar cells. In particular, we highlight our studies of the functions of PKD in several key pathobiologic processes associated with acute pancreatitis in experimental models. Results Our findings reveal that PKD signaling is required for NF-κB activation/inflammation, intracellular zymogen activation, and acinar cell necrosis in rodent experimental pancreatitis. Novel small-molecule PKD inhibitors attenuate the severity of pancreatitis in both in vitro and in vivo experimental models. Further, this review emphasizes our latest advances in the therapeutic application of PKD inhibitors to experimental pancreatitis after the initiation of pancreatitis. Conclusions These novel findings suggest that PKD signaling is a necessary modulator in key initiating pathobiologic processes of pancreatitis, and that it constitutes a novel therapeutic target for treatments of this disorder. PMID:26879861

  14. Polycystic Kidney Disease: Pathogenesis and Potential Therapies

    Science.gov (United States)

    Takiar, Vinita; Caplan, Michael J.

    2011-01-01

    Autosomal dominant polycystic kidney disease (ADPKD) is a prevalent, inherited condition for which there is currently no effective specific clinical therapy. The disease is characterized by the progressive development of fluid-filled cysts derived from renal tubular epithelial cells which gradually compress the parenchyma and compromise renal function. Current interests in the field focus on understanding and exploiting signaling mechanisms underlying disease pathogenesis as well as delineating the role of the primary cilium in cystogenesis. This review highlights the pathogenetic pathways underlying renal cyst formation as well as novel therapeutic targets for the treatment of PKD. PMID:21146605

  15. Identification of novel mutations in Chinese Hans with autosomal dominant polycystic kidney disease

    Directory of Open Access Journals (Sweden)

    Yu Chaowen

    2011-12-01

    Full Text Available Abstract Background Autosomal dominant polycystic kidney disease (ADPKD is the most common inherited renal disease with an incidence of 1 in 400 to 1000. The disease is genetically heterogeneous, with two genes identified: PKD1 (16p13.3 and PKD2 (4q21. Molecular diagnosis of the disease in at-risk individuals is complicated due to the structural complexity of PKD1 gene and the high diversity of the mutations. This study is the first systematic ADPKD mutation analysis of both PKD1 and PKD2 genes in Chinese patients using denaturing high-performance liquid chromatography (DHPLC. Methods Both PKD1 and PKD2 genes were mutation screened in each proband from 65 families using DHPLC followed by DNA sequencing. Novel variations found in the probands were checked in their family members available and 100 unrelated normal controls. Then the pathogenic potential of the variations of unknown significance was examined by evolutionary comparison, effects of amino acid substitutions on protein structure, and effects of splice site alterations using online mutation prediction resources. Results A total of 92 variations were identified, including 27 reported previously. Definitely pathogenic mutations (ten frameshift, ten nonsense, two splicing defects and one duplication were identified in 28 families, and probably pathogenic mutations were found in an additional six families, giving a total detection level of 52.3% (34/65. About 69% (20/29 of the mutations are first reported with a recurrent mutation rate of 31%. Conclusions Mutation study of PKD1 and PKD2 genes in Chinese Hans with ADPKD may contribute to a better understanding of the genetic diversity between different ethnic groups and enrich the mutation database. Besides, evaluating the pathogenic potential of novel variations should also facilitate the clinical diagnosis and genetic counseling of the disease.

  16. Molecular and cellular pathogenesis of autosomal dominant polycystic kidney disease

    Directory of Open Access Journals (Sweden)

    A.P. Bastos

    2011-07-01

    Full Text Available Autosomal dominant polycystic kidney disease (ADPKD is one of the most common human life-threatening monogenic disorders. The disease is characterized by bilateral, progressive renal cystogenesis and cyst and kidney enlargement, often leading to end-stage renal disease, and may include extrarenal manifestations. ADPKD is caused by mutation in one of two genes, PKD1 and PKD2, which encode polycystin-1 (PC1 and polycystin-2 (PC2, respectively. PC2 is a non-selective cation channel permeable to Ca2+, while PC1 is thought to function as a membrane receptor. The cyst cell phenotype includes increased proliferation and apoptosis, dedifferentiation, defective planar polarity, and a secretory pattern associated with extracellular matrix remodeling. The two-hit model for cyst formation has been recently extended by the demonstration that early gene inactivation leads to rapid and diffuse development of renal cysts, while inactivation in adult life is followed by focal and late cyst formation. Renal ischemia/reperfusion, however, can function as a third hit, triggering rapid cyst development in kidneys with Pkd1 inactivation induced in adult life. The PC1-PC2 complex behaves as a sensor in the primary cilium, mediating signal transduction via Ca2+ signaling. The intracellular Ca2+ homeostasis is impaired in ADPKD, being apparently responsible for the cAMP accumulation and abnormal cell proliferative response to cAMP. Activated mammalian target for rapamycin (mTOR and cell cycle dysregulation are also significant features of PKD. Based on the identification of pathways altered in PKD, a large number of preclinical studies have been performed and are underway, providing a basis for clinical trials in ADPKD and helping the design of future trials.

  17. Lysine methyltransferase SMYD2 promotes cyst growth in autosomal dominant polycystic kidney disease.

    Science.gov (United States)

    Li, Linda Xiaoyan; Fan, Lucy X; Zhou, Julie Xia; Grantham, Jared J; Calvet, James P; Sage, Julien; Li, Xiaogang

    2017-06-30

    Autosomal dominant polycystic kidney disease (ADPKD) is driven by mutations in PKD1 and PKD2 genes. Recent work suggests that epigenetic modulation of gene expression and protein function may play a role in ADPKD pathogenesis. In this study, we identified SMYD2, a SET and MYND domain protein with lysine methyltransferase activity, as a regulator of renal cyst growth. SMYD2 was upregulated in renal epithelial cells and tissues from Pkd1-knockout mice as well as in ADPKD patients. SMYD2 deficiency delayed renal cyst growth in postnatal kidneys from Pkd1 mutant mice. Pkd1 and Smyd2 double-knockout mice lived longer than Pkd1-knockout mice. Targeting SMYD2 with its specific inhibitor, AZ505, delayed cyst growth in both early- and later-stage Pkd1 conditional knockout mouse models. SMYD2 carried out its function via methylation and activation of STAT3 and the p65 subunit of NF-κB, leading to increased cystic renal epithelial cell proliferation and survival. We further identified two positive feedback loops that integrate epigenetic regulation and renal inflammation in cyst development: SMYD2/IL-6/STAT3/SMYD2 and SMYD2/TNF-α/NF-κB/SMYD2. These pathways provide mechanisms by which SMYD2 might be induced by cyst fluid IL-6 and TNF-α in ADPKD kidneys. The SMYD2 transcriptional target gene Ptpn13 also linked SMYD2 to other PKD-associated signaling pathways, including ERK, mTOR, and Akt signaling, via PTPN13-mediated phosphorylation.

  18. Microarray-based approach identifies microRNAs and their target functional patterns in polycystic kidney disease

    Directory of Open Access Journals (Sweden)

    Boehn Susanne NE

    2008-12-01

    Full Text Available Abstract Background MicroRNAs (miRNAs play key roles in mammalian gene expression and several cellular processes, including differentiation, development, apoptosis and cancer pathomechanisms. Recently the biological importance of primary cilia has been recognized in a number of human genetic diseases. Numerous disorders are related to cilia dysfunction, including polycystic kidney disease (PKD. Although involvement of certain genes and transcriptional networks in PKD development has been shown, not much is known how they are regulated molecularly. Results Given the emerging role of miRNAs in gene expression, we explored the possibilities of miRNA-based regulations in PKD. Here, we analyzed the simultaneous expression changes of miRNAs and mRNAs by microarrays. 935 genes, classified into 24 functional categories, were differentially regulated between PKD and control animals. In parallel, 30 miRNAs were differentially regulated in PKD rats: our results suggest that several miRNAs might be involved in regulating genetic switches in PKD. Furthermore, we describe some newly detected miRNAs, miR-31 and miR-217, in the kidney which have not been reported previously. We determine functionally related gene sets, or pathways to reveal the functional correlation between differentially expressed mRNAs and miRNAs. Conclusion We find that the functional patterns of predicted miRNA targets and differentially expressed mRNAs are similar. Our results suggest an important role of miRNAs in specific pathways underlying PKD.

  19. An efficient and comprehensive strategy for genetic diagnostics of polycystic kidney disease.

    Directory of Open Access Journals (Sweden)

    Tobias Eisenberger

    Full Text Available Renal cysts are clinically and genetically heterogeneous conditions. Autosomal dominant polycystic kidney disease (ADPKD is the most frequent life-threatening genetic disease and mainly caused by mutations in PKD1. The presence of six PKD1 pseudogenes and tremendous allelic heterogeneity make molecular genetic testing challenging requiring laborious locus-specific amplification. Increasing evidence suggests a major role for PKD1 in early and severe cases of ADPKD and some patients with a recessive form. Furthermore it is becoming obvious that clinical manifestations can be mimicked by mutations in a number of other genes with the necessity for broader genetic testing. We established and validated a sequence capture based NGS testing approach for all genes known for cystic and polycystic kidney disease including PKD1. Thereby, we demonstrate that the applied standard mapping algorithm specifically aligns reads to the PKD1 locus and overcomes the complication of unspecific capture of pseudogenes. Employing careful and experienced assessment of NGS data, the method is shown to be very specific and equally sensitive as established methods. An additional advantage over conventional Sanger sequencing is the detection of copy number variations (CNVs. Sophisticated bioinformatic read simulation increased the high analytical depth of the validation study and further demonstrated the strength of the approach. We further raise some awareness of limitations and pitfalls of common NGS workflows when applied in complex regions like PKD1 demonstrating that quality of NGS needs more than high coverage of the target region. By this, we propose a time- and cost-efficient diagnostic strategy for comprehensive molecular genetic testing of polycystic kidney disease which is highly automatable and will be of particular value when therapeutic options for PKD emerge and genetic testing is needed for larger numbers of patients.

  20. An efficient and comprehensive strategy for genetic diagnostics of polycystic kidney disease.

    Science.gov (United States)

    Eisenberger, Tobias; Decker, Christian; Hiersche, Milan; Hamann, Ruben C; Decker, Eva; Neuber, Steffen; Frank, Valeska; Bolz, Hanno J; Fehrenbach, Henry; Pape, Lars; Toenshoff, Burkhard; Mache, Christoph; Latta, Kay; Bergmann, Carsten

    2015-01-01

    Renal cysts are clinically and genetically heterogeneous conditions. Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent life-threatening genetic disease and mainly caused by mutations in PKD1. The presence of six PKD1 pseudogenes and tremendous allelic heterogeneity make molecular genetic testing challenging requiring laborious locus-specific amplification. Increasing evidence suggests a major role for PKD1 in early and severe cases of ADPKD and some patients with a recessive form. Furthermore it is becoming obvious that clinical manifestations can be mimicked by mutations in a number of other genes with the necessity for broader genetic testing. We established and validated a sequence capture based NGS testing approach for all genes known for cystic and polycystic kidney disease including PKD1. Thereby, we demonstrate that the applied standard mapping algorithm specifically aligns reads to the PKD1 locus and overcomes the complication of unspecific capture of pseudogenes. Employing careful and experienced assessment of NGS data, the method is shown to be very specific and equally sensitive as established methods. An additional advantage over conventional Sanger sequencing is the detection of copy number variations (CNVs). Sophisticated bioinformatic read simulation increased the high analytical depth of the validation study and further demonstrated the strength of the approach. We further raise some awareness of limitations and pitfalls of common NGS workflows when applied in complex regions like PKD1 demonstrating that quality of NGS needs more than high coverage of the target region. By this, we propose a time- and cost-efficient diagnostic strategy for comprehensive molecular genetic testing of polycystic kidney disease which is highly automatable and will be of particular value when therapeutic options for PKD emerge and genetic testing is needed for larger numbers of patients.

  1. Chronic Kidney Disease

    Science.gov (United States)

    You have two kidneys, each about the size of your fist. Their main job is to filter your blood. They remove wastes and ... help control blood pressure, and make hormones. Chronic kidney disease (CKD) means that your kidneys are damaged ...

  2. Proliferative kidney disease in brown trout: infection level, pathology and mortality under field conditions.

    Science.gov (United States)

    Schmidt-Posthaus, Heike; Hirschi, Regula; Schneider, Ernst

    2015-05-21

    Proliferative kidney disease (PKD) is an emerging disease threatening wild salmonid populations. In temperature-controlled aquaria, PKD can cause mortality rates of up to 85% in rainbow trout. So far, no data about PKD-related mortality in wild brown trout Salmo trutta fario are available. The aim of this study was to investigate mortality rates and pathology in brown trout kept in a cage within a natural river habitat known to harbor Tetracapsuloides bryosalmonae. Young-of-the-year (YOY) brown trout, free of T. bryosalmonae, were exposed in the River Wutach, in the northeast of Switzerland, during 3 summer months. Samples of wild brown trout caught by electrofishing near the cage location were examined in parallel. The incidence of PKD in cage-exposed animals (69%) was not significantly different to the disease prevalence of wild fish (82 and 80% in the upstream and downstream locations, respectively). The mortality in cage-exposed animals, however, was as low as 15%. At the termination of the exposure experiment, surviving fish showed histological lesions typical for PKD regression, suggesting that many YOY brown trout survive the initial infection. Our results at the River Wutach suggest that PKD in brown trout does not always result in high mortality under natural conditions.

  3. Glycogen synthase kinase-3β promotes cyst expansion in polycystic kidney disease.

    Science.gov (United States)

    Tao, Shixin; Kakade, Vijayakumar R; Woodgett, James R; Pandey, Pankaj; Suderman, Erin D; Rajagopal, Madhumitha; Rao, Reena

    2015-06-01

    Polycystic kidney diseases (PKDs) are inherited disorders characterized by the formation of fluid filled renal cysts. Elevated cAMP levels in PKDs stimulate progressive cyst enlargement involving cell proliferation and transepithelial fluid secretion often leading to end-stage renal disease. The glycogen synthase kinase-3 (GSK3) family of protein kinases consists of GSK3α and GSK3β isoforms and has a crucial role in multiple cellular signaling pathways. We previously found that GSK3β, a regulator of cell proliferation, is also crucial for cAMP generation and vasopressin-mediated urine concentration by the kidneys. However, the role of GSK3β in the pathogenesis of PKDs is not known. Here we found that GSK3β expression and activity were markedly upregulated and associated with cyst-lining epithelia in the kidneys of mice and humans with PKD. Renal collecting duct-specific gene knockout of GSK3β or pharmacological inhibition of GSK3 effectively slowed down the progression of PKD in mouse models of autosomal recessive or autosomal dominant PKD. GSK3 inactivation inhibited cAMP generation and cell proliferation resulting in reduced cyst expansion, improved renal function, and extended life span. GSK3β inhibition also reduced pERK, c-Myc, and cyclin-D1, known mitogens in proliferation of cystic epithelial cells. Thus, GSK3β has a novel functional role in PKD pathophysiology, and its inhibition may be therapeutically useful to slow down cyst expansion and progression of PKD.

  4. Autosomal dominant polycystic kidney disease caused by somatic and germline mosaicism.

    Science.gov (United States)

    Tan, A Y; Blumenfeld, J; Michaeel, A; Donahue, S; Bobb, W; Parker, T; Levine, D; Rennert, H

    2015-04-01

    Autosomal dominant polycystic kidney disease (ADPKD) is a heterogeneous genetic disorder caused by loss of function mutations of PKD1 or PKD2 genes. Although PKD1 is highly polymorphic and the new mutation rate is relatively high, the role of mosaicism is incompletely defined. Herein, we describe the molecular analysis of ADPKD in a 19-year-old female proband and her father. The proband had a PKD1 truncation mutation c.10745dupC (p.Val3584ArgfsX43), which was absent in paternal peripheral blood lymphocytes (PBL). However, very low quantities of this mutation were detected in the father's sperm DNA, but not in DNA from his buccal cells or urine sediment. Next generation sequencing (NGS) analysis determined the level of this mutation in the father's PBL, buccal cells and sperm to be ∼3%, 4.5% and 10%, respectively, consistent with somatic and germline mosaicism. The PKD1 mutation in ∼10% of her father's sperm indicates that it probably occurred early in embryogenesis. In ADPKD cases where a de novo mutation is suspected because of negative PKD gene testing of PBL, additional evaluation with more sensitive methods (e.g. NGS) of the proband PBL and paternal sperm can enhance detection of mosaicism and facilitate genetic counseling. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  5. At Risk for Kidney Disease?

    Science.gov (United States)

    ... Heart Disease Mineral & Bone Disorder Causes of Chronic Kidney Disease Diabetes and high blood pressure are the most ... blood vessels in your kidneys. Other causes of kidney disease Other causes of kidney disease include a genetic ...

  6. Preimplantation Genetic Diagnosis Counseling in Autosomal Dominant Polycystic Kidney Disease.

    Science.gov (United States)

    Murphy, Erin L; Droher, Madeline L; DiMaio, Miriam S; Dahl, Neera K

    2018-03-30

    Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common hereditary forms of chronic kidney disease. Mutations within PKD1 or PKD2 lead to innumerable fluid-filled cysts in the kidneys and in some instances, end-stage renal disease (ESRD). Affected individuals have a 50% chance of passing the mutation to each of their offspring. Assisted reproductive technology using preimplantation genetic diagnosis (PGD) allows these individuals to reduce this risk to 1% to 2%. We assess the disease burden of 8 individuals with ADPKD who have undergone genetic testing in preparation for PGD. Clinical features that predict high risk for progression to ESRD in patients with ADPKD include genotype, early onset of hypertension, a urologic event before age 35 years, and a large height-adjusted total kidney volume. Patients may have a family history of intracranial aneurysms or complications involving hepatic cysts, which may further influence the decision to pursue PGD. We also explore the cost, risks, and benefits of using PGD. All patients with ADPKD of childbearing potential, regardless of risk for progression to ESRD or risk for a significant disease burden, will likely benefit from genetic counseling. Copyright © 2018 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

  7. Mutational screening of PKD2 gene in the north Indian polycystic ...

    Indian Academy of Sciences (India)

    Sonam Raj

    2017-09-27

    Sep 27, 2017 ... Polycystic kidney disease (PKD) is a systemic disorder which adds majority of renal patients to end stage renal disease. ... This study was performed using PCR and automated DNA sequencing in 84 cases and .... protein is expressed in all segments of nephron except .... patient cohort from northern India.

  8. Autosomal dominant polycystic kidney disease: recent advances in clinical management [version 1; referees: 2 approved

    Directory of Open Access Journals (Sweden)

    Zhiguo Mao

    2016-08-01

    Full Text Available The first clinical descriptions of autosomal dominant polycystic kidney disease (ADPKD go back at least 500 years to the late 16th century. Advances in understanding disease presentation and pathophysiology have mirrored the progress of clinical medicine in anatomy, pathology, physiology, cell biology, and genetics. The identification of PKD1 and PKD2, the major genes mutated in ADPKD, has stimulated major advances, which in turn have led to the first approved drug for this disorder and a fresh reassessment of patient management in the 21st century. In this commentary, we consider how clinical management is likely to change in the coming decade.

  9. Diabetes and Kidney Disease

    Science.gov (United States)

    ... et.al. Clinical manifestations of kidney disease among US adults with diabetes. Journal of the American Medical Association. 2016;316( ... of Washington, Associate Director, Kidney Research Institute ... The National Institute of Diabetes and Digestive and Kidney Diseases Health Information Center ...

  10. Epigenetics of kidney disease.

    Science.gov (United States)

    Wanner, Nicola; Bechtel-Walz, Wibke

    2017-07-01

    DNA methylation and histone modifications determine renal programming and the development and progression of renal disease. The identification of the way in which the renal cell epigenome is altered by environmental modifiers driving the onset and progression of renal diseases has extended our understanding of the pathophysiology of kidney disease progression. In this review, we focus on current knowledge concerning the implications of epigenetic modifications during renal disease from early development to chronic kidney disease progression including renal fibrosis, diabetic nephropathy and the translational potential of identifying new biomarkers and treatments for the prevention and therapy of chronic kidney disease and end-stage kidney disease.

  11. Fibroblast Growth Factor 23 and Kidney Disease Progression in Autosomal Dominant Polycystic Kidney Disease.

    Science.gov (United States)

    Chonchol, Michel; Gitomer, Berenice; Isakova, Tamara; Cai, Xuan; Salusky, Isidro; Pereira, Renata; Abebe, Kaleab; Torres, Vicente; Steinman, Theodor I; Grantham, Jared J; Chapman, Arlene B; Schrier, Robert W; Wolf, Myles

    2017-09-07

    Increases in fibroblast growth factor 23 precede kidney function decline in autosomal dominant polycystic kidney disease; however, the role of fibroblast growth factor 23 in autosomal dominant polycystic kidney disease has not been well characterized. We measured intact fibroblast growth factor 23 levels in baseline serum samples from 1002 participants in the HALT-PKD Study A ( n =540; mean eGFR =91±17 ml/min per 1.73 m 2 ) and B ( n =462; mean eGFR =48±12 ml/min per 1.73 m 2 ). We used linear mixed and Cox proportional hazards models to test associations between fibroblast growth factor 23 and eGFR decline, percentage change in height-adjusted total kidney volume, and composite of time to 50% reduction in eGFR, onset of ESRD, or death. Median (interquartile range) intact fibroblast growth factor 23 was 44 (33-56) pg/ml in HALT-PKD Study A and 69 (50-93) pg/ml in Study B. In adjusted models, annualized eGFR decline was significantly faster in the upper fibroblast growth factor 23 quartile (Study A: quartile 4, -3.62; 95% confidence interval, -4.12 to -3.12 versus quartile 1, -2.51; 95% confidence interval, -2.71 to -2.30 ml/min per 1.73 m 2 ; P for trend kidney volume in adjusted models (quartile 4, 6.76; 95% confidence interval, 5.57 to 7.96 versus quartile 1, 6.04; 95% confidence interval, 5.55 to 6.54; P for trend =0.03). In Study B, compared with the lowest quartile, the highest fibroblast growth factor 23 quartile was associated with elevated risk for the composite outcome (hazard ratio, 3.11; 95% confidence interval, 1.84 to 5.25). Addition of fibroblast growth factor 23 to a model of annualized decline in eGFR≥3.0 ml/min per 1.73 m 2 did not improve risk prediction. Higher serum fibroblast growth factor 23 concentration was associated with kidney function decline, height-adjusted total kidney volume percentage increase, and death in patients with autosomal dominant polycystic kidney disease. However, fibroblast growth factor 23 did not substantially

  12. Kidney Disease Basics

    Science.gov (United States)

    ... disease, you can continue to live a productive life, work, spend time with friends and family, stay physically active, and do other things you enjoy. You may need to change what you eat and add healthy ... active, and enjoy life. Will my kidneys get better? Kidney disease is ...

  13. Obesity and kidney disease

    Directory of Open Access Journals (Sweden)

    Geraldo Bezerra da Silva Junior

    Full Text Available Abstract Obesity has been pointed out as an important cause of kidney diseases. Due to its close association with diabetes and hypertension, excess weight and obesity are important risk factors for chronic kidney disease (CKD. Obesity influences CKD development, among other factors, because it predisposes to diabetic nephropathy, hypertensive nephrosclerosis and focal and segmental glomerulosclerosis. Excess weight and obesity are associated with hemodynamic, structural and histological renal changes, in addition to metabolic and biochemical alterations that lead to kidney disease. Adipose tissue is dynamic and it is involved in the production of "adipokines", such as leptin, adiponectin, tumor necrosis factor-α, monocyte chemoattractant protein-1, transforming growth factor-β and angiotensin-II. A series of events is triggered by obesity, including insulin resistance, glucose intolerance, dyslipidemia, atherosclerosis and hypertension. There is evidence that obesity itself can lead to kidney disease development. Further studies are required to better understand the association between obesity and kidney disease.

  14. Increasing extracellular matrix collagen level and MMP activity induces cyst development in polycystic kidney disease.

    Science.gov (United States)

    Liu, Bin; Li, Chenghai; Liu, Zijuan; Dai, Zonghan; Tao, Yunxia

    2012-09-11

    Polycystic Kidney Disease (PKD) kidneys exhibit increased extracellular matrix (ECM) collagen expression and metalloproteinases (MMPs) activity. We investigated the role of these increases on cystic disease progression in PKD kidneys. We examined the role of type I collagen (collagen I) and membrane bound type 1 MMP (MT1-MMP) on cyst development using both in vitro 3 dimensional (3D) collagen gel culture and in vivo PCK rat model of PKD. We found that collagen concentration is critical in controlling the morphogenesis of MDCK cells cultured in 3D gels. MDCK cells did not form 3D structures at collagen I concentrations lower than 1 mg/ml but began forming tubules when the concentration reaches 1 mg/ml. Significantly, these cells began to form cyst when collagen I concentration reached to 1.2 mg/ml, and the ratios of cyst to tubule structures increased as the collagen I concentration increased. These cells exclusively formed cyst structures at a collagen I concentration of 1.8 mg/ml or higher. Overexpression of MT1-MMP in MDCK cells significantly induced cyst growth in 3D collagen gel culture. Conversely, inhibition of MMPs activity with doxycycline, a FDA approved pan-MMPs inhibitor, dramatically slowed cyst growth. More importantly, the treatment of PCK rats with doxycycline significantly decreased renal tubule cell proliferation and markedly inhibited the cystic disease progression. Our data suggest that increased collagen expression and MMP activity in PKD kidneys may induce cyst formation and expansion. Our findings also suggest that MMPs may serve as a therapeutic target for the treatment of human PKD.

  15. Increasing extracellular matrix collagen level and MMP activity induces cyst development in polycystic kidney disease

    Directory of Open Access Journals (Sweden)

    Liu Bin

    2012-09-01

    Full Text Available Abstract Background Polycystic Kidney Disease (PKD kidneys exhibit increased extracellular matrix (ECM collagen expression and metalloproteinases (MMPs activity. We investigated the role of these increases on cystic disease progression in PKD kidneys. Methods We examined the role of type I collagen (collagen I and membrane bound type 1 MMP (MT1-MMP on cyst development using both in vitro 3 dimensional (3D collagen gel culture and in vivo PCK rat model of PKD. Results We found that collagen concentration is critical in controlling the morphogenesis of MDCK cells cultured in 3D gels. MDCK cells did not form 3D structures at collagen I concentrations lower than 1 mg/ml but began forming tubules when the concentration reaches 1 mg/ml. Significantly, these cells began to form cyst when collagen I concentration reached to 1.2 mg/ml, and the ratios of cyst to tubule structures increased as the collagen I concentration increased. These cells exclusively formed cyst structures at a collagen I concentration of 1.8 mg/ml or higher. Overexpression of MT1-MMP in MDCK cells significantly induced cyst growth in 3D collagen gel culture. Conversely, inhibition of MMPs activity with doxycycline, a FDA approved pan-MMPs inhibitor, dramatically slowed cyst growth. More importantly, the treatment of PCK rats with doxycycline significantly decreased renal tubule cell proliferation and markedly inhibited the cystic disease progression. Conclusions Our data suggest that increased collagen expression and MMP activity in PKD kidneys may induce cyst formation and expansion. Our findings also suggest that MMPs may serve as a therapeutic target for the treatment of human PKD.

  16. Progression of autosomal dominant kidney disease: measurement of the stage transitions of chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Christopher M Blanchette

    2015-04-01

    Full Text Available Background: Autosomal dominant polycystic kidney disease (ADPKD is a progressive genetic disorder characterized by the development of numerous kidney cysts that result in kidney failure. Little is known regarding the key patient characteristics and utilization of healthcare resources for ADPKD patients along the continuum of disease progression. This observational study was designed to describe the characteristics of ADPKD patients and compare them with those of patients with other chronic kidney diseases. Methods: This retrospective cohort study involved patients with a claim for ADPKD or PKD unspecified from 1/1/2000–2/28/2013 and ≥6 months of previous continuous enrollment (baseline within a large database of administrative claims in the USA. A random sample of chronic kidney disease (CKD patients served as comparators. For a subset of ADPKD patients who had only a diagnosis code of unspecified PKD, abstraction of medical records was undertaken to estimate the proportion of patients who had medical chart-confirmed ADPKD. In patients with linked electronic laboratory data, the estimated glomerular filtration rate was calculated via serum creatinine values to determine CKD stage at baseline and during follow-up. Proportions of patients transitioning to another stage and the mean age at transition were calculated. Results: ADPKD patients were, in general, younger and had fewer physician visits, but had more specific comorbidities at observation start compared with CKD patients. ADPKD patients had a longer time in the milder stages and longer duration before recorded transition to a more severe stage compared with CKD patients. Patients with ADPKD at risk of rapid progression had a shorter time-to-end-stage renal disease than patients with CKD and ADPKD patients not at risk, but stage duration was similar between ADPKD patients at risk and those not at risk. Conclusions: These results suggest that distribution of patients by age at transition

  17. About Chronic Kidney Disease

    Science.gov (United States)

    ... detect CKD: blood pressure, urine albumin and serum creatinine. What causes CKD? The two main causes of chronic kidney disease are diabetes and high blood pressure , which are responsible for up to ...

  18. Polycystic kidney disease

    Science.gov (United States)

    ... don't have other diseases may be good candidates for a kidney transplant. Possible Complications Health problems ... www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. ...

  19. Testing for Kidney Disease

    Science.gov (United States)

    ... mean for you. If you have kidney disease, measuring the albumin in your urine helps your provider ... Staff Directory Budget & Legislative Information Advisory & Coordinating Committees Strategic Plans & Reports Research Areas FAQs Jobs at NIDDK ...

  20. Acquired Cystic Kidney Disease

    Science.gov (United States)

    ... including diabetes, high blood pressure, glomerulonephritis, and cys tic kidney diseases. Participants in clinical trials can play ... Life Options Rehabilitation Resource Center c/o Medical Education Institute, Inc. 414 D’Onofrio Drive, Suite 200 ...

  1. End-stage kidney disease

    Science.gov (United States)

    ... stage; Kidney failure - end stage; ESRD; ESKD Images Kidney anatomy References Fogarty DG, Taal MW. A stepped care approach to the management of chronic kidney disease. In: Skorecki K, Chertow GM, Marsden PA, ...

  2. Diabetic kidney disease.

    Science.gov (United States)

    Thomas, Merlin C; Brownlee, Michael; Susztak, Katalin; Sharma, Kumar; Jandeleit-Dahm, Karin A M; Zoungas, Sophia; Rossing, Peter; Groop, Per-Henrik; Cooper, Mark E

    2015-07-30

    The kidney is arguably the most important target of microvascular damage in diabetes. A substantial proportion of individuals with diabetes will develop kidney disease owing to their disease and/or other co-morbidity, including hypertension and ageing-related nephron loss. The presence and severity of chronic kidney disease (CKD) identify individuals who are at increased risk of adverse health outcomes and premature mortality. Consequently, preventing and managing CKD in patients with diabetes is now a key aim of their overall management. Intensive management of patients with diabetes includes controlling blood glucose levels and blood pressure as well as blockade of the renin-angiotensin-aldosterone system; these approaches will reduce the incidence of diabetic kidney disease and slow its progression. Indeed, the major decline in the incidence of diabetic kidney disease (DKD) over the past 30 years and improved patient prognosis are largely attributable to improved diabetes care. However, there remains an unmet need for innovative treatment strategies to prevent, arrest, treat and reverse DKD. In this Primer, we summarize what is now known about the molecular pathogenesis of CKD in patients with diabetes and the key pathways and targets implicated in its progression. In addition, we discuss the current evidence for the prevention and management of DKD as well as the many controversies. Finally, we explore the opportunities to develop new interventions through urgently needed investment in dedicated and focused research. For an illustrated summary of this Primer, visit: http://go.nature.com/NKHDzg.

  3. The Therapeutic Effect of the Antitumor Drug 11 Beta and Related Molecules on Polycystic Kidney Disease

    Science.gov (United States)

    2017-10-01

    models (Somlo, Yale). Preparation work to assemble a collection of probes specific for oxidative stress genes and other PKD specific genes (as part... Worked : 6 Contribution to Project: Performance of experiments including those related to mitochondrial biology in vivo and unfolded protein...1 AWARD NUMBER: W81XWH-15-1-0364 TITLE: THE THERAPEUTIC EFFECT OF THE ANTITUMOR DRUG 11 BETA AND RELATED MOLECULES ON POLYYSTIC KIDNEY DISEASE

  4. Inhibition of Aerobic Glycolysis Attenuates Disease Progression in Polycystic Kidney Disease.

    Directory of Open Access Journals (Sweden)

    Meliana Riwanto

    Full Text Available Dysregulated signaling cascades alter energy metabolism and promote cell proliferation and cyst expansion in polycystic kidney disease (PKD. Here we tested whether metabolic reprogramming towards aerobic glycolysis ("Warburg effect" plays a pathogenic role in male heterozygous Han:SPRD rats (Cy/+, a chronic progressive model of PKD. Using microarray analysis and qPCR, we found an upregulation of genes involved in glycolysis (Hk1, Hk2, Ldha and a downregulation of genes involved in gluconeogenesis (G6pc, Lbp1 in cystic kidneys of Cy/+ rats compared with wild-type (+/+ rats. We then tested the effect of inhibiting glycolysis with 2-deoxyglucose (2DG on renal functional loss and cyst progression in 5-week-old male Cy/+ rats. Treatment with 2DG (500 mg/kg/day for 5 weeks resulted in significantly lower kidney weights (-27% and 2-kidney/total-body-weight ratios (-20% and decreased renal cyst index (-48% compared with vehicle treatment. Cy/+ rats treated with 2DG also showed higher clearances of creatinine (1.98±0.67 vs 1.41±0.37 ml/min, BUN (0.69±0.26 vs 0.40±0.10 ml/min and uric acid (0.38±0.20 vs 0.21±0.10 ml/min, and reduced albuminuria. Immunoblotting analysis of kidney tissues harvested from 2DG-treated Cy/+ rats showed increased phosphorylation of AMPK-α, a negative regulator of mTOR, and restoration of ERK signaling. Assessment of Ki-67 staining indicated that 2DG limits cyst progression through inhibition of epithelial cell proliferation. Taken together, our results show that targeting the glycolytic pathway may represent a promising therapeutic strategy to control cyst growth in PKD.

  5. Rationale, design and objectives of ARegPKD, a European ARPKD registry study.

    Science.gov (United States)

    Ebner, Kathrin; Feldkoetter, Markus; Ariceta, Gema; Bergmann, Carsten; Buettner, Reinhard; Doyon, Anke; Duzova, Ali; Goebel, Heike; Haffner, Dieter; Hero, Barbara; Hoppe, Bernd; Illig, Thomas; Jankauskiene, Augustina; Klopp, Norman; König, Jens; Litwin, Mieczyslaw; Mekahli, Djalila; Ranchin, Bruno; Sander, Anja; Testa, Sara; Weber, Lutz Thorsten; Wicher, Dorota; Yuzbasioglu, Ayse; Zerres, Klaus; Dötsch, Jörg; Schaefer, Franz; Liebau, Max Christoph

    2015-02-18

    Autosomal recessive polycystic kidney disease (ARPKD) is a rare but frequently severe disorder that is typically characterized by cystic kidneys and congenital hepatic fibrosis but displays pronounced phenotypic heterogeneity. ARPKD is among the most important causes for pediatric end stage renal disease and a leading reason for liver-, kidney- or combined liver kidney transplantation in childhood. The underlying pathophysiology, the mechanisms resulting in the observed clinical heterogeneity and the long-term clinical evolution of patients remain poorly understood. Current treatment approaches continue to be largely symptomatic and opinion-based even in most-advanced medical centers. While large clinical trials for the frequent and mostly adult onset autosomal dominant polycystic kidney diseases have recently been conducted, therapeutic initiatives for ARPKD are facing the challenge of small and clinically variable cohorts for which reliable end points are hard to establish. ARegPKD is an international, mostly European, observational study to deeply phenotype ARPKD patients in a pro- and retrospective fashion. This registry study is conducted with the support of the German Society for Pediatric Nephrology (GPN) and the European Study Consortium for Chronic Kidney Disorders Affecting Pediatric Patients (ESCAPE Network). ARegPKD clinically characterizes long-term ARPKD courses by a web-based approach that uses detailed basic data questionnaires in combination with yearly follow-up visits. Clinical data collection is accompanied by associated biobanking and reference histology, thus setting roots for future translational research. The novel registry study ARegPKD aims to characterize miscellaneous subcohorts and to compare the applied treatment options in a large cohort of deeply characterized patients. ARegPKD will thus provide evidence base for clinical treatment decisions and contribute to the pathophysiological understanding of this severe inherited disorder.

  6. Anemia in Chronic Kidney Disease

    Science.gov (United States)

    ... Cysts Solitary Kidney Your Kidneys & How They Work Anemia in Chronic Kidney Disease What is anemia? Anemia is a condition in which the body ... function as well as they should. How is anemia related to chronic kidney disease? Anemia commonly occurs ...

  7. Molecular Diagnostics in Autosomal Dominant Polycystic Kidney Disease: Utility and Limitations

    Science.gov (United States)

    Zhao, Xiao; Paterson, Andrew D.; Zahirieh, Alireza; He, Ning; Wang, Kairong; Pei, York

    2008-01-01

    Background and objectives: Gene-based mutation screening is now available and has the potential to provide diagnostic confirmation or exclusion of autosomal dominant polycystic kidney disease. This study illustrates its utility and limitations in the clinical setting. Design, setting, participants, & measurements: Using a molecular diagnostic service, genomic DNA of one affected individual from each study family was screened for pathologic PKD1 and PKD2 mutations. Bidirectional sequencing was performed to identify sequence variants in all exons and splice junctions of both genes and to confirm the specific mutations in other family members. In two multiplex families, microsatellite markers were genotyped at both PDK1 and PKD2 loci, and pair-wise and multipoint linkage analysis was performed. Results: Three of five probands studied were referred for assessment of renal cystic disease without a family history of autosomal dominant polycystic kidney disease, and two others were younger at-risk members of families with autosomal dominant polycystic kidney disease being evaluated as living-related kidney donors. Gene-based mutation screening identified pathogenic mutations that provided confirmation or exclusion of disease in three probands, but in the other two, only unclassified variants were identified. In one proband in which mutation screening was indeterminate, DNA linkage studies provided strong evidence for disease exclusion. Conclusions: Gene-based mutation screening or DNA linkage analysis should be considered in individuals in whom the diagnosis of autosomal dominant polycystic kidney disease is uncertain because of a lack of family history or equivocal imaging results and in younger at-risk individuals who are being evaluated as living-related kidney donors. PMID:18077784

  8. Chronic Kidney Disease.

    Science.gov (United States)

    Webster, Angela C; Nagler, Evi V; Morton, Rachael L; Masson, Philip

    2017-03-25

    The definition and classification of chronic kidney disease (CKD) have evolved over time, but current international guidelines define this condition as decreased kidney function shown by glomerular filtration rate (GFR) of less than 60 mL/min per 1·73 m 2 , or markers of kidney damage, or both, of at least 3 months duration, regardless of the underlying cause. Diabetes and hypertension are the main causes of CKD in all high-income and middle-income countries, and also in many low-income countries. Incidence, prevalence, and progression of CKD also vary within countries by ethnicity and social determinants of health, possibly through epigenetic influence. Many people are asymptomatic or have non-specific symptoms such as lethargy, itch, or loss of appetite. Diagnosis is commonly made after chance findings from screening tests (urinary dipstick or blood tests), or when symptoms become severe. The best available indicator of overall kidney function is GFR, which is measured either via exogenous markers (eg, DTPA, iohexol), or estimated using equations. Presence of proteinuria is associated with increased risk of progression of CKD and death. Kidney biopsy samples can show definitive evidence of CKD, through common changes such as glomerular sclerosis, tubular atrophy, and interstitial fibrosis. Complications include anaemia due to reduced production of erythropoietin by the kidney; reduced red blood cell survival and iron deficiency; and mineral bone disease caused by disturbed vitamin D, calcium, and phosphate metabolism. People with CKD are five to ten times more likely to die prematurely than they are to progress to end stage kidney disease. This increased risk of death rises exponentially as kidney function worsens and is largely attributable to death from cardiovascular disease, although cancer incidence and mortality are also increased. Health-related quality of life is substantially lower for people with CKD than for the general population, and falls as GFR

  9. Screening for Chronic Kidney Disease

    Science.gov (United States)

    Understanding Task Force Recommendations Screening for Chronic Kidney Disease The U.S. Preventive Services Task Force (Task Force) has issued a final recommendation on Screening for Chronic Kidney Disease (CKD) . This recommendation ...

  10. National Kidney Disease Education Program

    Science.gov (United States)

    ... Living Tips About WIN NIDDK Information Clearinghouses National Kidney Disease Education Program Improving the understanding, detection, and ... Group Learn more about Working Groups Learn about Kidney Disease Find information for people with or at ...

  11. The Jeremiah Metzger Lecture. Polycystic kidney disease: old disease in a new context.

    Science.gov (United States)

    Grantham, Jared J

    2002-01-01

    I want to thank the organizers for inviting me to present the Jeremiah Metzger Lecture at this, the 114th meeting of the ACCA. It is a high honor, indeed, to join a list of very distinguished predecessors. And for this opportunity to tell you about my passion in medicine and science, I am most grateful. Most of you in this room have passing knowledge of polycystic kidney disease, probably hearing about it in your medical school Pathology course where you were shown an especially grotesque, enormously enlarged kidney either encased in transparent plastic or submerged in a bucket of formaldehyde. In that minute or two when PKD was discussed in lecture, you may have been told that this is a rare, hereditary disorder that causes kidney failure and that nothing can be done to alter that course. Unless you chose to specialize in General Internal Medicine or Nephrology, you may not have encountered PKD again until today, despite the fact there are approximately 600,000 PKD patients in the USA and over 10,000,000 worldwide, and it accounts for approximately 5% of non-diabetic dialysis and renal transplant patients (Table 1). I might have overlooked PKD as well had it not been for a close friend that I grew up with who had inherited the disease from his mother. He was very open about the fact that he had cysts in his kidneys that caused bleeding into the urine from time to time, especially after a solid hit during a game of tackle football. We remained friends long after I left home for college and medical school. At an early stage of my research career in medicine, while wondering how nephron segments processed glomerular filtrate, I inadvertently discovered that renal tubules could secrete as well as reabsorb salt and water. This was quite an unexpected finding at the time (1). But it occurred to [table: see text] me that this might be a means to fill renal cysts with fluid and so I decided to learn more about the pathology and pathogenesis of PKD. This didn't take long

  12. Anemia in Chronic Kidney Disease

    Science.gov (United States)

    ... artérielle Heart Disease Mineral & Bone Disorder Anemia in Chronic Kidney Disease What is anemia? Anemia is a condition in ... as they should. How is anemia related to chronic kidney disease? Anemia commonly occurs in people with chronic kidney ...

  13. Environmental pollution and kidney diseases.

    Science.gov (United States)

    Xu, Xin; Nie, Sheng; Ding, Hanying; Hou, Fan Fan

    2018-05-01

    The burden of disease and death attributable to environmental pollution is becoming a public health challenge worldwide, especially in developing countries. The kidney is vulnerable to environmental pollutants because most environmental toxins are concentrated by the kidney during filtration. Given the high mortality and morbidity of kidney disease, environmental risk factors and their effect on kidney disease need to be identified. In this Review, we highlight epidemiological evidence for the association between kidney disease and environmental pollutants, including air pollution, heavy metal pollution and other environmental risk factors. We discuss the potential biological mechanisms that link exposure to environmental pollutants to kidney damage and emphasize the contribution of environmental pollution to kidney disease. Regulatory efforts should be made to control environmental pollution and limit individual exposure to preventable or avoidable environmental risk. Population studies with accurate quantification of environmental exposure in polluted regions, particularly in developing countries, might aid our understanding of the dose-response relationship between pollutants and kidney diseases.

  14. Rare co-occurrence of osteogenesis imperfecta type I and autosomal dominant polycystic kidney disease.

    Science.gov (United States)

    Hoefele, Julia; Mayer, Karin; Marschall, Christoph; Alberer, Martin; Klein, Hanns-Georg; Kirschstein, Martin

    2016-11-01

    There are several clinical reports about the co-occurrence of autosomal dominant polycystic kidney disease (ADPKD) and connective tissue disorders. A simultaneous occurrence of osteogenesis imperfecta (OI) type I and ADPKD has not been observed so far. This report presents the first patient with OI type I and ADPKD. Mutational analysis of PKD1 and COL1A1 in the index patient revealed a heterozygous mutation in each of the two genes. Mutational analysis of the parents indicated the mother as a carrier of the PKD1 mutation and the father as a carrier of the COL1A1 mutation. The simultaneous occurrence of both disorders has an estimated frequency of 3.5:100 000 000. In singular cases, ADPKD can occur in combination with other rare disorders, e.g. connective tissue disorders.

  15. Kidney Disease: Early Detection and Treatment

    Science.gov (United States)

    ... Bar Home Current Issue Past Issues Special Section Kidney Disease: Early Detection and Treatment Past Issues / Winter ... called a "urine albumin-to-creatinine ratio." Treating Kidney Disease Kidney disease is usually a progressive disease, ...

  16. Pregnancy and Kidney Disease

    Science.gov (United States)

    ... who has a kidney transplant have a baby? Yes. If you have a kidney transplant, you are likely to have regular menstrual periods and good general health. Therefore, getting pregnant and having a child is possible. But ...

  17. An epidemic model for the interactions between thermal regime of rivers and transmission of Proliferative Kidney Disease in salmonid fish

    Science.gov (United States)

    Carraro, Luca; Bertuzzo, Enrico; Mari, Lorenzo; Gatto, Marino; Strepparava, Nicole; Hartikainen, Hanna; Rinaldo, Andrea

    2015-04-01

    Proliferative kidney disease (PKD) affects salmonid populations in European and North-American rivers. It is caused by the endoparasitic myxozoan Tetracapsuloides bryosalmonae, which exploits freshwater bryozoans (Fredericella sultana) and salmonids as primary and secondary hosts, respectively. Incidence and mortality, which can reach up to 90-100%, are known to be strongly related to water temperature. PKD has been present in brown trout population for a long time but has recently increased rapidly in incidence and severity causing a decline in fish catches in many countries. In addition, environmental changes are feared to cause PKD outbreaks at higher latitude and altitude regions as warmer temperatures promote disease development. This calls for a better comprehension of the interactions between disease dynamics and the thermal regime of rivers, in order to possibly devise strategies for disease management. In this perspective, a spatially explicit model of PKD epidemiology in riverine host metacommunities is proposed. The model aims at summarizing the knowledge on the modes of transmission of the disease and the life-cycle of the parasite, making the connection between temperature and epidemiological parameters explicit. The model accounts for both local population and disease dynamics of bryozoans and fish and hydrodynamic dispersion of the parasite spores and hosts along the river network. The model is time-hybrid, coupling inter-seasonal and intra-seasonal dynamics, the former being described in a continuous time domain, the latter seen as time steps of a discrete time domain. In order to test the model, a case study is conducted in river Wigger (Cantons of Aargau and Lucerne, Switzerland), where data about water temperature, brown trout and bryozoan populations and PKD prevalence are being collected.

  18. Genetics of Autosomal Recessive Polycystic Kidney Disease and Its Differential Diagnoses

    Directory of Open Access Journals (Sweden)

    Carsten Bergmann

    2018-02-01

    Full Text Available Autosomal recessive polycystic kidney disease (ARPKD is a hepatorenal fibrocystic disorder that is characterized by enlarged kidneys with progressive loss of renal function and biliary duct dilatation and congenital hepatic fibrosis that leads to portal hypertension in some patients. Mutations in the PKHD1 gene are the primary cause of ARPKD; however, the disease is genetically not as homogeneous as long thought and mutations in several other cystogenes can phenocopy ARPKD. The family history usually is negative, both for recessive, but also often for dominant disease genes due to de novo arisen mutations or recessive inheritance of variants in genes that usually follow dominant patterns such as the main ADPKD genes PKD1 and PKD2. Considerable progress has been made in the understanding of polycystic kidney disease (PKD. A reduced dosage of disease proteins leads to the disruption of signaling pathways underlying key mechanisms involved in cellular homeostasis, which may help to explain the accelerated and severe clinical progression of disease course in some PKD patients. A comprehensive knowledge of disease-causing genes is essential for counseling and to avoid genetic misdiagnosis, which is particularly important in the prenatal setting (e.g., preimplantation genetic diagnosis/PGD. For ARPKD, there is a strong demand for early and reliable prenatal diagnosis, which is only feasible by molecular genetic analysis. A clear genetic diagnosis is helpful for many families and improves the clinical management of patients. Unnecessary and invasive measures can be avoided and renal and extrarenal comorbidities early be detected in the clinical course. The increasing number of genes that have to be considered benefit from the advances of next-generation sequencing (NGS which allows simultaneous analysis of a large group of genes in a single test at relatively low cost and has become the mainstay for genetic diagnosis. The broad phenotypic and genetic

  19. Organoids: Modelling polycystic kidney disease

    Science.gov (United States)

    Romagnani, Paola

    2017-11-01

    Cysts were generated from organoids in vitro and the removal of adherent cues was shown to play a key role in polycystic kidney disease progression. These cysts resembled those of diseased tissue phenotypically and were capable of remodelling their microenvironment.

  20. Branched-chain amino acids enhance cyst development in autosomal dominant polycystic kidney disease.

    Science.gov (United States)

    Yamamoto, Junya; Nishio, Saori; Hattanda, Fumihiko; Nakazawa, Daigo; Kimura, Toru; Sata, Michio; Makita, Minoru; Ishikawa, Yasunobu; Atsumi, Tatsuya

    2017-08-01

    Autosomal dominant polycystic kidney disease (ADPKD) is characterized by the progressive development of kidney and liver cysts. The mammalian target of rapamycin (mTOR) cascade is one of the important pathways regulating cyst growth in ADPKD. Branched-chain amino acids (BCAAs), including leucine, play a crucial role to activate mTOR pathway. Therefore, we administered BCAA dissolved in the drinking water to Pkd1 flox/flox :Mx1-Cre (cystic) mice from four to 22 weeks of age after polyinosinic-polycytidylic acid-induced conditional Pkd1 knockout at two weeks of age. The BCAA group showed significantly greater kidney/body weight ratio and higher cystic index in both the kidney and liver compared to the placebo-treated mice. We found that the L-type amino acid transporter 1 that facilitates BCAA entry into cells is strongly expressed in cells lining the cysts. We also found increased cyst-lining cell proliferation and upregulation of mTOR and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathways in the BCAA group. In vitro, we cultured renal epithelial cell lines from Pkd1 null mice with or without leucine. Leucine was found to stimulate cell proliferation, as well as activate mTOR and MAPK/ERK pathways in these cells. Thus, BCAA accelerated disease progression by mTOR and MAPK/ERK pathways. Hence, BCAA may be harmful to patients with ADPKD. Copyright © 2017 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

  1. [Chronic kidney disease and kidney transplantation].

    Science.gov (United States)

    Thuret, R; Timsit, M O; Kleinclauss, F

    2016-11-01

    To report epidemiology and characteristics of end-stage renal disease (ESRD) patients and renal transplant candidates, and to evaluate access to waiting list and results of renal transplantation. An exhaustive systematic review of the scientific literature was performed in the Medline database (http://www.ncbi.nlm.nih.gov) and Embase (http://www.embase.com) using different associations of the following keywords: "chronic kidney disease, epidemiology, kidney transplantation, cost, survival, graft, brain death, cardiac arrest, access, allocation". French legal documents have been reviewed using the government portal (http://www.legifrance.gouv.fr). Articles were selected according to methods, language of publication and relevance. The reference lists were used to identify additional historical studies of interest. Both prospective and retrospective series, in French and English, as well as review articles and recommendations were selected. In addition, French national transplant and health agencies (http://www.agence-biomedecine.fr and http://www.has-sante.fr) databases were screened using identical keywords. A total of 3234 articles, 6 official reports and 3 newspaper articles were identified; after careful selection 99 publications were eligible for our review. The increasing prevalence of chronic kidney disease (CKD) leads to worsen organ shortage. Renal transplantation remains the best treatment option for ESRD, providing recipients with an increased survival and quality of life, at lower costs than other renal replacement therapies. The never-ending lengthening of the waiting list raises issues regarding treatment strategies and candidates' selection, and underlines the limits of organ sharing without additional source of kidneys available for transplantation. Allocation policies aim to reduce medical or geographical disparities regarding enrollment on a waiting list or access to an allotransplant. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

  2. Chronic kidney disease and anticoagulation

    DEFF Research Database (Denmark)

    Sciascia, Savino; Radin, Massimo; Schreiber, Karen

    2017-01-01

    Anticoagulation in patients with impaired kidney function can be challenging since drugs' pharmacokinetics and bioavailability are altered in this setting. Patients with chronic kidney disease (CKD) treated with conventional anticoagulant agents [vitamin K antagonist (VKA), low-molecular weight...... are eliminated via the kidneys pose additional challenges. More recently, two classes of direct oral anticoagulant agents (DOACs) have been investigated for the prevention and management of venous thromboembolic events: the direct factor Xa inhibitors rivaroxaban, apixaban and edoxaban, and the direct thrombin...

  3. Immune gene expression profiling of Proliferative Kidney Disease in rainbow trout Oncorhynchus mykiss reveals a dominance of anti-inflammatory, antibody and T helper cell-like activities.

    Science.gov (United States)

    Gorgoglione, Bartolomeo; Wang, Tiehui; Secombes, Christopher J; Holland, Jason W

    2013-07-16

    The myxozoan Tetracapsuloides bryosalmonae is the causative agent of Proliferative Kidney Disease (PKD) targeting primarily the kidney of infected fish where it causes a chronic lymphoid immunopathology. Although known to be associated with suppression of some cellular aspects of innate immunity and a prominent lymphocytic hyperplasia, there remains a considerable knowledge gap in our understanding of the underlying immune mechanisms driving PKD pathogenesis. To provide further insights, the expression profiles of a panel of innate/inflammatory and adaptive immune molecules were examined in rainbow trout Oncorhynchus mykiss following a natural exposure to the parasite. Relative to controls, fish with early to advanced stages of kidney pathology exhibited up-regulation of the inflammatory cytokines interleukin (IL)-6 and IL-11, although remaining refractory towards genes indicative of macrophage activity. Antimicrobial peptides (AMPs) and anti-inflammatory markers, including cathelicidin (CATH) and IL-10 were markedly up-regulated during clinical disease. Up-regulation of adaptive immune molecules, including cell markers and antibody genes reflect the lymphocytic dominance of this disease and the likely importance of lymphocyte subsets in PKD pathogenesis. Up-regulation of T helper (TH) cell-like response genes and transcription factors implies that T. bryosalmonae may elicit a complex interplay between TH cell subsets. This work, for the first time in the study of fish-myxozoan interactions, suggests that PKD pathogenesis is shaped by an anti-inflammatory phenotype, a profound B cell/antibody response and dysregulated TH cell-like activities. A better understanding of the functional roles of fish immune cells and molecules in PKD pathogenesis may facilitate future development of control measures against this disease.

  4. Immune gene expression profiling of Proliferative Kidney Disease in rainbow trout Oncorhynchus mykiss reveals a dominance of anti-inflammatory, antibody and T helper cell-like activities

    Science.gov (United States)

    2013-01-01

    The myxozoan Tetracapsuloides bryosalmonae is the causative agent of Proliferative Kidney Disease (PKD) targeting primarily the kidney of infected fish where it causes a chronic lymphoid immunopathology. Although known to be associated with suppression of some cellular aspects of innate immunity and a prominent lymphocytic hyperplasia, there remains a considerable knowledge gap in our understanding of the underlying immune mechanisms driving PKD pathogenesis. To provide further insights, the expression profiles of a panel of innate / inflammatory and adaptive immune molecules were examined in rainbow trout Oncorhynchus mykiss following a natural exposure to the parasite. Relative to controls, fish with early to advanced stages of kidney pathology exhibited up-regulation of the inflammatory cytokines interleukin (IL)-6 and IL-11, although remaining refractory towards genes indicative of macrophage activity. Antimicrobial peptides (AMPs) and anti-inflammatory markers, including cathelicidin (CATH) and IL-10 were markedly up-regulated during clinical disease. Up-regulation of adaptive immune molecules, including cell markers and antibody genes reflect the lymphocytic dominance of this disease and the likely importance of lymphocyte subsets in PKD pathogenesis. Up-regulation of T helper (TH) cell-like response genes and transcription factors implies that T. bryosalmonae may elicit a complex interplay between TH cell subsets. This work, for the first time in the study of fish-myxozoan interactions, suggests that PKD pathogenesis is shaped by an anti-inflammatory phenotype, a profound B cell / antibody response and dysregulated TH cell-like activities. A better understanding of the functional roles of fish immune cells and molecules in PKD pathogenesis may facilitate future development of control measures against this disease. PMID:23865616

  5. Diagnosis of diabetic kidney disease

    DEFF Research Database (Denmark)

    Persson, Frederik; Rossing, Peter

    2018-01-01

    Approximately 20% to 40% of patients with type 1 or type 2 diabetes mellitus develop diabetic kidney disease. This is a clinical syndrome characterized by persistent albuminuria (> 300 mg/24 h, or > 300 mg/g creatinine), a relentless decline in glomerular filtration rate (GFR), raised arterial...... sign of diabetic nephropathy, the first symptom is usually peripheral edema, which occurs at a very late stage. Regular, systematic screening for diabetic kidney disease is needed in order to identify patients at risk of or with presymptomatic diabetic kidney disease. Annual monitoring of urinary...

  6. Embolization of renal arteries before transplantation in patients with polycystic kidney disease: a single institution long-term experience

    Energy Technology Data Exchange (ETDEWEB)

    Petitpierre, F.; Cornelis, F.; Lasserre, A.S.; Tricaud, E.; Le Bras, Y.; Grenier, N. [Pellegrin Hospital, Department of Radiology, Bordeaux (France); Couzi, L.; Merville, P. [Pellegrin Hospital, Department of Nephrology, Bordeaux (France); Combe, C.; Ferriere, J.M. [Pellegrin Hospital, Department of Urology, Bordeaux (France)

    2015-11-15

    We aimed to retrospectively assess the long-term safety and efficacy of embolization of renal arteries (ERA) in patients with polycystic kidney disease (PKD) before renal transplantation. Between January 2008 and November 2013, 82 ERA procedures were performed on 76 kidneys in 73 patients (mean age 53 years, range: 34-72). All patients had terminal-stage PKD and were under dialysis and on the renal transplant waiting list with a temporary contraindication due to excessive renal volume. ERA was considered successful in 89.5 % (68/76) of embolized kidneys, meaning that the temporary contraindication for transplantation could be withdrawn for 65 patients (on average 5.6 months, range: 2.8-24.3, after ERA). Mean volume reduction was 40 (range: 2-69) at 3 months and 59 % (35-86) thereafter (both p < 0.001). Post-embolization syndrome occurred after 15 of 82 procedures (18.3 %). The severe complication rate was 4.9 %. Forty-three (67.7 %) transplantations were successfully conducted after ERA, with a mean follow-up of 26.2 months (range: 1.8-59.5), and the estimated 5-year graft survival rate was 95.3 % [95 % CI: 82.7-98.8]. ERA is a safe and effective alternative to nephrectomy before renal transplantation in patients with PKD. (orig.)

  7. Embolization of renal arteries before transplantation in patients with polycystic kidney disease: a single institution long-term experience

    International Nuclear Information System (INIS)

    Petitpierre, F.; Cornelis, F.; Lasserre, A.S.; Tricaud, E.; Le Bras, Y.; Grenier, N.; Couzi, L.; Merville, P.; Combe, C.; Ferriere, J.M.

    2015-01-01

    We aimed to retrospectively assess the long-term safety and efficacy of embolization of renal arteries (ERA) in patients with polycystic kidney disease (PKD) before renal transplantation. Between January 2008 and November 2013, 82 ERA procedures were performed on 76 kidneys in 73 patients (mean age 53 years, range: 34-72). All patients had terminal-stage PKD and were under dialysis and on the renal transplant waiting list with a temporary contraindication due to excessive renal volume. ERA was considered successful in 89.5 % (68/76) of embolized kidneys, meaning that the temporary contraindication for transplantation could be withdrawn for 65 patients (on average 5.6 months, range: 2.8-24.3, after ERA). Mean volume reduction was 40 (range: 2-69) at 3 months and 59 % (35-86) thereafter (both p < 0.001). Post-embolization syndrome occurred after 15 of 82 procedures (18.3 %). The severe complication rate was 4.9 %. Forty-three (67.7 %) transplantations were successfully conducted after ERA, with a mean follow-up of 26.2 months (range: 1.8-59.5), and the estimated 5-year graft survival rate was 95.3 % [95 % CI: 82.7-98.8]. ERA is a safe and effective alternative to nephrectomy before renal transplantation in patients with PKD. (orig.)

  8. The Therapeutic Effect of the Antitumor Drug 11beta and Related Molecules on Polycystic Kidney Disease

    Science.gov (United States)

    2016-10-01

    shown that two parent compounds, 11B-dichloro and 11B- dipropyl, are effective in preventing and delaying cyst growth in two different orthologous mouse...polycystic kidney disease (PKD). In collaboration with the Essigmann lab at MIT, we have shown that two parent compounds, 11B-dichloro and 11B-dipropyl, are...cultured at the permissible temperature (33 °C), then re-plated at 37 °C, in the absence of interferon gamma, conditions in which turn off the large T

  9. The effect of angiotensin-converting-enzyme inhibitors on progression of advanced polycystic kidney disease

    DEFF Research Database (Denmark)

    Jafar, Tazeen H; Stark, Paul C; Schmid, Christopher H

    2005-01-01

    BACKGROUND: It is not known whether angiotensin-converting-enzyme (ACE) inhibitors slow the progression of polycystic kidney disease (PKD). We performed a patient-level meta-analysis to compare the effect of antihypertensive regimens, including ACE inhibitors, to those without ACE inhibitors...... of doubling of baseline serum creatinine or onset of kidney failure). We also performed multivariable linear regression and Cox proportional hazards analyses. Based on previous findings, we searched for interactions between the treatment effect (effect of ACE inhibitors vs. controls) and baseline urine......%) in the ACE inhibitor group and 30 patients (41%) in the control group (P= 0.17). ACE inhibitors had a greater effect on lowering urine protein excretion and slowing kidney disease progression in patients with higher levels of baseline urine protein excretion (interaction P

  10. Sexuality and Chronic Kidney Disease

    Science.gov (United States)

    ... Events Advocacy Donate A to Z Health Guide Sexuality and Kidney Disease Tweet Share Print Email Can ... It's something everyone needs. Many people think that sexuality refers only to sexual intercourse. But sexuality includes ...

  11. Chronic Kidney Disease and Kidney Failure

    Science.gov (United States)

    ... death rates limited life expectancy. Some patients were lucky enough to get a kidney transplant, which greatly ... epidemic rates. Through the 1980s and 1990s, the number of patients developing end-stage kidney failure nearly ...

  12. HIV and chronic kidney disease

    OpenAIRE

    Naicker, Saraladevi; Rahmania, Sadaf; Kopp, Jeffrey B.

    2015-01-01

    Chronic kidney disease (CKD) is a frequent complication of HIV infection, occurring in 3.5 – 48.5%, and occurs as a complication of HIV infection, other co-morbid disease and infections and as a consequence of therapy of HIV infection and its complications. The classic involvement of the kidney by HIV infection is HIV-associated nephropathy (HIVAN), occurring typically in young adults of African ancestry with advanced HIV disease in association with APOL1 high-risk variants. HIV-immune comple...

  13. Chronic kidney disease

    African Journals Online (AJOL)

    disease, together with other related non -communicable diseases. (NCDs), poses not only a threat ... but because if we do not act against NCDs we will also be increasing individual and ... respiratory diseases and cancer. This is in recognition ...

  14. of chronic kidney disease advancement

    Directory of Open Access Journals (Sweden)

    Jolanta Szeliga-Król

    2016-09-01

    Full Text Available Background . Chronic kidney disease (CKD is at present a worldwide health problem. According to the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI, chronic kidney disease has five stages of advancement based on the estimated glomerular filtration rate (eGFR. The formulas that are most frequently used in determining eGFR are the Cockroft–Gault (CG formula, the simplified Modification of Diet in Renal Disease (MDRD formula, and the Chronic Kidney Disease Epidemiology (CKD-EPI Collaboration formula, which is considered the most accurate formula. Objectives . The aim of our study was to compare the CG, simplified MDRD and CKD-EPI formulas for determining eGFR and thus CKD advancement. Material and methods. The study was conducted on a group of 202 patients with previously diagnosed CKD. To calculate the eGFR, the CG, simplified MDRD, and CKD-EPI formulas were used. Patients were assigned a disease stage (from 1 to 5 according to the NKF KDOQI guidelines. Results . The calculated eGFR values varied depending on the formula, which resulted different assignations of patients to CKD stages. The largest difference regarded the qualification of the patients to the first and the fifth stage. A similar number of patients were classed as stage three by all formulas. Differences were also seen in how the formulas classified patients to the second and fourth stages. Conclusions . GFR estimation remains a problematic clinical concern. The CKD stage assigned to patients varies depending on the formula used, a fact which may be particularly significant for general practitioners. Laboratories should apply the CKD-EPI formula for eGFR calculation, as it gives the least false results.

  15. Metformin in chronic kidney disease

    DEFF Research Database (Denmark)

    Heaf, James

    2014-01-01

    Metformin has traditionally been regarded as contraindicated in chronic kidney disease (CKD), though guidelines in recent years have been relaxed to permit therapy if the glomerular filtration rate (GFR) is > 30 mL/min. The main problem is the perceived risk of lactic acidosis (LA). Epidemiological...

  16. Bowel Diseases and Kidneys

    Directory of Open Access Journals (Sweden)

    A.E. Dorofeiev

    2015-09-01

    Full Text Available This review of contemporary publications analyzes the prevalence of combinations of bowel and renal diseases. Special attention is paid to the problem of correlation between bowel diseases and urolithiasis. We consider the possible pathogenic mechanisms of lesions, such as genetically determined violations of intestinal absorption and secretion, changes in the intestinal microbiota, systemic inflammatory response, water and electrolyte disturbances.

  17. The Role of G-Protein-Coupled Receptor Proteolysis Site Cleavage of Polycystin-1 in Renal Physiology and Polycystic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Marie Trudel

    2016-01-01

    Full Text Available Polycystin-1 (PC1 plays an essential role in renal tubular morphogenesis, and PC1 dysfunction causes human autosomal dominant polycystic kidney disease. A fundamental characteristic of PC1 is post-translational modification via cleavage at the juxtamembrane GPCR proteolysis site (GPS motif that is part of the larger GAIN domain. Given the considerable biochemical complexity of PC1 molecules generated in vivo by this process, GPS cleavage has several profound implications on the intracellular trafficking and localization in association with their particular function. The critical nature of GPS cleavage is further emphasized by the increasing numbers of PKD1 mutations that significantly affect this cleavage process. The GAIN domain with the GPS motif therefore represents the key structural element with fundamental importance for PC1 and might be polycystic kidney disease’s (PKD Achilles’ heel in a large spectrum of PKD1 missense mutations. We highlight the central roles of PC1 cleavage for the regulation of its biogenesis, intracellular trafficking and function, as well as its significance in polycystic kidney disease.

  18. Complex interaction between proliferative kidney disease, water temperature and concurrent nematode infection in brown trout.

    Science.gov (United States)

    Schmidt-Posthaus, Heike; Steiner, Pascale; Müller, Barbara; Casanova-Nakayama, Ayako

    2013-04-29

    Proliferative kidney disease (PKD) is a temperature-dependent disease caused by the myxozoan Tetracapsuloides bryosalmonae. It is an emerging threat to wild brown trout Salmo trutta fario populations in Switzerland. Here we examined (1) how PKD prevalence and pathology in young-of-the-year (YOY) brown trout relate to water temperature, (2) whether wild brown trout can completely recover from T. bryosalmonae-induced renal lesions and eliminate T. bryosalmonae over the winter months, and (3) whether this rate and/or extent of the recovery is influenced by concurrent infection. A longitudinal field study on a wild brown trout cohort was conducted over 16 mo. YOY and age 1+ fish were sampled from 7 different field sites with various temperature regimes, and monitored for infection with T. bryosalmonae and the nematode Raphidascaris acus. T. bryosamonae was detectable in brown trout YOY from all sampling sites, with similar renal pathology, independent of water temperature. During winter months, recovery was mainly influenced by the presence or absence of concurrent infection with R. acus larvae. While brown trout without R. acus regenerated completely, concurrently infected brown trout showed incomplete recovery, with chronic renal lesions and incomplete translocation of T. bryosalmonae from the renal interstitium into the tubular lumen. Water temperature seemed to influence complete excretion of T. bryosalmonae, with spores remaining in trout from summer-warm rivers, but absent in trout from summer-cool rivers. In the following summer months, we found PKD infections in 1+ brown trout from all investigated river sites. The pathological lesions indicated a re-infection rather than a proliferation of remaining T. bryosalmonae. However, disease prevalence in 1+ trout was lower than in YOY.

  19. NAFLD and Chronic Kidney Disease.

    Science.gov (United States)

    Marcuccilli, Morgan; Chonchol, Michel

    2016-04-14

    Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in developed countries and it is now considered a risk factor for cardiovascular disease. Evidence linking NAFLD to the development and progression of chronic kidney disease (CKD) is emerging as a popular area of scientific interest. The rise in simultaneous liver-kidney transplantation as well as the significant cost associated with the presence of chronic kidney disease in the NAFLD population make this entity a worthwhile target for screening and therapeutic intervention. While several cross-sectional and case control studies have been published to substantiate these theories, very little data exists on the underlying cause of NAFLD and CKD. In this review, we will discuss the most recent publications on the diagnosis of NAFLD as well new evidence regarding the pathophysiology of NAFLD and CKD as an inflammatory disorder. These mechanisms include the role of obesity, the renin-angiotensin system, and dysregulation of fructose metabolism and lipogenesis in the development of both disorders. Further investigation of these pathways may lead to novel therapies that aim to target the NAFLD and CKD. However, more prospective studies that include information on both renal and liver histology will be necessary in order to understand the relationship between these diseases.

  20. Integrative Approach with Electrophysiological and Theoretical Methods Reveals a New Role of S4 Positively Charged Residues in PKD2L1 Channel Voltage-Sensing.

    Science.gov (United States)

    Numata, Tomohiro; Tsumoto, Kunichika; Yamada, Kazunori; Kurokawa, Tatsuki; Hirose, Shinichi; Nomura, Hideki; Kawano, Mitsuhiro; Kurachi, Yoshihisa; Inoue, Ryuji; Mori, Yasuo

    2017-08-29

    Numerical model-based simulations provide important insights into ion channel gating when experimental limitations exist. Here, a novel strategy combining numerical simulations with patch clamp experiments was used to investigate the net positive charges in the putative transmembrane segment 4 (S4) of the atypical, positively-shifted voltage-dependence of polycystic kidney disease 2-like 1 (PKD2L1) channel. Charge-neutralising mutations (K452Q, K455Q and K461Q) in S4 reduced gating charges, positively shifted the Boltzmann-type activation curve [i.e., open probability (P open )-V curve] and altered the time-courses of activation/deactivation of PKD2L1, indicating that this region constitutes part of a voltage sensor. Numerical reconstruction of wild-type (WT) and mutant PKD2L1-mediated currents necessitated, besides their voltage-dependent gating parameters, a scaling factor that describes the voltage-dependence of maximal conductance, G max . Subsequent single-channel conductance (γ) measurements revealed that voltage-dependence of G max in WT can be explained by the inward-rectifying property of γ, which is greatly changed in PKD2L1 mutants. Homology modelling based on PKD2 and Na V Ab structures suggest that such voltage dependence of P open and γ in PKD2L1 could both reflect the charged state of the S4 domain. The present conjunctive experimental and theoretical approaches provide a framework to explore the undetermined mechanism(s) regulating TRP channels that possess non-classical voltage-dependent properties.

  1. Sour ageusia in two individuals implicates ion channels of the ASIC and PKD families in human sour taste perception at the anterior tongue.

    Directory of Open Access Journals (Sweden)

    Taufiqul Huque

    2009-10-01

    Full Text Available The perception of sour taste in humans is incompletely understood at the receptor cell level. We report here on two patients with an acquired sour ageusia. Each patient was unresponsive to sour stimuli, but both showed normal responses to bitter, sweet, and salty stimuli.Lingual fungiform papillae, containing taste cells, were obtained by biopsy from the two patients, and from three sour-normal individuals, and analyzed by RT-PCR. The following transcripts were undetectable in the patients, even after 50 cycles of amplification, but readily detectable in the sour-normal subjects: acid sensing ion channels (ASICs 1a, 1beta, 2a, 2b, and 3; and polycystic kidney disease (PKD channels PKD1L3 and PKD2L1. Patients and sour-normals expressed the taste-related phospholipase C-beta2, the delta-subunit of epithelial sodium channel (ENaC and the bitter receptor T2R14, as well as beta-actin. Genomic analysis of one patient, using buccal tissue, did not show absence of the genes for ASIC1a and PKD2L1. Immunohistochemistry of fungiform papillae from sour-normal subjects revealed labeling of taste bud cells by antibodies to ASICs 1a and 1beta, PKD2L1, phospholipase C-beta2, and delta-ENaC. An antibody to PKD1L3 labeled tissue outside taste bud cells.These data suggest a role for ASICs and PKDs in human sour perception. This is the first report of sour ageusia in humans, and the very existence of such individuals ("natural knockouts" suggests a cell lineage for sour that is independent of the other taste modalities.

  2. Chronic Kidney Disease

    Science.gov (United States)

    ... and ankles. What causes CKD? The most common causes of CKD are high blood pressure, diabetes, and heart disease. Infections and ... they suspect CKD. Blood pressure test: Checks for high blood pressure. Urine ... is in your urine. Serum creatinine: Checks to see how much waste is in ...

  3. CKD in diabetes: diabetic kidney disease versus nondiabetic kidney disease.

    Science.gov (United States)

    Anders, Hans-Joachim; Huber, Tobias B; Isermann, Berend; Schiffer, Mario

    2018-06-01

    The increasing global prevalence of type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) has prompted research efforts to tackle the growing epidemic of diabetic kidney disease (DKD; also known as diabetic nephropathy). The limited success of much of this research might in part be due to the fact that not all patients diagnosed with DKD have renal dysfunction as a consequence of their diabetes mellitus. Patients who present with CKD and diabetes mellitus (type 1 or type 2) can have true DKD (wherein CKD is a direct consequence of their diabetes status), nondiabetic kidney disease (NDKD) coincident with diabetes mellitus, or a combination of both DKD and NDKD. Preclinical studies using models that more accurately mimic these three entities might improve the ability of animal models to predict clinical trial outcomes. Moreover, improved insights into the pathomechanisms that are shared by these entities - including sodium-glucose cotransporter 2 (SGLT2) and renin-angiotensin system-driven glomerular hyperfiltration and tubular hyper-reabsorption - as well as those that are unique to individual entities might lead to the identification of new treatment targets. Acknowledging that the clinical entity of CKD plus diabetes mellitus encompasses NDKD as well as DKD could help solve some of the urgent unmet medical needs of patients affected by these conditions.

  4. Chronic Kidney Disease in Pregnancy.

    Science.gov (United States)

    Koratala, Abhilash; Bhattacharya, Deepti; Kazory, Amir

    2017-09-01

    With the increasing prevalence of chronic kidney disease (CKD) worldwide, the number of pregnant women with various degrees of renal dysfunction is expected to increase. There is a bidirectional relation between CKD and pregnancy in which renal dysfunction negatively affects pregnancy outcomes, and the pregnancy can have a deleterious impact on various aspects of kidney disease. It has been shown that even mild renal dysfunction can increase considerably the risk of adverse maternal and fetal outcomes. Moreover, data suggest that a history of recovery from acute kidney injury is associated with adverse pregnancy outcomes. In addition to kidney dysfunction, maternal hypertension and proteinuria predispose women to negative outcomes and are important factors to consider in preconception counseling and the process of risk stratification. In this review, we provide an overview of the physiologic renal changes during pregnancy as well as available data regarding CKD and pregnancy outcomes. We also highlight the important management strategies in women with certain selected renal conditions that are seen commonly during the childbearing years. We call for future research on underexplored areas such as the concept of renal functional reserve to develop a potential clinical tool for prognostication and risk stratification of women at higher risk for complications during pregnancy.

  5. First record of proliferative kidney disease agent Tetracapsuloides bryosalmonae in wild brown trout and European grayling in Finland.

    Science.gov (United States)

    Vasemägi, Anti; Nousiainen, Ilkka; Saura, Ari; Vähä, Juha-Pekka; Valjus, Jorma; Huusko, Ari

    2017-06-19

    The myxozoan endoparasite Tetracapsuloides bryosalmonae causes temperature-driven proliferative kidney disease (PKD) in salmonid fishes. Despite the economic and ecological importance of PKD, information about the distribution of the parasite is still scarce. Here, we report for the first time the occurrence of T. bryosalmonae in wild brown trout Salmo trutta and European grayling Thymallus thymallus populations in Finland. We detected T. bryosalmonae at high prevalence in both brown trout and European grayling from the transboundary Finnish-Russian River Koutajoki system (Rivers Oulankajoki, Kuusinkijoki, Kitkajoki, Maaninkajoki, and Juumajoki) in north-eastern Finland. In southern Finland, T. bryosalmonae was detected in River Siuntionjoki young-of-the-year brown trout collected both in 2015 and 2016 (100% prevalence), while the parasite was not observed in fish from 3 other rivers (Ingarskila, Mustajoki, and Vantaanjoki) flowing to the Gulf of Finland. Our results, together with those from recent studies of Atlantic salmon, indicate that T. bryosalmonae is distributed over much higher latitudes in northern Europe than previously appreciated. We expect that increasing water temperatures will likely cause new PKD outbreaks in these more northerly regions in the future.

  6. Characteristics of intracranial aneurysms in the else kröner-fresenius registry of autosomal dominant polycystic kidney disease.

    Science.gov (United States)

    Neumann, Hartmut P H; Malinoc, Angelica; Bacher, Janina; Nabulsi, Zinaida; Ivanovas, Vera; Bruechle, Nadine Ortiz; Mader, Irina; Hoffmann, Michael M; Riegler, Peter; Kraemer-Guth, Annette; Burchardi, Christian; Schaeffner, Elke; Martin, Rodolfo S; Azurmendi, Pablo J; Zerres, Klaus; Jilg, Cordula; Eng, Charis; Gläsker, Sven

    2012-01-01

    Patients who harbor intracranial aneurysms (IAs) run a risk for aneurysm rupture and subsequent subarachnoid hemorrhage which frequently results in permanent deficits or death. Prophylactic treatment of unruptured aneurysms is possible and recommended depending on the size and location of the aneurysm as well as patient age and condition. IAs are major manifestations of autosomal dominant polycystic kidney disease (ADPKD). Current guidelines do not suggest surveillance of IAs in ADPKD except in the setting of family history if IA was known in any relative with ADPKD. Management of IAs in ADPKD is problematic because limited data exist from large studies. We established the Else Kröner-Fresenius Registry for ADPKD in Germany. Clinical data were assessed for age at diagnosis of IAs, stage of renal insufficiency, and number, location and size of IAs as well as family history of cerebral events. Patients with symptomatic or asymptomatic IAs were included. All patients with ADPKD-related IAs were offered mutation scanning of the susceptibility genes for ADPKD, the PKD1 and PKD2 genes. Of 463 eligible ADPKD patients from the population base of Germany, 32 (7%) were found to have IAs, diagnosed at the age of 2-71 years, 19 females and 13 males. Twenty (63%) of these 32 patients were symptomatic, whereas IAs were detected in an asymptomatic stage in 12 patients. IAs were multifocal in 12 and unifocal in 20 patients. In 26 patients (81%), IAs were diagnosed before end-stage renal failure. Twenty-five out of 27 unrelated index cases (93%) had no IAs or cerebral events documented in their relatives with ADPKD. In 16 unrelated index patients and 3 relatives, we detected germline mutations. The mutations were randomly distributed across the PKD1 gene in 14 and the PKD2 gene in 2 index cases. Questionnaires answered for 320/441 ADPKD patients without IAs revealed that only 45/320 (14%) had MR angiography. In ADPKD, rupture of IAs occurs frequently before the start of dialysis

  7. Characteristics of Intracranial Aneurysms in the Else Kröner-Fresenius Registry of Autosomal Dominant Polycystic Kidney Disease

    Science.gov (United States)

    Neumann, Hartmut P.H.; Malinoc, Angelica; Bacher, Janina; Nabulsi, Zinaida; Ivanovas, Vera; Bruechle, Nadine Ortiz; Mader, Irina; Hoffmann, Michael M.; Riegler, Peter; Kraemer-Guth, Annette; Burchardi, Christian; Schaeffner, Elke; Martin, Rodolfo S.; Azurmendi, Pablo J.; Zerres, Klaus; Jilg, Cordula; Eng, Charis; Gläsker, Sven

    2012-01-01

    Background Patients who harbor intracranial aneurysms (IAs) run a risk for aneurysm rupture and subsequent subarachnoid hemorrhage which frequently results in permanent deficits or death. Prophylactic treatment of unruptured aneurysms is possible and recommended depending on the size and location of the aneurysm as well as patient age and condition. IAs are major manifestations of autosomal dominant polycystic kidney disease (ADPKD). Current guidelines do not suggest surveillance of IAs in ADPKD except in the setting of family history if IA was known in any relative with ADPKD. Management of IAs in ADPKD is problematic because limited data exist from large studies. Methods We established the Else Kröner-Fresenius Registry for ADPKD in Germany. Clinical data were assessed for age at diagnosis of IAs, stage of renal insufficiency, and number, location and size of IAs as well as family history of cerebral events. Patients with symptomatic or asymptomatic IAs were included. All patients with ADPKD-related IAs were offered mutation scanning of the susceptibility genes for ADPKD, the PKD1 and PKD2 genes. Results Of 463 eligible ADPKD patients from the population base of Germany, 32 (7%) were found to have IAs, diagnosed at the age of 2–71 years, 19 females and 13 males. Twenty (63%) of these 32 patients were symptomatic, whereas IAs were detected in an asymptomatic stage in 12 patients. IAs were multifocal in 12 and unifocal in 20 patients. In 26 patients (81%), IAs were diagnosed before end-stage renal failure. Twenty-five out of 27 unrelated index cases (93%) had no IAs or cerebral events documented in their relatives with ADPKD. In 16 unrelated index patients and 3 relatives, we detected germline mutations. The mutations were randomly distributed across the PKD1 gene in 14 and the PKD2 gene in 2 index cases. Questionnaires answered for 320/441 ADPKD patients without IAs revealed that only 45/320 (14%) had MR angiography. Conclusion In ADPKD, rupture of IAs occurs

  8. Characteristics of Intracranial Aneurysms in the Else Kröner-Fresenius Registry of Autosomal Dominant Polycystic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Hartmut P.H. Neumann

    2012-10-01

    Full Text Available Background: Patients who harbor intracranial aneurysms (IAs run a risk for aneurysm rupture and subsequent subarachnoid hemorrhage which frequently results in permanent deficits or death. Prophylactic treatment of unruptured aneurysms is possible and recommended depending on the size and location of the aneurysm as well as patient age and condition. IAs are major manifestations of autosomal dominant polycystic kidney disease (ADPKD. Current guidelines do not suggest surveillance of IAs in ADPKD except in the setting of family history if IA was known in any relative with ADPKD. Management of IAs in ADPKD is problematic because limited data exist from large studies. Methods: We established the Else Kröner-Fresenius Registry for ADPKD in Germany. Clinical data were assessed for age at diagnosis of IAs, stage of renal insufficiency, and number, location and size of IAs as well as family history of cerebral events. Patients with symptomatic or asymptomatic IAs were included. All patients with ADPKD-related IAs were offered mutation scanning of the susceptibility genes for ADPKD, the PKD1 and PKD2 genes. Results: Of 463 eligible ADPKD patients from the population base of Germany, 32 (7% were found to have IAs, diagnosed at the age of 2–71 years, 19 females and 13 males. Twenty (63% of these 32 patients were symptomatic, whereas IAs were detected in an asymptomatic stage in 12 patients. IAs were multifocal in 12 and unifocal in 20 patients. In 26 patients (81%, IAs were diagnosed before end-stage renal failure. Twenty-five out of 27 unrelated index cases (93% had no IAs or cerebral events documented in their relatives with ADPKD. In 16 unrelated index patients and 3 relatives, we detected germline mutations. The mutations were randomly distributed across the PKD1 gene in 14 and the PKD2 gene in 2 index cases. Questionnaires answered for 320/441 ADPKD patients without IAs revealed that only 45/320 (14% had MR angiography. Conclusion: In ADPKD

  9. Wasting in chronic kidney disease

    OpenAIRE

    Mak, RH; Ikizler, AT; Kovesdy, CP; Raj, DS; Stenvinkel, P; Kalantar-Zadeh, K

    2011-01-01

    Wasting/cachexia is prevalent among patients with chronic kidney disease (CKD). It is to be distinguished from malnutrition, which is defined as the consequence of insufficient food intake or an improper diet. Malnutrition is characterized by hunger, which is an adaptive response, whereas anorexia is prevalent in patients with wasting/cachexia. Energy expenditure decreases as a protective mechanism in malnutrition whereas it remains inappropriately high in cachexia/wasting. In malnutrition, f...

  10. MicroRNA-106b-5p regulates cisplatin chemosensitivity by targeting polycystic kidney disease-2 in non-small-cell lung cancer.

    Science.gov (United States)

    Yu, Shaorong; Qin, Xiaobing; Chen, Tingting; Zhou, Leilei; Xu, Xiaoyue; Feng, Jifeng

    2017-09-01

    Systemic therapy with cytotoxic agents remains one of the main treatment methods for non-small-cell lung cancer (NSCLC). Cisplatin is a commonly used chemotherapeutic agent, that, when combined with other drugs, is an effective treatment for NSCLC. However, effective cancer therapy is hindered by a patient's resistance to cisplatin. Unfortunately, the potential mechanism underlying such resistance remains unclear. In this study, we explored the mechanism of microRNA-106b-5p (miR-106b-5p), which is involved in the resistance to cisplatin in the A549 cell line of NSCLC. Quantitative real-time PCR was used to test the expression of miR-106-5p in the A549 and the A549/DDP cell line of NSCLC. The cell counting kit-8 assay was used to detect cell viability. Flow cytometry was used to measure cell cycle and cell apoptosis. Luciferase reporter assays and western blot were performed to confirm whether polycystic kidney disease-2 (PKD2) is a direct target gene of miR-106b-5p. Immunohistochemistry was performed to examine the distribution of PKD2 expression in patients who are sensitive and resistant to cisplatin. The experiments indicated that the expression of miR-106b-5p was significantly decreased in A549/DDP compared with that in A549. MiR-106b-5p affected the tolerance of cells to cisplatin by negatively regulating PKD2. Upregulation of miR-106b-5p or downregulation of PKD2 expression can cause A549/DDP cells to become considerably more sensitive to cisplatin. The results showed that miR-106b-5p enhanced the sensitivity of A549/DDP cells to cisplatin by targeting the expression of PKD2. These findings suggest that the use of miR-106b-5p may be a promising clinical strategy in the treatment of NSCLC.

  11. Structure of the polycystic kidney disease TRP channel Polycystin-2 (PC2).

    Science.gov (United States)

    Grieben, Mariana; Pike, Ashley C W; Shintre, Chitra A; Venturi, Elisa; El-Ajouz, Sam; Tessitore, Annamaria; Shrestha, Leela; Mukhopadhyay, Shubhashish; Mahajan, Pravin; Chalk, Rod; Burgess-Brown, Nicola A; Sitsapesan, Rebecca; Huiskonen, Juha T; Carpenter, Elisabeth P

    2017-02-01

    Mutations in either polycystin-1 (PC1 or PKD1) or polycystin-2 (PC2, PKD2 or TRPP1) cause autosomal-dominant polycystic kidney disease (ADPKD) through unknown mechanisms. Here we present the structure of human PC2 in a closed conformation, solved by electron cryomicroscopy at 4.2-Å resolution. The structure reveals a novel polycystin-specific 'tetragonal opening for polycystins' (TOP) domain tightly bound to the top of a classic transient receptor potential (TRP) channel structure. The TOP domain is formed from two extensions to the voltage-sensor-like domain (VSLD); it covers the channel's endoplasmic reticulum lumen or extracellular surface and encloses an upper vestibule, above the pore filter, without blocking the ion-conduction pathway. The TOP-domain fold is conserved among the polycystins, including the homologous channel-like region of PC1, and is the site of a cluster of ADPKD-associated missense variants. Extensive contacts among the TOP-domain subunits, the pore and the VSLD provide ample scope for regulation through physical and chemical stimuli.

  12. Skin changes in chronic kidney disease

    OpenAIRE

    Joanna M. Przepiórka-Kosińska; Katarzyna M. Chyl-Surdacka; Joanna Bartosińska; Dorota Krasowska; Grażyna Chodorowska

    2017-01-01

    Chronic kidney disease causes skin changes which may sometimes be the first sign of kidney failure. Specific skin changes include acquired perforating dermatosis, porphyria cutanea tarda, pseudoporphyria, calcinosis and nephrogenic systemic fibrosis. The majority of patients present with cutaneous manifestations which are classified as non-specific, including xerosis, pruritus, pigmentation disturbances, nail plate abnormalities, uraemic frost and gynaecomastia. Treatment improving kidney fun...

  13. Skin changes in chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Joanna M. Przepiórka-Kosińska

    2017-04-01

    Full Text Available Chronic kidney disease causes skin changes which may sometimes be the first sign of kidney failure. Specific skin changes include acquired perforating dermatosis, porphyria cutanea tarda, pseudoporphyria, calcinosis and nephrogenic systemic fibrosis. The majority of patients present with cutaneous manifestations which are classified as non-specific, including xerosis, pruritus, pigmentation disturbances, nail plate abnormalities, uraemic frost and gynaecomastia. Treatment improving kidney function (dialysis therapy or kidney transplantation also leads to the resolution of skin lesions.

  14. Expression of Nek1 during kidney development and cyst formation in multiple nephron segments in the Nek1-deficient kat2J mouse model of polycystic kidney disease.

    Science.gov (United States)

    Chen, Yumay; Chiang, Huai-Chin; Litchfield, Patricia; Pena, Michelle; Juang, Charity; Riley, Daniel J

    2014-07-17

    Neks, mammalian orthologs of the fungal protein kinase never-in-mitosis A, have been implicated in the pathogenesis of polycystic kidney disease. Among them, Nek1 is the primary protein inactivated in kat2J mouse models of PKD. We report the expression pattern of Nek1 and characterize the renal cysts that develop in kat2J mice. Nek1 is detectable in all murine tissues but its expression in wild type and kat2J heterozygous kidneys decrease as the kidneys mature, especially in tubular epithelial cells. In the embryonic kidney, Nek1 expression is most prominent in cells that will become podocytes and proximal tubules. Kidney development in kat2J homozygous mice is aberrant early, before the appearance of gross cysts: developing cortical zones are thin, populated by immature glomeruli, and characterized by excessive apoptosis of several cell types. Cysts in kat2J homozygous mice form postnatally in Bowman's space as well as different tubular subtypes. Late in life, kat2J heterozygous mice form renal cysts and the cells lining these cysts lack staining for Nek1. The primary cilia of cells lining cysts in kat2J homozygous mice are morphologically diverse: in some cells they are unusually long and in others there are multiple cilia of varying lengths. Our studies indicate that Nek1 deficiency leads to disordered kidney maturation, and cysts throughout the nephron.

  15. Hereditary Causes of Kidney Stones and Chronic Kidney Disease

    Science.gov (United States)

    Edvardsson, Vidar O.; Goldfarb, David S.; Lieske, John C.; Beara-Lasic, Lada; Anglani, Franca; Milliner, Dawn S.; Palsson, Runolfur

    2013-01-01

    Adenine phosphoribosyltransferase (APRT) deficiency, cystinuria, Dent disease, familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) and primary hyperoxaluria (PH) are rare but important causes of severe kidney stone disease and/or chronic kidney disease in children. Recurrent kidney stone disease and nephrocalcinosis, particularly in pre-pubertal children, should alert the physician to the possibility of an inborn error of metabolism as the underlying cause. Unfortunately, the lack of recognition and knowledge of the five disorders has frequently resulted in an unacceptable delay in diagnosis and treatment, sometimes with grave consequences. A high index of suspicion coupled with early diagnosis may reduce or even prevent the serious long-term complications of these diseases. In this paper, we review the epidemiology, clinical features, diagnosis, treatment and outcome of patients with APRT deficiency, cystinuria, Dent disease, FHHNC and PH with emphasis on childhood manifestations. PMID:23334384

  16. Periodontal Disease and Decreased Kidney Function in Japanese Elderly

    NARCIS (Netherlands)

    Iwasaki, Masanori; Taylor, George W.; Nesse, Willem; Vissink, Arjan; Yoshihara, Akihiro; Miyazaki, Hideo

    Background: Early detection of decreased kidney function can help prevent the progression of kidney disease to kidney failure and cardiovascular events. Potentially significant associations between kidney function and periodontal disease have been reported in cross-sectional studies. However, no

  17. Fetal polycystic kidney disease: Pathological overview

    Directory of Open Access Journals (Sweden)

    Sunita B Patil

    2013-01-01

    Full Text Available Polycystic kidney disease is a rare developmental anomaly inherited as autosomal dominant or autosomal recessive. It is characterized by cystic dilatation of the collecting ducts frequently associated with hepatic involvement and progression to renal failure. It is included in the differential diagnosis of cystic diseases of the kidney. We report a case of polycystic kidney disease, in 22 weeks fetus incidentally detected on routine antenatal ultrasonography and confirmed by fetal autopsy. This report elucidates the importance of early diagnosis and intervention in cystic kidney diseases.

  18. [Skin and chronic kidney disease].

    Science.gov (United States)

    Rizzo, Raffaella; Mancini, Elena; Santoro, Antonio

    2014-01-01

    Kidneys and skin are seldom considered associated, but their relationship is more closer than generally believed. In some immunological diseases (SLE...) and genetic syndromes (tuberous sclerosis, Fabrys disease...) the cutaneous manifestations are integral parts of the clinical picture. In advanced uremia, besides the well-known itching skin lesions, calciphylaxis may appear, a typical example of cutaneous involvement secondary to the metabolic complications (calcium-phosphate imbalance) of the renal disease. Nephrogenic systemic fibrosis appears only in patients with renal failure and it has a very severe prognosis due to the systemic organ involvement. Moreover, there is a heterogeneous group of metabolic diseases, with renal involvement, that may be accompanied by skin lesions, either related to the disease itself or to its complications (diabetes mellitus, porphyrias). In systemic amyloidosis, fibrils may deposit even in dermis leading to different skin lesions. In some heroin abusers, in the presence of suppurative lesions in the sites of needle insertion, renal amyloidosis should be suspected, secondary to the chronic inflammation. Atheroembolic disease is nowadays frequently observed, as a consequence of the increasing number of invasive intravascular manoeuvres. Skin manifestations like livedo reticularis or the blue toe syndrome are the most typical signs, but often renal dysfunction is also present. In all these conditions, the skin lesion may be a first sign, a warning, that should arouse the suspicion of a more complex pathology, even with renal involvement. Being aware of this relationship is fundamental to accelerate the diagnostic process.

  19. Prevalence of chronic kidney disease after preeclampsia.

    Science.gov (United States)

    Lopes van Balen, Veronica Agatha; Spaan, Julia Jeltje; Cornelis, Tom; Spaanderman, Marc Erich August

    2017-06-01

    Preeclampsia (PE), an endothelial disease that affects kidney function during pregnancy, is correlated to an increased future risk of cardiovascular and chronic kidney disease. The Kidney Disease Improving Global Outcomes (KDIGO) 2012 guideline emphasizes the combined role of glomerular filtration rate (GFR) and albuminuria in determining the frequency of monitoring of kidney function. In this study we evaluated the prevalence of CKD in women with a history of PE. We investigated how many seemingly healthy women required monitoring of kidney function according to the KDIGO guideline. We included 775 primiparous women with a history of PE. They were at least 4 months postpartum, and had no pre-existing hypertension, diabetes or kidney disease. We estimated GFR by the CKD-Epidemiology equation and urinary albumin loss by albumin creatinine ratio in a 24-h urine collection. Most women, 669 (86.3 %), had a normal GFR and absent albuminuria. Based on the KDIGO guideline, 13.7 % would require at least yearly monitoring of kidney function. Only 1.4 % were classified to be at high risk for kidney function deterioration. Monitoring of kidney function seems relevant for about one in seven women with a history of PE, mainly due to albuminuria. Albuminuria should be evaluated postpartum to identify those women that need further monitoring of kidney function.

  20. Viruses & kidney disease: beyond HIV

    Science.gov (United States)

    Waldman, Meryl; Marshall, Vickie; Whitby, Denise; Kopp, Jeffrey B.

    2008-01-01

    HIV-infected patients may acquire new viral co-infections; they may also experience the reactivation or worsening of existing viral infections, including active, smoldering, or latent infections. HIV-infected patients may be predisposed to these viral infections due to immunodeficiency or to risk factors common to HIV and other viruses. A number of these affect the kidney, either by direct infection or by deposition of immune complexes. In this review we discuss the renal manifestations and treatment of hepatitis C virus, BK virus, adenovirus, cytomegalovirus, and parvovirus B19 in patients with HIV disease. We also discuss an approach to the identification of new viral renal pathogens, using a viral gene chip to identify viral DNA or RNA. PMID:19013331

  1. Polycystin 1 loss of function is directly linked to an imbalance in G-protein signaling in the kidney.

    Science.gov (United States)

    Zhang, Bo; Tran, Uyen; Wessely, Oliver

    2018-03-22

    The development of the kidney relies on the establishment and maintenance of a precise tubular diameter of its functional units, the nephrons. This process is disrupted in polycystic kidney disease (PKD), resulting in dilations of the nephron and renal cyst formation. In the course of exploring G-protein-coupled signaling in the Xenopus pronephric kidney, we discovered that loss of the G-protein α subunit, Gnas, results in a PKD phenotype. Polycystin 1, one of the genes mutated in human PKD, encodes a protein resembling a G-protein-coupled receptor. Furthermore, deletion of the G-protein-binding domain present in the intracellular C terminus of polycystin 1 impacts functionality. A comprehensive analysis of all the G-protein α subunits expressed in the Xenopus pronephric kidney demonstrates that polycystin 1 recruits a select subset of G-protein α subunits and that their knockdown - as in the case of Gnas - results in a PKD phenotype. Mechanistically, the phenotype is caused by increased endogenous G-protein β/γ signaling and can be reversed by pharmacological inhibitors as well as knocking down Gnb1. Together, our data support the hypothesis that G proteins are recruited to the intracellular domain of PKD1 and that this interaction is crucial for its function in the kidney. © 2018. Published by The Company of Biologists Ltd.

  2. Disease modeling in genetic kidney diseases: zebrafish.

    Science.gov (United States)

    Schenk, Heiko; Müller-Deile, Janina; Kinast, Mark; Schiffer, Mario

    2017-07-01

    Growing numbers of translational genomics studies are based on the highly efficient and versatile zebrafish (Danio rerio) vertebrate model. The increasing types of zebrafish models have improved our understanding of inherited kidney diseases, since they not only display pathophysiological changes but also give us the opportunity to develop and test novel treatment options in a high-throughput manner. New paradigms in inherited kidney diseases have been developed on the basis of the distinct genome conservation of approximately 70 % between zebrafish and humans in terms of existing gene orthologs. Several options are available to determine the functional role of a specific gene or gene sets. Permanent genome editing can be induced via complete gene knockout by using the CRISPR/Cas-system, among others, or via transient modification by using various morpholino techniques. Cross-species rescues succeeding knockdown techniques are employed to determine the functional significance of a target gene or a specific mutation. This article summarizes the current techniques and discusses their perspectives.

  3. Epidemiology of hypertensive kidney disease.

    Science.gov (United States)

    Udani, Suneel; Lazich, Ivana; Bakris, George L

    2011-01-01

    The prevalence of hypertension, chronic kidney disease (CKD) and end-stage renal disease (ESRD) attributable to hypertension continues to rise worldwide. Identifying the precise prevalence of CKD attributable to hypertension is difficult owing to the absence of uniform criteria to establish a diagnosis of hypertensive nephropathy. Despite the increasing prevalence of CKD-associated hypertension, awareness of hypertension among individuals with CKD remains suboptimal and rates of blood-pressure control remain poor. Targeted subgroups involved in studies of CKD seem to reach better rates of blood-pressure control, suggesting that this therapeutic goal can be achieved in patients with CKD. Elevated blood-pressure levels are associated with CKD progression. However, the optimal blood-pressure level and pharmacological agent remains unclear. Physicians treating patients with CKD must recognize the importance of maintaining optimal salt and volume balance to achieve blood-pressure goals. Furthermore, agents that modify the renin-angiotensin-aldosterone axis can be an important adjunct to therapy and physicians must monitor expected changes in serum creatinine and electrolyte levels after their administration. Hypertension remains a common factor complicating CKD. Future investigations identifying early signs of hypertension-related CKD, increasing awareness of the effects of hypertension in CKD and determining optimal therapeutic interventions might help reduce the incidence of hypertensive nephropathy.

  4. Definition and classification of chronic kidney disease : A position statement from Kidney Disease: Improving Global Outcomes (KDIGO)

    NARCIS (Netherlands)

    Levey, Andrew S.; Eckardt, Kai Uwe; Tsukamoto, Yusuke; Levin, Adeera; Coresh, Josef; Rossert, Jerome; de Zeeuw, Dick; Hostetter, Thomas H.; Lameire, Norbert; Eknoyan, Garabed

    Chronic kidney disease (CKD) is a worldwide public health problem, with adverse outcomes of kidney failure, cardiovascular disease (CVD), and premature death. A simple definition and classification of kidney disease is necessary for international development and implementation of clinical practice

  5. Kidney injury molecule-1 in renal disease

    NARCIS (Netherlands)

    Waanders, Femke; van Timmeren, Mirjan M.; Stegeman, Coen A.; Bakker, Stephan J. L.; van Goor, Harry

    Kidney injury molecule-1 (KIM-1) is a marker for renal proximal tubular damage, the hallmark of virtually all proteinuric, toxic and ischaemic kidney diseases. KIM-1 has gained increasing interest because of its possible pathophysiological role in modulating tubular damage and repair. In this

  6. [The use of diuretics in kidney disease].

    Science.gov (United States)

    Heramb, Lene; Hallan, Stein; Aasarød, Knut

    2014-04-29

    Diuretics are an important part of the therapy for a number of medical conditions such as heart, liver and kidney failure and hypertension. This article presents updated knowledge on the use of diuretics in kidney disease. The article is based on a literature search in PubMed, information obtained from textbooks on neurophysiology and kidney disease and on the authors' clinical experience. Kidney disease affects the pharmacokinetics and pharmacodynamics of diuretics, and this must be taken into account when selecting a drug and determining the dosage. This applies particularly to nephrotic syndrome and severe chronic renal disease (GFR diuretics is crucial to the rational use of diuretics in renal disease. Dose titration under close clinical monitoring and an optimal dosage interval make it possible to find the lowest possible effective dose and reduce the occurrence of side effects.

  7. Cholesterol Crystal Embolism and Chronic Kidney Disease.

    Science.gov (United States)

    Li, Xuezhu; Bayliss, George; Zhuang, Shougang

    2017-05-24

    Renal disease caused by cholesterol crystal embolism (CCE) occurs when cholesterol crystals become lodged in small renal arteries after small pieces of atheromatous plaques break off from the aorta or renal arteries and shower the downstream vascular bed. CCE is a multisystemic disease but kidneys are particularly vulnerable to atheroembolic disease, which can cause an acute, subacute, or chronic decline in renal function. This life-threatening disease may be underdiagnosed and overlooked as a cause of chronic kidney disease (CKD) among patients with advanced atherosclerosis. CCE can result from vascular surgery, angiography, or administration of anticoagulants. Atheroembolic renal disease has various clinical features that resemble those found in other kidney disorders and systemic diseases. It is commonly misdiagnosed in clinic, but confirmed by characteristic renal biopsy findings. Therapeutic options are limited, and prognosis is considered to be poor. Expanding knowledge of atheroembolic renal disease due to CCE opens perspectives for recognition, diagnosis, and treatment of this cause of progressive renal insufficiency.

  8. Vitamins and Minerals in Kidney Disease

    Science.gov (United States)

    ... Donate A to Z Health Guide Vitamins and Minerals in Kidney Disease Tweet Share Print Email Are ... you need to know. What are vitamins and minerals? Vitamins and minerals are substances your body needs ...

  9. Management of patients with chronic kidney disease

    African Journals Online (AJOL)

    management of the complications of CKD, e.g. renal anaemia, ... ARTICLE. Management of patients with chronic kidney disease. T Gerntholtz,1 FCP (SA); G Paget,2 ..... Telmisartan, ramipril, or both in patients at high risk for vascular events.

  10. Diagnostic approach to chronic kidney disease

    African Journals Online (AJOL)

    syndrome may suggest disorders such as polycystic kidney disease,. Alport syndrome, focal ... metabolic syndrome assists with the evaluation of the patient's cardiovascular risk .... found during heavy exercise, fever and stress. • Common ...

  11. Common acquired kidney diseases in children

    African Journals Online (AJOL)

    5. Common acquired kidney diseases in children. Examination of the urine is probably the most important investigation ... result from the same streptococcal infection. .... musculoskeletal system. ... Prediction of histopathology from clinical.

  12. Percutaneous Nephrolithotomy and Chronic Kidney Disease

    DEFF Research Database (Denmark)

    Sairam, Krish; Scoffone, Cesare M; Alken, Peter

    2012-01-01

    by glomerular filtration rate, including chronic kidney disease stages 0/I/II-greater than 60, stage III-30 to 59 and stages IV/V-less than 30 ml/minute/1.73 m(2). Patient characteristics, operative characteristics, outcomes and morbidity were assessed. RESULTS: Estimated glomerular filtration rate data were...... available on 5,644 patients, including 4,436 with chronic kidney disease stages 0/I/II, 994 with stage III and 214 with stages IV/V. A clinically significant minority of patients with nephrolithiasis presented with severe chronic kidney disease. A greater number of patients with stages IV/V previously...... underwent percutaneous nephrolithotomy, ureteroscopy or nephrostomy and had positive urine cultures than less severely affected patients, consistent with the higher incidence of staghorn stones in these patients. Patients with chronic kidney disease stages IV/V had statistically significantly worse...

  13. Chronic Disease and Childhood Development: Kidney Disease and Transplantation.

    Science.gov (United States)

    Klein, Susan D.; Simmons, Roberta G.

    As part of a larger study of transplantation and chronic disease and the family, 124 children (10-18 years old) who were chronically ill with kidney disease (n=72) or were a year or more post-transplant (n=52) were included in a study focusing on the effects of chronic kidney disease and transplantation on children's psychosocial development. Ss…

  14. PKD2 mutation in an Iranian autosomal dominant polycystic kidney disease family with misleading linkage analysis data

    Directory of Open Access Journals (Sweden)

    Mona Entezam

    2016-06-01

    Conclusion: Although analysis of additive informative polymorphic markers can overcome the misleading haplotype data, it is limited because of the lack of other highly polymorphic microsatellite markers closer to the gene. Direct mutation screening can identify the causative mutation in the apparently unlinked pedigree; moreover, it is the only approach to achieve the confirmed diagnosis in individuals with equivocal imaging results.

  15. Wnt Signaling in Kidney Development and Disease.

    Science.gov (United States)

    Wang, Yongping; Zhou, Chengji J; Liu, Youhua

    2018-01-01

    Wnt signal cascade is an evolutionarily conserved, developmental pathway that regulates embryogenesis, injury repair, and pathogenesis of human diseases. It is well established that Wnt ligands transmit their signal via canonical, β-catenin-dependent and noncanonical, β-catenin-independent mechanisms. Mounting evidence has revealed that Wnt signaling plays a key role in controlling early nephrogenesis and is implicated in the development of various kidney disorders. Dysregulations of Wnt expression cause a variety of developmental abnormalities and human diseases, such as congenital anomalies of the kidney and urinary tract, cystic kidney, and renal carcinoma. Multiple Wnt ligands, their receptors, and transcriptional targets are upregulated during nephron formation, which is crucial for mediating the reciprocal interaction between primordial tissues of ureteric bud and metanephric mesenchyme. Renal cysts are also associated with disrupted Wnt signaling. In addition, Wnt components are important players in renal tumorigenesis. Activation of Wnt/β-catenin is instrumental for tubular repair and regeneration after acute kidney injury. However, sustained activation of this signal cascade is linked to chronic kidney diseases and renal fibrosis in patients and experimental animal models. Mechanistically, Wnt signaling controls a diverse array of biologic processes, such as cell cycle progression, cell polarity and migration, cilia biology, and activation of renin-angiotensin system. In this chapter, we have reviewed recent findings that implicate Wnt signaling in kidney development and diseases. Targeting this signaling may hold promise for future treatment of kidney disorders in patients. Copyright © 2018 Elsevier Inc. All rights reserved.

  16. Longitudinal Assessment of Left Ventricular Mass in Autosomal Dominant Polycystic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Taimur Dad

    2018-05-01

    Full Text Available Introduction: The high burden of cardiovascular morbidity and mortality in autosomal dominant polycystic kidney disease (ADPKD is related to development of hypertension and left ventricular hypertrophy. Blood pressure reduction has been shown to reduce left ventricular mass in ADPKD; however, moderators and predictors of response to lower blood pressure are unknown. Methods: This was a post hoc cohort analysis of HALT PKD study A, a randomized placebo controlled trial examining the effect of low blood pressure and single versus dual renin−angiotensin blockade in early ADPKD. Participants were hypertensive ADPKD patients 15 to 49 years of age with estimated glomerular filtration rate (eGFR > 60 ml/min per 1.73 m2 across 7 centers in the United States. Predictors included age, sex, baseline eGFR, systolic blood pressure, total kidney volume, serum potassium, and urine sodium, potassium, albumin, and aldosterone. Outcome was left ventricular mass index (LVMI measured using 1.5-T magnetic resonance imaging at months 0, 24, 48, and 60. Results: Reduction in LVMI was associated with higher baseline systolic blood pressure and larger kidney volume regardless of blood pressure control group assignment (P < 0.001 for both. Male sex and baseline eGFR were associated with a positive annual slope in LVMI (P < 0.001 and P = 0.07, respectively. Conclusion: Characteristics associated with higher risk of progression in ADPKD, including higher systolic blood pressure, larger kidney volume, and lower eGFR are associated with improvement in LVMI with intensive blood pressure control, whereas male sex is associated with a smaller slope of reduction in LVMI. Keywords: autosomal dominant polycystic kidney disease, hypertension, left ventricular hypertrophy, left ventricular mass index

  17. Experimental research on preimplantation genetic diagnosis for autosomal dominant polycys-tic kidney disease%常染色体显性多囊肾疾病行胚胎植入前遗传学诊断的实验研究

    Institute of Scientific and Technical Information of China (English)

    朱琴; 徐炳森; 黄学锋; 周颖

    2009-01-01

    目的:建立由PKD1突变所致常染色体显性多囊肾疾病(autosomal dominant polycystic kidney disease,ADPKD)的胚胎植入前遗传学诊断(preimplantation genetic diagnosis,PGD)方法.方法:①通过微卫星连锁分析确定2个多囊肾家系的ADPKD致病基因.检测的微卫星包括为与PKD1连锁的KG8、 SM6、CW4和CW2以及与PKD2连锁的D4S1534、D4S1563、D4S414和D4S423.②对18个淋巴细胞和1个PKD1 突变所致ADPKD成员行常规体外受精胚胎移植后的5个废弃胚胎15个卵裂球行多重巢式PCR和毛细管电泳检测与PKD1连锁的微卫星分型.结果:①KG8、CW4和CW2 可作为连锁微卫星分析外周血和单个细胞的PKD1突变;②2个家系的致病基因均为PKD1;③单个卵裂球扩增成功率为86.67%(13/15),单个淋巴细胞扩增成功率为88.89%(16/18),CW4等位基因脱扣率为25%(4/16),CW2未发现等位基因脱扣,均未发现污染,2个胚胎携带致病基因.结论:PKD1连锁的微卫星分型可作为PKD1突变所致ADPKD的PGD诊断方法.

  18. Phosphorus Regulation in Chronic Kidney Disease.

    Science.gov (United States)

    Suki, Wadi N; Moore, Linda W

    2016-01-01

    Serum phosphorus levels stay relatively constant through the influence of multiple factors-such as parathyroid hormone, fibroblast growth factor 23, and vitamin D-on the kidney, bone, and digestive system. Whereas normal serum phosphorus ranges between 3 mg/dL to 4.5 mg/dL, large cross-sectional studies have shown that even people with normal kidney function are sometimes found to have levels ranging between 1.6 mg/dL and 6.2 mg/dL. While this may partially be due to diet and the factors mentioned above, total understanding of these atypical ranges of serum phosphorus remains uncertain. Risks for bone disease are high in people aged 50 and older, and this group comprises a large proportion of people who also have chronic kidney disease. Consuming diets low in calcium and high in phosphorus, especially foods with phosphate additives, further exacerbates bone turnover. Existing bone disease increases the risk for high serum phosphorus, and higher serum phosphorus has been associated with increased adverse events and cardiovascular-related mortality both in people with chronic kidney disease and in those with no evidence of disease. Once kidney function has deteriorated to end-stage disease (Stage 5), maintaining normal serum phosphorus requires dietary restrictions, phosphate-binding medications, and dialysis. Even so, normal serum phosphorus remains elusive in many patients with Stage 5 kidney disease, and researchers are testing novel targets that may inhibit intestinal transport of phosphorus to achieve better phosphate control. Protecting and monitoring bone health should also aid in controlling serum phosphorus as kidney disease advances.

  19. Mutations in DZIP1L, which encodes a ciliary transition zone protein, cause autosomal recessive polycystic kidney disease

    Science.gov (United States)

    Lu, Hao; Galeano, Maria C. Rondón; Ott, Elisabeth; Kaeslin, Geraldine; Kausalya, P. Jaya; Kramer, Carina; Ortiz-Brüchle, Nadina; Hilger, Nadescha; Metzis, Vicki; Hiersche, Milan; Tay, Shang Yew; Tunningley, Robert; Vij, Shubha; Courtney, Andrew D.; Whittle, Belinda; Wühl, Elke; Vester, Udo; Hartleben, Björn; Neuber, Steffen; Frank, Valeska; Little, Melissa H.; Epting, Daniel; Papathanasiou, Peter; Perkins, Andrew C.; Wright, Graham D.; Hunziker, Walter; Gee, Heon Yung; Otto, Edgar A.; Zerres, Klaus; Hildebrandt, Friedhelm; Roy, Sudipto; Wicking, Carol; Bergmann, Carsten

    2017-01-01

    Autosomal recessive polycystic kidney disease (ARPKD), usually considered to be a genetically homogeneous disease caused by mutations in PKHD1, has been associated with ciliary dysfunction. Here, we describe mutations in the DAZ interacting protein 1-like (DZIP1L) gene in patients with ARPKD, findings we have further validated by loss-of-function studies in mice and zebrafish. DZIP1L localizes to centrioles and at the distal end of basal bodies, and interacts with septin2, a protein implicated in maintenance of the periciliary diffusion barrier at the ciliary transition zone. Consistent with a defect in the diffusion barrier, we found that the ciliary membrane translocation of the PKD proteins, polycystin-1 and −2, is compromised in DZIP1L mutant cells. Together, these data provide the first conclusive evidence that ARPKD is not a homogeneous disorder, and establishes DZIP1L as a second gene involved in its pathogenesis. PMID:28530676

  20. Mutations in DZIP1L, which encodes a ciliary-transition-zone protein, cause autosomal recessive polycystic kidney disease.

    Science.gov (United States)

    Lu, Hao; Galeano, Maria C Rondón; Ott, Elisabeth; Kaeslin, Geraldine; Kausalya, P Jaya; Kramer, Carina; Ortiz-Brüchle, Nadina; Hilger, Nadescha; Metzis, Vicki; Hiersche, Milan; Tay, Shang Yew; Tunningley, Robert; Vij, Shubha; Courtney, Andrew D; Whittle, Belinda; Wühl, Elke; Vester, Udo; Hartleben, Björn; Neuber, Steffen; Frank, Valeska; Little, Melissa H; Epting, Daniel; Papathanasiou, Peter; Perkins, Andrew C; Wright, Graham D; Hunziker, Walter; Gee, Heon Yung; Otto, Edgar A; Zerres, Klaus; Hildebrandt, Friedhelm; Roy, Sudipto; Wicking, Carol; Bergmann, Carsten

    2017-07-01

    Autosomal recessive polycystic kidney disease (ARPKD), usually considered to be a genetically homogeneous disease caused by mutations in PKHD1, has been associated with ciliary dysfunction. Here, we describe mutations in DZIP1L, which encodes DAZ interacting protein 1-like, in patients with ARPKD. We further validated these findings through loss-of-function studies in mice and zebrafish. DZIP1L localizes to centrioles and to the distal ends of basal bodies, and interacts with septin2, a protein implicated in maintenance of the periciliary diffusion barrier at the ciliary transition zone. In agreement with a defect in the diffusion barrier, we found that the ciliary-membrane translocation of the PKD proteins polycystin-1 and polycystin-2 is compromised in DZIP1L-mutant cells. Together, these data provide what is, to our knowledge, the first conclusive evidence that ARPKD is not a homogeneous disorder and further establish DZIP1L as a second gene involved in ARPKD pathogenesis.

  1. National Institute of Diabetes and Digestive and Kidney Diseases

    Science.gov (United States)

    ... Events Follow Us National Institute of Diabetes and Digestive and Kidney Diseases NIDDK conducts and supports research ... to improve health. Learn more Health Topics Diabetes Digestive Diseases Kidney Disease Weight Management Liver Disease Urologic ...

  2. SECRETED KLOTHO AND CHRONIC KIDNEY DISEASE

    Science.gov (United States)

    Hu, Ming Chang; Kuro-o, Makoto; Moe, Orson W.

    2013-01-01

    Soluble Klotho (sKl) in the circulation can be generated directly by alterative splicing of the Klotho transcript or the extracellular domain of membrane Klotho can be released from membrane-anchored Klotho on the cell surface. Unlike membrane Klotho which functions as a coreceptor for fibroblast growth factor-23 (FGF23), sKl, acts as hormonal factor and plays important roles in anti-aging, anti-oxidation, modulation of ion transport, and Wnt signaling. Emerging evidence reveals that Klotho deficiency is an early biomarker for chronic kidney diseases as well as a pathogenic factor. Klotho deficiency is associated with progression and chronic complications in chronic kidney disease including vascular calcification, cardiac hypertrophy, and secondary hyperparathyroidism. In multiple experimental models, replacement of sKl, or manipulated up-regulation of endogenous Klotho protect the kidney from renal insults, preserve kidney function, and suppress renal fibrosis, in chronic kidney disease. Klotho is a highly promising candidate on the horizon as an early biomarker, and as a novel therapeutic agent for chronic kidney disease. PMID:22396167

  3. Allopurinol Against Progression of Chronic Kidney Disease.

    Science.gov (United States)

    Golmohammadi, Sima; Almasi, Afshin; Manouchehri, M; Omrani, Hamid Reza; Zandkarimi, Mohammad Reza

    2017-07-01

    Hyperuricemia is common in approximately 50% of patients with kidney failure due to decreased uric acid excretion, and it has been recently known as an independent factor in the progression of renal insufficiency. Allopurinol inhibits the production of uric acid. The aim of this study was to evaluate the effect of allopurinol on chronic kidney disease progression. In a clinical trial, patients with stages 3 and 4 of chronic kidney disease were divided into two groups to receive allopurinol, 100 mg, daily and placebo for 12 months. Patients' kidney function and serum uric acid levels were assessed at baseline and 3, 6, and 12 months after initial administration. Subgroups of patients with severe and mild glomerular filtration rate (GFR) impairment (GFR, 15 mL/min/1.73 m2 to 30 mL/min/1.73 m2 and 30 mL/min/1.73 m2 to 60 mL/min/1.73 m2, respectively), were compared between the groups. Serum uric acid levels decreased significantly during after 12 months of allopurinol administration (P = .004). In patients with severe GFR impairment, serum creatinine levels did not decrease significantly and there was no significant increase in GFR, but in those with mild GFR impairment, serum creatinine levels decreased and GFR increase significantly (P kidney disease progression and could be administered with other effective medications for controlling the kidney disease.

  4. Chronic Kidney Disease and Medicines

    Science.gov (United States)

    ... help you meet your blood pressure goals, which is good for your kidneys, and can lower your chances of having a heart attack or stroke . For tips on quitting, go to Smokefree.gov . Find healthy ways to cope with stress and depression Long-term stress can raise your ...

  5. Microvascular pericytes in healthy and diseased kidneys

    Science.gov (United States)

    Pan, Szu-Yu; Chang, Yu-Ting; Lin, Shuei-Liong

    2014-01-01

    Pericytes are interstitial mesenchymal cells found in many major organs. In the kidney, microvascular pericytes are defined anatomically as extensively branched, collagen-producing cells in close contact with endothelial cells. Although many molecular markers have been proposed, none of them can identify the pericytes with satisfactory specificity or sensitivity. The roles of microvascular pericytes in kidneys were poorly understood in the past. Recently, by using genetic lineage tracing to label collagen-producing cells or mesenchymal cells, the elusive characteristics of the pericytes have been illuminated. The purpose of this article is to review recent advances in the understanding of microvascular pericytes in the kidneys. In healthy kidney, the pericytes are found to take part in the maintenance of microvascular stability. Detachment of the pericytes from the microvasculature and loss of the close contact with endothelial cells have been observed during renal insult. Renal microvascular pericytes have been shown to be the major source of scar-forming myofibroblasts in fibrogenic kidney disease. Targeting the crosstalk between pericytes and neighboring endothelial cells or tubular epithelial cells may inhibit the pericyte–myofibroblast transition, prevent peritubular capillary rarefaction, and attenuate renal fibrosis. In addition, renal pericytes deserve attention for their potential to produce erythropoietin in healthy kidneys as pericytes stand in the front line, sensing the change of oxygenation and hemoglobin concentration. Further delineation of the mechanisms underlying the reduced erythropoietin production occurring during pericyte–myofibroblast transition may be promising for the development of new treatment strategies for anemia in chronic kidney disease. PMID:24465134

  6. Circulating CXCL16 in Diabetic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Usama Elewa

    2016-09-01

    Full Text Available Background/Aims: Chronic kidney disease and, specifically, diabetic kidney disease, is among the fastest increasing causes of death worldwide. A better understanding of the factors contributing to the high mortality may help design novel monitoring and therapeutic approaches. CXCL16 is both a cholesterol receptor and a chemokine with a potential role in vascular injury and inflammation. We aimed at identifying predictors of circulating CXCL16 levels in diabetic patients with chronic kidney disease. Methods: We have now studied plasma CXCL16 in 134 European patients with diabetic kidney disease with estimated glomerular filtration rate (eGFR categories G1-G4 and albuminuria categories A1-A3, in order to identify factors influencing plasma CXCL16 in this population. Results: Plasma CXCL16 levels were 4.0±0.9 ng/ml. Plasma CXCL16 increased with increasing eGFR category from G1 to G4 (that is, with decreasing eGFR values and with increasing albuminuria category. Plasma CXCL16 was higher in patients with prior cardiovascular disease (4.33±1.03 vs 3.88±0.86 ng/ml; p=0.013. In multivariate analysis, eGFR and serum albumin had an independent and significant negative correlation with plasma CXCL16. Conclusion: In diabetic kidney disease patients, GFR and serum albumin independently predicted plasma CXCL16 levels.

  7. MR imaging of adult glomerulocystic kidney disease

    International Nuclear Information System (INIS)

    Egashira, K.; Nakata, H.; Hashimoto, O.; Kaizu, K.; University of Occupational and Environmental Health School of Medicine, Kitakyushu

    1991-01-01

    A 59-year-old man with hypertension and severe renal dysfunction was diagnosed as having adult glomerulocystic kidney disease. MR imaging of the kidney showed a diffuse reduction of the intensity of the renal cortex with a loss of normal cortico-medullary differentiation of T1-weighted images. Numerous small cortical cysts were also demonstrated. These MR findings complemented the results of the biopsy and were useful for making a definitive diagnosis. (orig.)

  8. Kidney Function and Plasma Copeptin Levels in Healthy Kidney Donors and Autosomal Dominant Polycystic Kidney Disease Patients

    NARCIS (Netherlands)

    Zittema, Debbie; van den Berg, Else; Meijer, Esther; Boertien, Wendy E.; Muller Kobold, Anneke C.; Franssen, Casper F. M.; de Jong, Paul E.; Bakker, Stephan J. L.; Navis, Gerjan; Gansevoort, Ron T.

    Background and objectives Plasma copeptin, a marker of arginine vasopressin, is elevated in patients with autosomal dominant polycystic kidney disease and predicts disease progression. It is unknown whether elevated copeptin levels result from decreased kidney clearance or as compensation for

  9. Local television news reporting of kidney disease.

    Science.gov (United States)

    Jaffery, Jonathan B; Jacobson, Lynn M; Goldstein, Kenneth M; Pribble, James M

    2006-12-01

    Local television is the primary news source for the majority of Americans. This study aims to describe how local news reports on kidney disease. Using our searchable database of health-related late local news segments from 2002, we identified stories with the key words kidney, hypertension, blood pressure, or diabetes. This database is a representative sample of the late local news on 122 stations in the 50 largest US media markets, comprising 60% of the population. The content of each identified story was reviewed to determine whether it mentioned: (1) chronic kidney disease (CKD), (2) screening for kidney disease, or (3) kidney disease as a potential complication (for blood pressure- or diabetes-related stories). Only 2 of 1,799 database news stories (0.11%) included "kidney" as a summary key word; neither referred to CKD, screening, or complications of other diseases. Of 19 stories about hypertension or blood pressure (1.06% of all stories) and the 14 stories about diabetes (0.78% of all stories), none mentioned these criteria. Despite efforts to increase public awareness of and screening for CKD, local television news (the most important news source for a majority of Americans) did little to help achieve these goals. Further work will be needed to confirm whether this paucity of coverage varies over time and determine why so little attention is given to CKD. Educating physicians and public relations personnel who advocate for kidney disease about journalists' needs may be an important step to help advance public awareness of CKD.

  10. Berberine slows cell growth in autosomal dominant polycystic kidney disease cells

    International Nuclear Information System (INIS)

    Bonon, Anna; Mangolini, Alessandra; Pinton, Paolo; Senno, Laura del; Aguiari, Gianluca

    2013-01-01

    Highlights: •Berberine at appropriate doses slows cell proliferation in ADPKD cystic cells. •Reduction of cell growth by berberine occurs by inhibition of ERK and p70-S6 kinase. •Higher doses of berberine cause an overall cytotoxic effect. •Berberine overdose induces apoptotic bodies formation and DNA fragmentation. •Antiproliferative properties of this drug make it a new candidate for ADPKD therapy. -- Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary monogenic disorder characterized by development and enlargement of kidney cysts that lead to loss of renal function. It is caused by mutations in two genes (PKD1 and PKD2) encoding for polycystin-1 and polycystin-2 proteins which regulate different signals including cAMP, mTOR and EGFR pathways. Abnormal activation of these signals following PC1 or PC2 loss of function causes an increased cell proliferation which is a typical hallmark of this disease. Despite the promising findings obtained in animal models with targeted inhibitors able to reduce cystic cell growth, currently, no specific approved therapy for ADPKD is available. Therefore, the research of new more effective molecules could be crucial for the treatment of this severe pathology. In this regard, we have studied the effect of berberine, an isoquinoline quaternary alkaloid, on cell proliferation and apoptosis in human and mouse ADPKD cystic cell lines. Berberine treatment slows cell proliferation of ADPKD cystic cells in a dose-dependent manner and at high doses (100 μg/mL) it induces cell death in cystic cells as well as in normal kidney tubule cells. However, at 10 μg/mL, berberine reduces cell growth in ADPKD cystic cells only enhancing G 0 /G 1 phase of cell cycle and inhibiting ERK and p70-S6 kinases. Our results indicate that berberine shows a selected antiproliferative activity in cellular models for ADPKD, suggesting that this molecule and similar natural compounds could open new opportunities

  11. Berberine slows cell growth in autosomal dominant polycystic kidney disease cells

    Energy Technology Data Exchange (ETDEWEB)

    Bonon, Anna; Mangolini, Alessandra [Department of Biomedical and Specialty Surgical Sciences, University of Ferrara, 44121 Ferrara (Italy); Pinton, Paolo [Department of Morphology, Surgery and Experimental Medicine, Section of General Pathology, University of Ferrara, 44121 Ferrara (Italy); Senno, Laura del [Department of Biomedical and Specialty Surgical Sciences, University of Ferrara, 44121 Ferrara (Italy); Aguiari, Gianluca, E-mail: dsn@unife.it [Department of Biomedical and Specialty Surgical Sciences, University of Ferrara, 44121 Ferrara (Italy)

    2013-11-22

    Highlights: •Berberine at appropriate doses slows cell proliferation in ADPKD cystic cells. •Reduction of cell growth by berberine occurs by inhibition of ERK and p70-S6 kinase. •Higher doses of berberine cause an overall cytotoxic effect. •Berberine overdose induces apoptotic bodies formation and DNA fragmentation. •Antiproliferative properties of this drug make it a new candidate for ADPKD therapy. -- Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary monogenic disorder characterized by development and enlargement of kidney cysts that lead to loss of renal function. It is caused by mutations in two genes (PKD1 and PKD2) encoding for polycystin-1 and polycystin-2 proteins which regulate different signals including cAMP, mTOR and EGFR pathways. Abnormal activation of these signals following PC1 or PC2 loss of function causes an increased cell proliferation which is a typical hallmark of this disease. Despite the promising findings obtained in animal models with targeted inhibitors able to reduce cystic cell growth, currently, no specific approved therapy for ADPKD is available. Therefore, the research of new more effective molecules could be crucial for the treatment of this severe pathology. In this regard, we have studied the effect of berberine, an isoquinoline quaternary alkaloid, on cell proliferation and apoptosis in human and mouse ADPKD cystic cell lines. Berberine treatment slows cell proliferation of ADPKD cystic cells in a dose-dependent manner and at high doses (100 μg/mL) it induces cell death in cystic cells as well as in normal kidney tubule cells. However, at 10 μg/mL, berberine reduces cell growth in ADPKD cystic cells only enhancing G{sub 0}/G{sub 1} phase of cell cycle and inhibiting ERK and p70-S6 kinases. Our results indicate that berberine shows a selected antiproliferative activity in cellular models for ADPKD, suggesting that this molecule and similar natural compounds could open new

  12. Src family kinases in chronic kidney disease.

    Science.gov (United States)

    Wang, Jun; Zhuang, Shougang

    2017-09-01

    Src family kinases (SFKs) belong to nonreceptor protein tyrosine kinases and have been implicated in the regulation of numerous cellular processes, including cell proliferation, differentiation, migration and invasion, and angiogenesis. The role and mechanisms of SFKs in tumorgenesis have been extensively investigated, and some SFK inhibitors are currently under clinical trials for tumor treatment. Recent studies have also demonstrated the importance of SFKs in regulating the development of various fibrosis-related chronic diseases (e.g., idiopathic pulmonary fibrosis, liver fibrosis, renal fibrosis, and systemic sclerosis). In this article, we summarize the roles of SFKs in various chronic kidney diseases, including glomerulonephritis, diabetic nephropathy, human immunodeficiency virus-associated nephropathy, autosomal dominant form of polycystic kidney disease, and obesity-associated kidney disease, and discuss the mechanisms involved. Copyright © 2017 the American Physiological Society.

  13. [Nutritional management of kidney diseases in children].

    Science.gov (United States)

    Borovik, T E; Kutafina, E K; Tsygin, A N; Sergeeva, T V; Baranov, A A; Namazova-Baranova, L S; Voznesenskaya, T S; Zakharova, I N; Semenova, N N; Zvonkova, N G; Yatsyk, S P

    2016-01-01

    The prevalence of various kidney diseases in children remains high in recent decades. Adequate nutrition management can enhance the effectiveness of drug treatment, slow the frequency of relapses andprevent the progression of the disease. The article is devoted to modern approaches to diet therapy in various kidney diseases in children with the defeat of tubular and glomerular appa ratus. For the first time the therapeutic diets for children with various kidney diseases are presented. Particular attention is paid to diet therapy in nephrotic syndrome (steroid-responsive and steroid-refractory). Dietary approaches with modern formulas for enteral nutrition in cases of steroid therapy complications in children with renal insufficiency (in predialysis stage and on dialysis) are described. Differentiated nutritional approaches for patients with different types of crystalluria are separately presented.

  14. Growth Retardation in Children with Kidney Disease

    Directory of Open Access Journals (Sweden)

    Paulina Salas

    2013-01-01

    Full Text Available Growth failure is almost inextricably linked with chronic kidney disease (CKD and end-stage renal disease (ESRD. Growth failure in CKD has been associated with both increased morbidity and mortality. Growth failure in the setting of kidney disease is multifactorial and is related to poor nutritional status as well as comorbidities, such as anemia, bone and mineral disorders, and alterations in hormonal responses, as well as to aspects of treatment such as steroid exposure. This review covers updated management of growth failure in these children including adequate nutrition, treatment of metabolic alterations, and early administration of recombinant human growth hormone (GH.

  15. Viruses & kidney disease: beyond HIV

    OpenAIRE

    Waldman, Meryl; Marshall, Vickie; Whitby, Denise; Kopp, Jeffrey B.

    2008-01-01

    HIV-infected patients may acquire new viral co-infections; they may also experience the reactivation or worsening of existing viral infections, including active, smoldering, or latent infections. HIV-infected patients may be predisposed to these viral infections due to immunodeficiency or to risk factors common to HIV and other viruses. A number of these affect the kidney, either by direct infection or by deposition of immune complexes. In this review we discuss the renal manifestations and t...

  16. Epidemiology of chronic kidney disease in children

    NARCIS (Netherlands)

    Harambat, Jérôme; van Stralen, Karlijn J.; Kim, Jon Jin; Tizard, E. Jane

    2012-01-01

    In the past 30 years there have been major improvements in the care of children with chronic kidney disease (CKD). However, most of the available epidemiological data stem from end-stage renal disease (ESRD) registries and information on the earlier stages of pediatric CKD is still limited. The

  17. Lupus and Kidney Disease (Lupus Nephritis)

    Science.gov (United States)

    ... disease. Your family history and things in your environment such as infections, viruses, toxic chemicals or pollutants ( ... to show how well your kidneys are filtering wastes Check for antiphospholipid antibodies and anti-nuclear antibodies (ANA) at least once during your disease. ...

  18. Long-term effect of coffee consumption on autosomal dominant polycystic kidneys disease progression: results from the Suisse ADPKD, a Prospective Longitudinal Cohort Study.

    Science.gov (United States)

    Girardat-Rotar, Laura; Puhan, Milo A; Braun, Julia; Serra, Andreas L

    2018-02-01

    Previous in vitro experiments of human polycystic kidney disease (PKD) cells reported that caffeine is a risk factor for the promotion of cyst enlargement in patients with autosomal dominant PKD (ADPKD). The relentless progression of ADPKD inclines the majority of physicians to advocate minimization of caffeine consumption despite the absence of clinical data supporting such a recommendation so far. This is the first clinical study to assess prospectively the association between coffee consumption and disease progression in a longitudinal ADPKD cohort. Information on coffee consumption and disease progression was collected at each follow-up visit using standardized measurement methods. The main model for the outcomes, kidney size (height-adjusted total kidney volume, htTKV) and kidney function (estimated glomerular filtration rate, eGFR), was a linear mixed model. Patients entered the on-going Swiss ADPKD study between 2006 and June 2014 and had at least 1 visit every year. The sample size of the study population was 151 with a median follow-up of 4 visits per patient and a median follow-up time of 4.38 years. After multivariate adjustment for age, smoking, hypertension, sex, body mass index and an interaction term (coffee*visit), coffee drinkers did not have a statistically significantly different kidney size compared to non-coffee drinkers (difference of -33.03 cm 3 height adjusted TKV, 95% confidence interval (CI) from -72.41 to 6.34, p = 0.10). After the same adjustment, there was no statistically significant difference in eGFR between coffee and non-coffee drinkers (2.03 ml/min/1.73 m 2 , 95% CI from -0.31 to 4.31, p = 0.089). Data derived from our prospective longitudinal study do not confirm that drinking coffee is a risk factor for ADPKD progression.

  19. Performance of an Artificial Multi-observer Deep Neural Network for Fully Automated Segmentation of Polycystic Kidneys.

    Science.gov (United States)

    Kline, Timothy L; Korfiatis, Panagiotis; Edwards, Marie E; Blais, Jaime D; Czerwiec, Frank S; Harris, Peter C; King, Bernard F; Torres, Vicente E; Erickson, Bradley J

    2017-08-01

    Deep learning techniques are being rapidly applied to medical imaging tasks-from organ and lesion segmentation to tissue and tumor classification. These techniques are becoming the leading algorithmic approaches to solve inherently difficult image processing tasks. Currently, the most critical requirement for successful implementation lies in the need for relatively large datasets that can be used for training the deep learning networks. Based on our initial studies of MR imaging examinations of the kidneys of patients affected by polycystic kidney disease (PKD), we have generated a unique database of imaging data and corresponding reference standard segmentations of polycystic kidneys. In the study of PKD, segmentation of the kidneys is needed in order to measure total kidney volume (TKV). Automated methods to segment the kidneys and measure TKV are needed to increase measurement throughput and alleviate the inherent variability of human-derived measurements. We hypothesize that deep learning techniques can be leveraged to perform fast, accurate, reproducible, and fully automated segmentation of polycystic kidneys. Here, we describe a fully automated approach for segmenting PKD kidneys within MR images that simulates a multi-observer approach in order to create an accurate and robust method for the task of segmentation and computation of TKV for PKD patients. A total of 2000 cases were used for training and validation, and 400 cases were used for testing. The multi-observer ensemble method had mean ± SD percent volume difference of 0.68 ± 2.2% compared with the reference standard segmentations. The complete framework performs fully automated segmentation at a level comparable with interobserver variability and could be considered as a replacement for the task of segmentation of PKD kidneys by a human.

  20. Hypoglycemia, chronic kidney disease, and diabetes mellitus.

    Science.gov (United States)

    Alsahli, Mazen; Gerich, John E

    2014-11-01

    Hypoglycemia is a major problem associated with substantial morbidity and mortality in patients with diabetes and is often a major barrier to achieving optimal glycemic control. Chronic kidney disease not only is an independent risk factor for hypoglycemia but also augments the risk of hypoglycemia that is already present in people with diabetes. This article summarizes our current knowledge of the epidemiology, pathogenesis, and morbidity of hypoglycemia in patients with diabetes and chronic kidney disease and reviews therapeutic considerations in this situation. PubMed and MEDLINE were searched for literature published in English from January 1989 to May 2014 for diabetes mellitus, hypoglycemia, chronic kidney disease, and chronic renal insufficiency. Copyright © 2014 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.

  1. Wait too long to talk about kidney disease and you could be waiting for a kidney.

    Science.gov (United States)

    ... Home Current Issue Past Issues Public Service Announcement Kidney Disease Past Issues / Summer 2006 Table of Contents ... Javascript on. Wait too long to talk about kidney disease and you could be waiting for a ...

  2. CDKD: a clinical database of kidney diseases

    Directory of Open Access Journals (Sweden)

    Singh Sanjay

    2012-04-01

    Full Text Available Abstract Background The main function of the kidneys is to remove waste products and excess water from the blood. Loss of kidney function leads to various health issues, such as anemia, high blood pressure, bone disease, disorders of cholesterol. The main objective of this database system is to store the personal and laboratory investigatory details of patients with kidney disease. The emphasis is on experimental results relevant to quantitative renal physiology, with a particular focus on data relevant for evaluation of parameters in statistical models of renal function. Description Clinical database of kidney diseases (CDKD has been developed with patient confidentiality and data security as a top priority. It can make comparative analysis of one or more parameters of patient’s record and includes the information of about whole range of data including demographics, medical history, laboratory test results, vital signs, personal statistics like age and weight. Conclusions The goal of this database is to make kidney-related physiological data easily available to the scientific community and to maintain & retain patient’s record. As a Web based application it permits physician to see, edit and annotate a patient record from anywhere and anytime while maintaining the confidentiality of the personal record. It also allows statistical analysis of all data.

  3. Diabetes and chronic kidney disease

    African Journals Online (AJOL)

    2007-08-16

    Aug 16, 2007 ... chronic dialysis or transplantation due to significant extrarenal disease, mainly .... including coronary heart disease, silent myocardial ischaemia and left ... diabetics and should be kept in mind: • renal papillary necrosis.

  4. Direct renin inhibition in chronic kidney disease

    DEFF Research Database (Denmark)

    Persson, Frederik; Rossing, Peter; Parving, Hans-Henrik

    2013-01-01

    that renin inhibition could hold potential for improved treatment in patients with chronic kidney disease, with diabetic nephropathy as an obvious group of patients to investigate, as the activity of the renin-angiotensin-aldosterone system is enhanced in these patients and as there is an unmet need....... In addition, combination treatment seemed safe and effective also in patients with impaired kidney function. These initial findings formed the basis for the design of a large morbidity and mortality trial investigating aliskiren as add-on to standard treatment. The study has just concluded, but was terminated...... early as a beneficial effect was unlikely and there was an increased frequency of side effects. Also in non-diabetic kidney disease a few intervention studies have been carried out, but there is no ongoing hard outcome study. In this review we provide the current evidence for renin inhibition in chronic...

  5. Potential Deleterious Effects of Vasopressin in Chronic Kidney Disease and Particularly Autosomal Dominant Polycystic Kidney Disease

    NARCIS (Netherlands)

    Meijer, E.; Boertien, W. E.; Zietse, R.; Gansevoort, R. T.

    2011-01-01

    The antidiuretic hormone vasopressin is crucial for regulating free water clearance in normal physiology. However, it has also been hypothesized that vasopressin has deleterious effects on the kidney. Vasopressin is elevated in animals and patients with chronic kidney disease. Suppression of

  6. Calcium Balance in Chronic Kidney Disease.

    Science.gov (United States)

    Hill Gallant, Kathleen M; Spiegel, David M

    2017-06-01

    The kidneys play a critical role in the balance between the internal milieu and external environment. Kidney failure is known to disrupt a number of homeostatic mechanisms that control serum calcium and normal bone metabolism. However, our understanding of calcium balance throughout the stages of chronic kidney disease is limited and the concept of balance itself, especially with a cation as complex as calcium, is often misunderstood. Both negative and positive calcium balance have important implications in patients with chronic kidney disease, where negative balance may increase risk of osteoporosis and fracture and positive balance may increase risk of vascular calcification and cardiovascular events. Here, we examine the state of current knowledge about calcium balance in adults throughout the stages of chronic kidney disease and discuss recommendations for clinical strategies to maintain balance as well as future research needs in this area. Recent calcium balance studies in adult patients with chronic kidney disease show that neutral calcium balance is achieved with calcium intake near the recommended daily allowance. Increases in calcium through diet or supplements cause high positive calcium balance, which may put patients at risk for vascular calcification. However, heterogeneity in calcium balance exists among these patients. Given the available calcium balance data in this population, it appears clinically prudent to aim for recommended calcium intakes around 1000 mg/day to achieve neutral calcium balance and avoid adverse effects of either negative or positive calcium balance. Assessment of patients' dietary calcium intake could further equip clinicians to make individualized recommendations for meeting recommended intakes.

  7. Heart failure in patients with kidney disease.

    Science.gov (United States)

    Tuegel, Courtney; Bansal, Nisha

    2017-12-01

    Heart failure (HF) is a leading cause of morbidity and mortality in patients with chronic kidney disease (CKD), and the population of CKD patients with concurrent HF continues to grow. The accurate diagnosis of HF is challenging in patients with CKD in part due to a lack of validated imaging and biomarkers specifically in this population. The pathophysiology between the heart and the kidneys is complex and bidirectional. Patients with CKD have greater prevalence of traditional HF risk factors as well as unique kidney-specific risk factors including malnutrition, acid-base alterations, uraemic toxins, bone mineral changes, anemia and myocardial stunning. These risk factors also contribute to the decline of kidney function seen in patients with subclinical and clinical HF. More targeted HF therapies may improve outcomes in patients with kidney disease as current HF therapies are underutilised in this population. Further work is also needed to develop novel HF therapies for the CKD population. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

  8. Averting the legacy of kidney disease – focus on childhood

    Directory of Open Access Journals (Sweden)

    Julie R. Ingelfinger

    2016-03-01

    Full Text Available World Kidney Day 2016 focuses on kidney disease in childhood and the antecedents of adult kidney disease that can begin in earliest childhood. Chronic kidney disease in childhood differs from that in adults, as the largest diagnostic group among children includes congenital anomalies and inherited disorders, with glomerulopathies and kidney disease in the setting of diabetes being relatively uncommon. In addition, many children with acute kidney injury will ultimately develop sequelae that may lead to hypertension and chronic kidney disease in later childhood or in adult life. Children born early or who are small-for date newborns have relatively increased risk for the development of chronic kidney disease later in life. Persons with a high-risk birth and early childhood history should be watched closely in order to help detect early signs of kidney disease in time to provide effective prevention or treatment. Successful therapy is feasible for advanced chronic kidney disease in childhood; there is evidence that children fare better than adults, if they receive kidney replacement therapy including dialysis and transplantation, while only a minority of children may require this ultimate intervention. Because there are disparities in access to care, effort is needed so that those children with kidney disease, wherever they live, may be treated effectively, irrespective of their geographic or economic circumstances. Our hope is that World Kidney Day will inform the general public, policy makers and caregivers about the needs and possibilities surrounding kidney disease in childhood.

  9. Kidney biomimicry--a rediscovered scientific field that could provide hope to patients with kidney disease.

    Science.gov (United States)

    Stenvinkel, Peter; Johnson, Richard J

    2013-11-01

    Most studies on kidney disease have relied on classic experimental studies in mice and rats or clinical studies in humans. From such studies much understanding of the physiology and pathophysiology of kidney disease has been obtained. However, breakthroughs in the prevention and treatment of kidney diseases have been relatively few, and new approaches to fight kidney disease are needed. Here we discuss kidney biomimicry as a new approach to understand kidney disease. Examples are given of how various animals have developed ways to prevent or respond to kidney failure, how to protect themselves from hypoxia or oxidative stress and from the scourge of hyperglycemia. We suggest that investigation of evolutionary biology and comparative physiology might provide new insights for the prevention and treatment of kidney disease. Copyright © 2013 IMSS. Published by Elsevier Inc. All rights reserved.

  10. Dengue-associated kidney disease.

    Science.gov (United States)

    Lizarraga, Karlo J; Nayer, Ali

    2014-01-01

    A mosquito-borne viral illness highly prevalent in the tropics and subtropics, dengue is considered a major global health threat by the World Health Organization. Directory of Open Access Journals (DOAJ), Google Scholar, PubMed (NLM), LISTA (EBSCO) and Web of Science have been searched. An RNA virus from the genus Flavivirus, dengue virus is transmitted by Aedes aegypti,the yellow fever mosquito. Dengue is asymptomatic in as many as one half of infected individuals. Dengue fever is an acute febrile illness accompanied by constitutional symptoms. Dengue hemorrhagic fever and dengue shock syndrome are the severe forms of dengue infection.Dengue infection has been associated with a variety of renal disorders. Acute renal failure is a potential complication of severe dengue infection and is typically associated with hypotension, rhabdomyolysis, or hemolysis. Acute renal failure complicates severe dengue infection in 2-5% of the cases and carries a high mortality rate. Proteinuria has been detected in as high as 74% of patients with severe dengue infection. Hematuria has been reported in up to 12.5% of patients. Various types of glomerulonephritis have been reported during or shortly after dengue infection in humans and mouse models of dengue infection. Mesangial proliferation and immune complex deposition are the dominant histologic features of dengue-associated glomerulonephritis. On a rare occasion, dengue infection is associated with systemic autoimmune disorders involving the kidneys. In the vast majority of cases, dengue infection and associated renal disorders are self-limited.

  11. Genetics Home Reference: uromodulin-associated kidney disease

    Science.gov (United States)

    ... disease Related Information How are genetic conditions and genes named? Additional Information & Resources MedlinePlus (3 links) Health Topic: Gout Health Topic: Kidney Diseases Health Topic: Kidney Failure ...

  12. Dermatological diseases in patients with chronic kidney disease.

    Science.gov (United States)

    Gagnon1, Amy L; Desai, Tejas

    2013-04-01

    There are a variety of dermatological diseases that are more commonly seen in patients with chronic kidney disease (CKD) and renal transplants than the general population. Directory of Open Access Journals (DOAJ), Google Scholar, Pubmed (NLM), LISTA (EBSCO) and Web of Science has been searched. Some cutaneous diseases are clearly unique to this population. Of them, Lindsay's Nails, xerosis cutis, dryness of the skin, nephrogenic systemic fibrosis and acquired perforating dermatosis have been described in chronic kidney disease patients. The most common malignancy found in all transplant recipients is non-melanoma skin cancer. It is important for patients and physicians to recognize the manifestations of skin disease in patients suffering from chronic kidney disease to mitigate the morbidity associated with these conditions.

  13. Autosomal Dominant Polycystic Kidney Disease

    Science.gov (United States)

    ... NIH Director Organization Budget History NIH Almanac Public Involvement Outreach & Education Visitor Information RePORT NIH Fact Sheets Home > Autosomal ... other than the observation that 50 percent of children born to an affected parent would develop the disease. Diagnosis of well-established ...

  14. Flavonoids in Kidney Health and Disease

    Directory of Open Access Journals (Sweden)

    Félix Vargas

    2018-04-01

    Full Text Available This review summarizes the latest advances in knowledge on the effects of flavonoids on renal function in health and disease. Flavonoids have antihypertensive, antidiabetic, and antiinflammatory effects, among other therapeutic activities. Many of them also exert renoprotective actions that may be of interest in diseases such as glomerulonephritis, diabetic nephropathy, and chemically-induced kidney insufficiency. They affect several renal factors that promote diuresis and natriuresis, which may contribute to their well-known antihypertensive effect. Flavonoids prevent or attenuate the renal injury associated with arterial hypertension, both by decreasing blood pressure and by acting directly on the renal parenchyma. These outcomes derive from their interference with multiple signaling pathways known to produce renal injury and are independent of their blood pressure-lowering effects. Oral administration of flavonoids prevents or ameliorates adverse effects on the kidney of elevated fructose consumption, high fat diet, and types I and 2 diabetes. These compounds attenuate the hyperglycemia-disrupted renal endothelial barrier function, urinary microalbumin excretion, and glomerular hyperfiltration that results from a reduction of podocyte injury, a determinant factor for albuminuria in diabetic nephropathy. Several flavonoids have shown renal protective effects against many nephrotoxic agents that frequently cause acute kidney injury (AKI or chronic kidney disease (CKD, such as LPS, gentamycin, alcohol, nicotine, lead or cadmium. Flavonoids also improve cisplatin- or methotrexate-induced renal damage, demonstrating important actions in chemotherapy, anticancer and renoprotective effects. A beneficial prophylactic effect of flavonoids has been also observed against AKI induced by surgical procedures such as ischemia/reperfusion (I/R or cardiopulmonary bypass. In several murine models of CKD, impaired kidney function was significantly improved by

  15. Antiphospholipid syndrome and kidney disease.

    Science.gov (United States)

    Bienaimé, Frank; Legendre, Christophe; Terzi, Fabiola; Canaud, Guillaume

    2017-01-01

    The antiphospholipid syndrome is a common autoimmune disease caused by pathogenic antiphospholipid antibodies, leading to recurrent thrombosis and/or obstetrical complications. Importantly for nephrologists, antiphospholipid antibodies are associated with various renal manifestations including large renal vessel thrombosis, renal artery stenosis, and a constellation of intrarenal lesions that has been termed antiphospholipid nephropathy. This last condition associates various degrees of acute thrombotic microangiopathy, proliferative and fibrotic lesions of the intrarenal vessels, and ischemic modifications of the renal parenchyma. The course of the disease can range from indolent nephropathy to devastating acute renal failure. The pejorative impact of antiphospholipid antibody-related renal complication is well established in the context of systemic lupus erythematous or after renal transplantation. In contrast, the exact significance of isolated antiphospholipid nephropathy remains uncertain. The evidence to guide management of the renal complications of antiphospholipid syndrome is limited. However, the recent recognition of the heterogeneous molecular mechanisms underlying the progression of intrarenal vascular lesions in antiphospholipid syndrome have opened promising tracks for patient monitoring and targeted therapeutic intervention. Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

  16. Diabetic Kidney Disease: A Syndrome Rather Than a Single Disease

    Science.gov (United States)

    Piccoli, Giorgina B.; Grassi, Giorgio; Cabiddu, Gianfranca; Nazha, Marta; Roggero, Simona; Capizzi, Irene; De Pascale, Agostino; Priola, Adriano M.; Di Vico, Cristina; Maxia, Stefania; Loi, Valentina; Asunis, Anna M.; Pani, Antonello; Veltri, Andrea

    2015-01-01

    The term "diabetic kidney" has recently been proposed to encompass the various lesions, involving all kidney structures that characterize protean kidney damage in patients with diabetes. While glomerular diseases may follow the stepwise progression that was described several decades ago, the tenet that proteinuria identifies diabetic nephropathy is disputed today and should be limited to glomerular lesions. Improvements in glycemic control may have contributed to a decrease in the prevalence of glomerular lesions, initially described as hallmarks of diabetic nephropathy, and revealed other types of renal damage, mainly related to vasculature and interstitium, and these types usually present with little or no proteinuria. Whilst glomerular damage is the hallmark of microvascular lesions, ischemic nephropathies, renal infarction, and cholesterol emboli syndrome are the result of macrovascular involvement, and the presence of underlying renal damage sets the stage for acute infections and drug-induced kidney injuries. Impairment of the phagocytic response can cause severe and unusual forms of acute and chronic pyelonephritis. It is thus concluded that screening for albuminuria, which is useful for detecting "glomerular diabetic nephropathy", does not identify all potential nephropathies in diabetes patients. As diabetes is a risk factor for all forms of kidney disease, diagnosis in diabetic patients should include the same combination of biochemical, clinical, and imaging tests as employed in non-diabetic subjects, but with the specific consideration that chronic kidney disease (CKD) may develop more rapidly and severely in diabetic patients. PMID:26676663

  17. Role of Smad signaling in kidney disease.

    Science.gov (United States)

    Zhang, Yanhua; Wang, Songyan; Liu, Shengmao; Li, Chunguang; Wang, Ji

    2015-12-01

    Smads are the key intermediates of canonical transforming growth factor-beta (TGF-β) signaling. These intermediates are divided into three distinct subgroups based on their role in TGF-β family signal transduction: Receptor-regulated Smads (R-Smads) 1, 2, 3, 5 and 8, common Smad4, and inhibitory Smads6 and 7. TGF-β signaling through Smad pathway involves phosphorylation, ubiquitination, sumoylation, acetylation, and protein-protein interactions with mitogen-activated protein kinases, PI3K-Akt/PKB, and Wnt/GSK-3. Several studies have suggested that upregulation or downregulation of TGF-β/Smad signaling pathways may be a pathogenic mechanism in the progression of chronic kidney disease. Smad2 and 3 are the two major downstream R-Smads in TGF-β-mediated renal fibrosis, while Smad7 also controls renal inflammation. In this review, we characterize the role of Smads in kidney disease, describe the molecular mechanisms, and discuss the potential of Smads as a therapeutic target in chronic kidney disease.

  18. Chronic kidney disease in disadvantaged populations

    Directory of Open Access Journals (Sweden)

    G. Garcia-Garcia

    2015-05-01

    Full Text Available The increased burden of chronic kidney disease (CKD in disadvantaged populations is due to both global factors and population-specific issues. Low socioeconomic status and poor access to care contribute to health care disparities and exacerbate the negative effects of genetic or biological predisposition. Provision of appropriate renal care to these populations requires a two-pronged approach: expanding the reach of dialysis through development of low-cost alternatives that can be practiced in remote locations, and implementation and evaluation of cost-effective prevention strategies. Kidney transplantation should be promoted by expansion of deceased donor transplant programs and use of inexpensive, generic immunosuppressive drugs. The message of World Kidney Day 2015 is that a concerted attack against the diseases that lead to end-stage renal disease, by increasing community outreach, better education, improved economic opportunity, and access to preventive medicine for those at highest risk, could end the unacceptable relationship between CKD and disadvantage in these communities.

  19. Ivabradine, heart failure and chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Luca Di Lullo

    2015-12-01

    Full Text Available The incidence and prevalence of congestive heart failure are actually increasing worldwide, especially in Western countries. In Europe and the United States, congestive heart failure represents a disabling clinical disease, accountable for increased hospitalization and health care costs. European guidelines have underlined the importance of pharmacological treatment to improve both patients’ outcomes and quality of life. The latest clinical trials to evaluate ivabradine’s efficacy have underlined its usefulness as a stand-alone medication and in combination with conventional congestive heart failure therapy, including in chronic kidney disease patients.

  20. Kidney Disease and Diabetes - What You Need to Know

    Science.gov (United States)

    ... Bar Home Current Issue Past Issues Special Section Kidney Disease and Diabetes: What You Need to Know ... page please turn Javascript on. March is National Kidney Month , a good time to check if you ...

  1. Cyclodextrin Protects Podocytes in Diabetic Kidney Disease

    Science.gov (United States)

    Merscher-Gomez, Sandra; Guzman, Johanna; Pedigo, Christopher E.; Lehto, Markku; Aguillon-Prada, Robier; Mendez, Armando; Lassenius, Mariann I.; Forsblom, Carol; Yoo, TaeHyun; Villarreal, Rodrigo; Maiguel, Dony; Johnson, Kevin; Goldberg, Ronald; Nair, Viji; Randolph, Ann; Kretzler, Matthias; Nelson, Robert G.; Burke, George W.; Groop, Per-Henrik; Fornoni, Alessia

    2013-01-01

    Diabetic kidney disease (DKD) remains the most common cause of end-stage kidney disease despite multifactorial intervention. We demonstrated that increased cholesterol in association with downregulation of ATP-binding cassette transporter ABCA1 occurs in normal human podocytes exposed to the sera of patients with type 1 diabetes and albuminuria (DKD+) when compared with diabetic patients with normoalbuminuria (DKD−) and similar duration of diabetes and lipid profile. Glomerular downregulation of ABCA1 was confirmed in biopsies from patients with early DKD (n = 70) when compared with normal living donors (n = 32). Induction of cholesterol efflux with cyclodextrin (CD) but not inhibition of cholesterol synthesis with simvastatin prevented podocyte injury observed in vitro after exposure to patient sera. Subcutaneous administration of CD to diabetic BTBR (black and tan, brachiuric) ob/ob mice was safe and reduced albuminuria, mesangial expansion, kidney weight, and cortical cholesterol content. This was followed by an improvement of fasting insulin, blood glucose, body weight, and glucose tolerance in vivo and improved glucose-stimulated insulin release in human islets in vitro. Our data suggest that impaired reverse cholesterol transport characterizes clinical and experimental DKD and negatively influences podocyte function. Treatment with CD is safe and effective in preserving podocyte function in vitro and in vivo and may improve the metabolic control of diabetes. PMID:23835338

  2. Interactions between thyroid disorders and kidney disease

    Directory of Open Access Journals (Sweden)

    Gopal Basu

    2012-01-01

    Full Text Available There are several interactions between thyroid and kidney functions in each other organ′s disease states. Thyroid hormones affect renal development and physiology. Thyroid hormones have pre-renal and intrinsic renal effects by which they increase the renal blood flow and the glomerular filtration rate (GFR. Hypothyroidism is associated with reduced GFR and hyperthyroidism results in increased GFR as well as increased renin - angiotensin - aldosterone activation. Chronic kidney disease (CKD is characterized by a low T3 syndrome which is now considered a part of an atypical nonthyroidal illness. CKD patients also have increased incidence of primary hypothyroidism and subclinical hypothyroidism. The physiological benefits of a hypothyroid state in CKD, and the risk of CKD progression with hyperthyroidism emphasize on a conservative approach in the treatment of thyroid hormone abnormalities in CKD. Thyroid dysfunction is also associated with glomerulonephritis often by a common autoimmune etiology. Several drugs could affect both thyroid and kidney functions. There are few described interactions between thyroid and renal malignancies. A detailed knowledge of all these interactions is important for both the nephrologists and endocrinologists for optimal management of the patient.

  3. NOS3 Polymorphisms and Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Alejandro Marín Medina

    2018-05-01

    Full Text Available ABSTRACT Chronic kidney disease (CKD is a multifactorial pathophysiologic irreversible process that often leads to a terminal state in which the patient requires renal replacement therapy. Most cases of CKD are due to chronic-degenerative diseases and endothelial dysfunction is one of the factors that contribute to its pathophysiology. One of the most important mechanisms for proper functioning of the endothelium is the regulation of the synthesis of nitric oxide. This compound is synthesized by the enzyme nitric oxide synthase, which has 3 isoforms. Polymorphisms in the NOS3 gene have been implicated as factors that alter the homeostasis of this mechanism. The Glu298Asp polymorphisms 4 b/a and -786T>C of the NOS3 gene have been associated with a more rapid deterioration of kidney function in patients with CKD. These polymorphisms have been evaluated in patients with CKD of determined and undetermined etiology and related to a more rapid deterioration of kidney function.

  4. Exploring metabolic dysfunction in chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Slee Adrian D

    2012-04-01

    Full Text Available Abstract Impaired kidney function and chronic kidney disease (CKD leading to kidney failure and end-stage renal disease (ESRD is a serious medical condition associated with increased morbidity, mortality, and in particular cardiovascular disease (CVD risk. CKD is associated with multiple physiological and metabolic disturbances, including hypertension, dyslipidemia and the anorexia-cachexia syndrome which are linked to poor outcomes. Specific hormonal, inflammatory, and nutritional-metabolic factors may play key roles in CKD development and pathogenesis. These include raised proinflammatory cytokines, such as interleukin-1 and −6, tumor necrosis factor, altered hepatic acute phase proteins, including reduced albumin, increased C-reactive protein, and perturbations in normal anabolic hormone responses with reduced growth hormone-insulin-like growth factor-1 axis activity. Others include hyperactivation of the renin-angiotensin aldosterone system (RAAS, with angiotensin II and aldosterone implicated in hypertension and the promotion of insulin resistance, and subsequent pharmacological blockade shown to improve blood pressure, metabolic control and offer reno-protective effects. Abnormal adipocytokine levels including leptin and adiponectin may further promote the insulin resistant, and proinflammatory state in CKD. Ghrelin may be also implicated and controversial studies suggest activities may be reduced in human CKD, and may provide a rationale for administration of acyl-ghrelin. Poor vitamin D status has also been associated with patient outcome and CVD risk and may indicate a role for supplementation. Glucocorticoid activities traditionally known for their involvement in the pathogenesis of a number of disease states are increased and may be implicated in CKD-associated hypertension, insulin resistance, diabetes risk and cachexia, both directly and indirectly through effects on other systems including activation of the mineralcorticoid

  5. Kidney disease and obesity: epidemiology, mechanisms and treatment.

    Science.gov (United States)

    Câmara, Niels Olsen Saraiva; Iseki, Kunitoshi; Kramer, Holly; Liu, Zhi-Hong; Sharma, Kumar

    2017-03-01

    The theme of World Kidney Day 2017 is 'kidney disease and obesity: healthy lifestyle for healthy kidneys'. To mark this event, Nature Reviews Nephrology invited five leading researchers to describe changes in the epidemiology of obesity-related kidney disease, advances in current understanding of the mechanisms and current approaches to the management of affected patients. The researchers also highlight new advances that could lead to the development of novel treatments and identify areas in which further basic and clinical studies are needed.

  6. Mineral & Bone Disorder in Chronic Kidney Disease

    Science.gov (United States)

    ... Clinical trials that are currently open and are recruiting can be viewed at www.ClinicalTrials.gov . This ... about Kidney Failure and How it’s Treated Treatment Methods for Kidney Failure: Hemodialysis Treatment Methods for Kidney ...

  7. The Kidney-Vascular-Bone Axis in the Chronic Kidney Disease-Mineral Bone Disorder.

    Science.gov (United States)

    Seifert, Michael E; Hruska, Keith A

    2016-03-01

    The last 25 years have been characterized by dramatic improvements in short-term patient and allograft survival after kidney transplantation. Long-term patient and allograft survival remains limited by cardiovascular disease and chronic allograft injury, among other factors. Cardiovascular disease remains a significant contributor to mortality in native chronic kidney disease as well as cardiovascular mortality in chronic kidney disease more than doubles that of the general population. The chronic kidney disease (CKD)-mineral bone disorder (MBD) is a syndrome recently coined to embody the biochemical, skeletal, and cardiovascular pathophysiology that results from disrupting the complex systems biology between the kidney, skeleton, and cardiovascular system in native and transplant kidney disease. The CKD-MBD is a unique kidney disease-specific syndrome containing novel cardiovascular risk factors, with an impact reaching far beyond traditional notions of renal osteodystrophy and hyperparathyroidism. This overview reviews current knowledge of the pathophysiology of the CKD-MBD, including emerging concepts surrounding the importance of circulating pathogenic factors released from the injured kidney that directly cause cardiovascular disease in native and transplant chronic kidney disease, with potential application to mechanisms of chronic allograft injury and vasculopathy.

  8. Chronic Kidney Disease and Lipid Disorders.

    Science.gov (United States)

    Zubovic, Sandra Vegar; Kristic, Spomenka; Prevljak, Sabina; Pasic, Irmina Sefic

    2016-06-01

    Chronic kidney disease (CKD) represents a serious public health problem due to the increase in incidence and prevalence of this disease worldwide. Given the significant morbidity and mortality from cardiovascular disease (CVD) in the population of patients with CKD, and the fact that dyslipidemia itself is a risk factor for CVD, increases the importance of lipid metabolism study in patients with CKD. Evaluate the lipid status of patients with chronic kidney disease. A one-year prospective study included 150 adult patients who were in various stages of chronic renal failure (stage I to IV). Estimate of creatinine clearance was performed using Cockroft-Goult formula. The classification of patients according to stages of chronic renal insufficiency was performed in accordance with the criteria of Kidney Disease Outcomes Quality Initiative (K/DOQI). Of the total number of patients (N=150) there was 71 males and 79 females. The mean age of patients was 55.43 years. Average values of serum cholesterol were highest in patients with stage II renal disease and the lowest in patients classified as stage IV (5.76±1.60 mmol/L vs. 5.07±1.88 mmol/L). Analysis of the average value of triglycerides in blood show a slight increase through the stages of CKD in a manner that patients classified into stage I have low serum triglyceride levels (1.73±1.17 mmol/L (range 0.61 to 5.5 mmol/L), and patients classified in stage III the highest value 2.13±1.11 mmol/L (range 0.62 to 4.66 mmol/L). Average cholesterol levels does not statistically significantly change with progression of chronic renal disease. There is an almost linear increase in average triglyceride levels in chronic renal disease. Triglyceride levels in serum begins to increase in the early stage of chronic renal disease and reach the peak in stage IV.

  9. Quantitative MRI of kidneys in renal disease.

    Science.gov (United States)

    Kline, Timothy L; Edwards, Marie E; Garg, Ishan; Irazabal, Maria V; Korfiatis, Panagiotis; Harris, Peter C; King, Bernard F; Torres, Vicente E; Venkatesh, Sudhakar K; Erickson, Bradley J

    2018-03-01

    To evaluate the reproducibility and utility of quantitative magnetic resonance imaging (MRI) sequences for the assessment of kidneys in young adults with normal renal function (eGFR ranged from 90 to 130 mL/min/1.73 m 2 ) and patients with early renal disease (autosomal dominant polycystic kidney disease). This prospective case-control study was performed on ten normal young adults (18-30 years old) and ten age- and sex-matched patients with early renal parenchymal disease (autosomal dominant polycystic kidney disease). All subjects underwent a comprehensive kidney MRI protocol, including qualitative imaging: T1w, T2w, FIESTA, and quantitative imaging: 2D cine phase contrast of the renal arteries, and parenchymal diffusion weighted imaging (DWI), magnetization transfer imaging (MTI), blood oxygen level dependent (BOLD) imaging, and magnetic resonance elastography (MRE). The normal controls were imaged on two separate occasions ≥24 h apart (range 24-210 h) to assess reproducibility of the measurements. Quantitative MR imaging sequences were found to be reproducible. The mean ± SD absolute percent difference between quantitative parameters measured ≥24 h apart were: MTI-derived ratio = 4.5 ± 3.6%, DWI-derived apparent diffusion coefficient (ADC) = 6.5 ± 3.4%, BOLD-derived R2* = 7.4 ± 5.9%, and MRE-derived tissue stiffness = 7.6 ± 3.3%. Compared with controls, the ADPKD patient's non-cystic renal parenchyma (NCRP) had statistically significant differences with regard to quantitative parenchymal measures: lower MTI percent ratios (16.3 ± 4.4 vs. 23.8 ± 1.2, p quantitative measurements was obtained in all cases. Significantly different quantitative MR parenchymal measurement parameters between ADPKD patients and normal controls were obtained by MT, DWI, BOLD, and MRE indicating the potential for detecting and following renal disease at an earlier stage than the conventional qualitative imaging techniques.

  10. Averting the legacy of kidney disease: focus on childhood

    Science.gov (United States)

    Ingelfinger, Julie R; Kalantar-Zadeh, Kamyar; Schaefer, Franz

    2016-01-01

    World Kidney Day 2016 focuses on kidney disease in childhood and the antecedents of adult kidney disease that can begin in earliest childhood. Chronic kidney disease (CKD) in childhood differs from that in adults, as the largest diagnostic group among children includes congenital anomalies and inherited disorders, with glomerulopathies and kidney disease in the setting of diabetes being relatively uncommon. In addition, many children with acute kidney injury will ultimately develop sequelae that may lead to hypertension and CKD in later childhood or in adult life. Children born early or who are small-for date newborns have relatively increased risk for the development of CKD later in life. Persons with a high-risk birth and early childhood history should be watched closely in order to help detect early signs of kidney disease in time to provide effective prevention or treatment. Successful therapy is feasible for advanced CKD in childhood; there is evidence that children fare better than adults, if they receive kidney replacement therapy including dialysis and transplantation, while only a minority of children may require this ultimate intervention. Because there are disparities in access to care, effort is needed so that those children with kidney disease, wherever they live, may be treated effectively, irrespective of their geographic or economic circumstances. Our hope is that World Kidney Day will inform the general public, policy makers and caregivers about the needs and possibilities surrounding kidney disease in childhood. PMID:28031959

  11. Averting the legacy of kidney disease - focus on childhood

    Directory of Open Access Journals (Sweden)

    J.R. Ingelfinger

    2016-01-01

    Full Text Available World Kidney Day 2016 focuses on kidney disease in childhood and the antecedents of adult kidney disease that can begin in earliest childhood. Chronic kidney disease (CKD in childhood differs from that in adults, in that the largest diagnostic group among children includes congenital anomalies and inherited disorders, with glomerulopathies and kidney disease as a consequence of diabetes being relatively uncommon. In addition, many children with acute kidney injury will ultimately develop sequelae that may lead to hypertension and CKD in later childhood or in adult life. Children born early or who are small-for-date newborns have relatively increased risk for the development of CKD later in life. Persons with a high-risk birth and early childhood history should be watched closely in order to help detect early signs of kidney disease in time to provide effective prevention or treatment. Successful therapy is feasible for advanced CKD in childhood; there is evidence that children fare better than adults, if they receive kidney replacement therapy including dialysis and transplantation, although only a minority of children may require this ultimate intervention. Because there are disparities in access to care, effort is needed so that children with kidney disease, wherever they live, may be treated effectively, irrespective of their geographic or economic circumstances. Our hope is that the World Kidney Day will inform the general public, policy makers and caregivers about the needs and possibilities surrounding kidney disease in childhood.

  12. Keep Your Kidneys Healthy: Catch Kidney Disease Early

    Science.gov (United States)

    ... your blood. Each kidney contains about a million tiny filters that can process around 40 gallons of fluid every day—about enough to fill a house’s hot water heater. When blood passes through the ...

  13. Chronic kidney disease in HIV patients

    Science.gov (United States)

    Bakri, S.; Rasyid, H.; Kasim, H.; Katu, S.

    2018-03-01

    Chronic kidney disease (CKD) is a health problem in human immunodeficiency virus (HIV) population. Prediction of CKD in HIV patients needsto have done. This study aimis to identify the prevalence of CKD in HIV patients.Thisis a cross-sectional studyofmale and female, age 18-60 years old, diagnosedHIVat Wahidin Sudirohusodo & Hasanuddin University Hospital Makassar. Diagnosed as CKD if estimated glomerular filtration rate (eGFR) HIV patients included in the analyses. Distribution of CKD, showed 3 (3.5%) subjects with eGFRHIV populations in Makassar is still quite low.

  14. Vitamin K status in chronic kidney disease.

    Science.gov (United States)

    McCabe, Kristin M; Adams, Michael A; Holden, Rachel M

    2013-11-07

    The purpose of this review is to summarize the research to date on vitamin K status in chronic kidney disease (CKD). This review includes a summary of the data available on vitamin K status in patients across the spectrum of CKD as well as the link between vitamin K deficiency in CKD and bone dynamics, including mineralization and demineralization, as well as ectopic mineralization. It also describes two current clinical trials that are underway evaluating vitamin K treatment in CKD patients. These data may inform future clinical practice in this population.

  15. Thyroid Disorders and Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Mohamed Mohamedali

    2014-01-01

    Full Text Available Thyroid hormones play a very important role regulating metabolism, development, protein synthesis, and influencing other hormone functions. The two main hormones produced by the thyroid are triiodothyronine (T3 and thyroxine (T4. These hormones can also have significant impact on kidney disease so it is important to consider the physiological association of thyroid dysfunction in relation to chronic kidney disease (CKD. CKD has been known to affect the pituitary-thyroid axis and the peripheral metabolism of thyroid hormones. Low T3 levels are the most common laboratory finding followed by subclinical hypothyroidism in CKD patients. Hyperthyroidism is usually not associated with CKD but has been known to accelerate it. One of the most important links between thyroid disorders and CKD is uremia. Patients who are appropriately treated for thyroid disease have a less chance of developing renal dysfunction. Clinicians need to be very careful in treating patients with low T3 levels who also have an elevation in TSH, as this can lead to a negative nitrogen balance. Thus, clinicians should be well educated on the role of thyroid hormones in relation to CKD so that proper treatment can be delivered to the patient.

  16. Phosphorus and Nutrition in Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Emilio González-Parra

    2012-01-01

    Full Text Available Patients with renal impairment progressively lose the ability to excrete phosphorus. Decreased glomerular filtration of phosphorus is initially compensated by decreased tubular reabsorption, regulated by PTH and FGF23, maintaining normal serum phosphorus concentrations. There is a close relationship between protein and phosphorus intake. In chronic renal disease, a low dietary protein content slows the progression of kidney disease, especially in patients with proteinuria and decreases the supply of phosphorus, which has been directly related with progression of kidney disease and with patient survival. However, not all animal proteins and vegetables have the same proportion of phosphorus in their composition. Adequate labeling of food requires showing the phosphorus-to-protein ratio. The diet in patients with advanced-stage CKD has been controversial, because a diet with too low protein content can favor malnutrition and increase morbidity and mortality. Phosphorus binders lower serum phosphorus and also FGF23 levels, without decreasing diet protein content. But the interaction between intestinal dysbacteriosis in dialysis patients, phosphate binder efficacy, and patient tolerance to the binder could reduce their efficiency.

  17. Obesity and kidney disease: hidden consequences of the epidemic ...

    African Journals Online (AJOL)

    Obesity has also been shown to be a risk factor for nephrolithiasis, and for a number of malignancies including kidney cancer. This year World Kidney Day promotes education on the harmful consequences of obesity and its association with kidney disease, advocating a healthy lifestyle and health policy measures that ...

  18. Polycystic kidney disease in the medaka (Oryzias latipes pc mutant caused by a mutation in the Gli-Similar3 (glis3 gene.

    Directory of Open Access Journals (Sweden)

    Hisashi Hashimoto

    Full Text Available Polycystic kidney disease (PKD is a common hereditary disease in humans. Recent studies have shown an increasing number of ciliary genes that are involved in the pathogenesis of PKD. In this study, the Gli-similar3 (glis3 gene was identified as the causal gene of the medaka pc mutant, a model of PKD. In the pc mutant, a transposon was found to be inserted into the fourth intron of the pc/glis3 gene, causing aberrant splicing of the pc/glis3 mRNA and thus a putatively truncated protein with a defective zinc finger domain. pc/glis3 mRNA is expressed in the epithelial cells of the renal tubules and ducts of the pronephros and mesonephros, and also in the pancreas. Antisense oligonucleotide-mediated knockdown of pc/glis3 resulted in cyst formation in the pronephric tubules of medaka fry. Although three other glis family members, glis1a, glis1b and glis2, were found in the medaka genome, none were expressed in the embryonic or larval kidney. In the pc mutant, the urine flow rate in the pronephros was significantly reduced, which was considered to be a direct cause of renal cyst formation. The cilia on the surface of the renal tubular epithelium were significantly shorter in the pc mutant than in wild-type, suggesting that shortened cilia resulted in a decrease in driving force and, in turn, a reduction in urine flow rate. Most importantly, EGFP-tagged pc/glis3 protein localized in primary cilia as well as in the nucleus when expressed in mouse renal epithelial cells, indicating a strong connection between pc/glis3 and ciliary function. Unlike human patients with GLIS3 mutations, the medaka pc mutant shows none of the symptoms of a pancreatic phenotype, such as impaired insulin expression and/or diabetes, suggesting that the pc mutant may be suitable for use as a kidney-specific model for human GLIS3 patients.

  19. CHRONIC KIDNEY DISEASE RAAS blockade and diastolic heart failure in chronic kidney disease

    NARCIS (Netherlands)

    Franssen, Casper F. M.; Navis, Gerjan

    New data from Ahmed et al. show that discharge prescriptions for renin-angiotensin-aldosterone inhibitor therapy are associated with a significant reduction in all-cause mortality in elderly patients with diastolic heart failure and chronic kidney disease (CKD). These observational data support the

  20. Central blood pressure and chronic kidney disease

    Science.gov (United States)

    Ohno, Yoichi; Kanno, Yoshihiko; Takenaka, Tsuneo

    2016-01-01

    In this review, we focused on the relationship between central blood pressure and chronic kidney diseases (CKD). Wave reflection is a major mechanism that determines central blood pressure in patients with CKD. Recent medical technology advances have enabled non-invasive central blood pressure measurements. Clinical trials have demonstrated that compared with brachial blood pressure, central blood pressure is a stronger risk factor for cardiovascular (CV) and renal diseases. CKD is characterized by a diminished renal autoregulatory ability, an augmented direct transmission of systemic blood pressure to glomeruli, and an increase in proteinuria. Any elevation in central blood pressure accelerates CKD progression. In the kidney, interstitial inflammation induces oxidative stress to handle proteinuria. Oxidative stress facilitates atherogenesis, increases arterial stiffness and central blood pressure, and worsens the CV prognosis in patients with CKD. A vicious cycle exists between CKD and central blood pressure. To stop this cycle, vasodilator antihypertensive drugs and statins can reduce central blood pressure and oxidative stress. Even in early-stage CKD, mineral and bone disorders (MBD) may develop. MBD promotes oxidative stress, arteriosclerosis, and elevated central blood pressure in patients with CKD. Early intervention or prevention seems necessary to maintain vascular health in patients with CKD. PMID:26788468

  1. Natural History of Progression of Chronic Kidney Disease in Stages ...

    African Journals Online (AJOL)

    Natural History of Progression of Chronic Kidney Disease in Stages 4 and 5. ... Conclusion: Low serum bicarbonate level and high urinary protein excretion at baseline are independent predictors of progression in stage 4 and 5 CKD. Keywords: Chronic kidney disease; End stage renal disease; Glomerular filtration rate; ...

  2. Sleep disorders and chronic kidney disease.

    Science.gov (United States)

    Maung, Stephanie C; El Sara, Ammar; Chapman, Cherylle; Cohen, Danielle; Cukor, Daniel

    2016-05-06

    Sleep disorders have a profound and well-documented impact on overall health and quality of life in the general population. In patients with chronic disease, sleep disorders are more prevalent, with an additional morbidity and mortality burden. The complex and dynamic relationship between sleep disorders and chronic kidney disease (CKD) remain relatively little investigated. This article presents an overview of sleep disorders in patients with CKD, with emphasis on relevant pathophysiologic underpinnings and clinical presentations. Evidence-based interventions will be discussed, in the context of individual sleep disorders, namely sleep apnea, insomnia, restless leg syndrome and excessive daytime sleepiness. Limitations of the current knowledge as well as future research directions will be highlighted, with a final discussion of different conceptual frameworks of the relationship between sleep disorders and CKD.

  3. Skin manifestations of chronic kidney disease.

    Science.gov (United States)

    Robles-Mendez, J C; Vazquez-Martinez, O; Ocampo-Candiani, J

    2015-10-01

    Skin manifestations associated with chronic kidney disease are very common. Most of these conditions present in the end stages and may affect the patient's quality of life. Knowledge of these entities can contribute to establishing an accurate diagnosis and prognosis. Severe renal pruritus is associated with increased mortality and a poor prognosis. Nail exploration can provide clues about albumin and urea levels. Nephrogenic systemic fibrosis is a preventable disease associated with gadolinium contrast. Comorbidities, such as diabetes mellitus and secondary hyperparathyroidism, can lead to acquired perforating dermatosis and calciphylaxis, respectively. Effective and innovative treatments are available for all of these conditions. Copyright © 2015 Elsevier España, S.L.U. and AEDV. All rights reserved.

  4. Targeting of regulated necrosis in kidney disease

    Directory of Open Access Journals (Sweden)

    Diego Martin-Sanchez

    2018-03-01

    (p. ej., con determinados inhibidores de la caspasa pueden desencadenar una necrosis y, por lo tanto, una lesión renal mediada por inflamación. En segundo lugar, y lo que es más revolucionario, ha surgido el concepto de necrosis regulada. Se han descrito varias modalidades de necrosis regulada como necroptosis, ferroptosis, piroptosis y necrosis regulada por transición de permeabilidad mitocondrial. De forma análoga a la apoptosis, la necrosis regulada se modula a través de moléculas específicas que actúan como dianas terapéuticas. Al contrario que la apoptosis, la necrosis regulada puede ser extremadamente proinflamatoria y, lo que es importante para el trasplante renal, inmunogénica. Además, la necrosis regulada puede desencadenar una necrosis sincronizada, en la que todas las células del interior de un túbulo concreto mueren de manera sincronizada. Revisaremos las diferentes modalidades de necrosis regulada, la evidencia de una función en las diversas formas de lesión renal y las nuevas oportunidades de intervención terapéutica. Keywords: Apoptosis, Ferroptosis, Necroptosis, Kidney, Acute kidney injury, Chronic kidney disease, Transplantation, Acute rejection, Delayed graft function, Palabras clave: Apoptosis, Ferroptosis, Necroptosis, Riñón, Lesión renal aguda, Enfermedad renal crónica, Trasplante, Rechazo agudo, Función retardada del injerto

  5. Affected parent sex and severity of autosomal dominant polycystic kidney disease: a retrospective cohort study
.

    Science.gov (United States)

    Nowak, Kristen L; Chonchol, Michel; You, Zhiying; Gupta, Malika; Gitomer, Berenice

    2018-03-01

    Parental inheritance may differentially affect autosomal dominant polycystic kidney disease (-ADPKD) severity via genetic imprinting or in utero epigenetic modifications; however, evidence is inconsistent. We conducted a longitudinal retrospective cohort study to assess the association between sex of the affected parent and time to hypertension diagnosis, end-stage renal disease (ESRD), and death in patients with the PKD1 genotype. 814 individuals who participated in research at the University of Colorado were studied. Kaplan-Meier survival analysis was performed. The predictor was parental sex, and outcomes were diagnosis of hypertension, progression to ESRD, and death. We also examined associations in four strata according to affected parent and participant sex, as previous studies have reported earlier onset of ESRD in males compared to females. The median follow-up for each outcome was as follows: hypertension, 30 (interquartile range (IQR): 18, 37); ESRD, 43 (IQR: 31, 52), death 39 (IQR: 25, 52) years of age. Among affected offspring in the entire cohort, there was no difference in hypertension diagnosis (p = 0.97) or progression to ESRD (p = 0.79) according to affected parent sex; however, participants with an affected mother were more likely to die than participants with an affected father (p father (p < 0.01) but not when the affected parent was the mother (p ≥ 0.11). Our results are largely in contrast to the hypothesis that severity of ADPKD is worse with maternal inheritance of disease.
.

  6. Clinical approach to kidney disease in kidney recipients in Spain

    Directory of Open Access Journals (Sweden)

    Josep M. Campistol

    2015-05-01

    Conclusions: Secondary markers and factors resulting in CKD progression, particularly anemia, are still frequently uncontrolled after kidney transplantation. Only about 2% of patients benefit from a therapeutic intervention based on a biopsy. Clinical perception differs from objective measures, which results in an obvious clinical inertia regarding risk factor control in such patients.

  7. End Stage and Chronic Kidney Disease: Associations with Renal Cancer

    International Nuclear Information System (INIS)

    Russo, Paul

    2012-01-01

    There is a well known association between end stage renal disease and the development of kidney cancer in the native kidney of patients requiring renal replacement therapy. There is now emerging evidence that lesser degrees of renal insufficiency (chronic kidney disease, CKD) are also associated with an increased likelihood of cancer in general and kidney cancer in particular. Nephropathological changes are commonly observed in the non-tumor bearing portions of kidney resected at the time of partial and radical nephrectomy (RN). In addition, patients with renal cancer are more likely to have CKD at the time of diagnosis and treatment than the general population. The exact mechanism by which renal insufficiency transforms normal kidney cells into tumor cells is not known. Possible mechanisms include uremic immune inhibition or increased exposure to circulating toxins not adequately cleared by the kidneys. Surgeons managing kidney tumors must have an increased awareness of their patient’s renal functional status as they plan their resection. Kidney sparing approaches, including partial nephrectomy (PN) or active surveillance in older and morbidly ill patients, can prevent CKD or delay the further decline in renal function which is well documented with RN. Despite emerging evidence that PN provides equivalent local tumor control to RN while at the same time preventing CKD, this operation remains under utilized in the United States and abroad. Increased awareness of the bi directional relationship between kidney function and kidney cancer is essential in the contemporary management of kidney cancer.

  8. Emerging role of autophagy in kidney function, diseases and aging

    Science.gov (United States)

    Huber, Tobias B.; Edelstein, Charles L.; Hartleben, Björn; Inoki, Ken; Jiang, Man; Koya, Daisuke; Kume, Shinji; Lieberthal, Wilfred; Pallet, Nicolas; Quiroga, Alejandro; Ravichandran, Kameswaran; Susztak, Katalin; Yoshida, Sei; Dong, Zheng

    2012-01-01

    Autophagy is a highly conserved process that degrades cellular long-lived proteins and organelles. Accumulating evidence indicates that autophagy plays a critical role in kidney maintenance, diseases and aging. Ischemic, toxic, immunological, and oxidative insults can cause an induction of autophagy in renal epithelial cells modifying the course of various kidney diseases. This review summarizes recent insights on the role of autophagy in kidney physiology and diseases alluding to possible novel intervention strategies for treating specific kidney disorders by modifying autophagy. PMID:22692002

  9. Chronic kidney disease in disadvantaged populations.

    Science.gov (United States)

    Garcia-Garcia, Guillermo; Jha, Vivekanand

    2015-01-01

    The increased burden of CKD in disadavantaged populations is due to both global factors and population-specific issues. Low socioeconomic status and poor access to care contribute to health care disparities, and exacerbate the negative effects of genetic or biologic predisposition. Provision of appropriate renal care to these populations requires a two-pronged approach: expanding the reach of dialysis through development of low-cost alternatives that can be practiced in remote locations, and implementation and evaluation of cost-effective prevention strategies. Kidney transplantation should be promoted by expanding deceased donor transplant programs and use of inexpensive, generic immunosuppressive drugs. The message of WKD 2015 is that a concerted attack against the diseases that lead to ESRD, by increasing community outreach, better education, improved economic opportunity, and access to preventive medicine for those at highest risk, could end the unacceptable relationship between CKD and disadvantage in these communities.

  10. Drug dosing in chronic kidney disease.

    Science.gov (United States)

    Gabardi, Steven; Abramson, Stuart

    2005-05-01

    Patients with chronic kidney disease (CKD) are at high risk for adverse drug reactions and drug-drug interactions. Drug dosing in these patients often proves to be a difficult task. Renal dysfunction-induced changes in human pathophysiology regularly results may alter medication pharmacodynamics and handling. Several pharmacokinetic parameters are adversely affected by CKD, secondary to a reduced oral absorption and glomerular filtration; altered tubular secretion; and reabsorption and changes in intestinal, hepatic, and renal metabolism. In general, drug dosing can be accomplished by multiple methods; however, the most common recommendations are often to reduce the dose or expand the dosing interval, or use both methods simultaneously. Some medications need to be avoided all together in CKD either because of lack of efficacy or increased risk of toxicity. Nevertheless, specific recommendations are available for dosing of certain medications and are an important resource, because most are based on clinical or pharmacokinetic trials.

  11. Viruses and kidney disease: beyond HIV.

    Science.gov (United States)

    Waldman, Meryl; Marshall, Vickie; Whitby, Denise; Kopp, Jeffrey B

    2008-11-01

    Human immunodeficiency virus (HIV)-infected patients may acquire new viral co-infections; they also may experience the reactivation or worsening of existing viral infections, including active, smoldering, or latent infections. HIV-infected patients may be predisposed to these viral infections owing to immunodeficiency or risk factors common to HIV and other viruses. A number of these affect the kidney, either by direct infection or by deposition of immune complexes. In this review we discuss the renal manifestations and treatment of hepatitis C virus, BK virus, adenovirus, cytomegalovirus, and parvovirus B19 in patients with HIV disease. We also discuss an approach to the identification of new viral renal pathogens, using a viral gene chip to identify viral DNA or RNA.

  12. Contribution of stone size to chronic kidney disease in kidney stone formers.

    Science.gov (United States)

    Ahmadi, Farrokhlagha; Etemadi, Samira Motedayen; Lessan-Pezeshki, Mahbob; Mahdavi-Mazdeh, Mitra; Ayati, Mohsen; Mir, Alireza; Yazdi, Hadi Rokni

    2015-01-01

    To determine whether stone burden correlates with the degree of chronic kidney disease in kidney stone formers. A total of 97 extracorporeal shockwave lithotripsy candidates aged 18 years and older were included. Size, number and location of the kidney stones, along with cumulative stone size, defined as the sum of diameters of all stones) were determined. Estimated glomerular filtration rate was determined using the Chronic Kidney Disease Epidemiology Collaboration cystatin C/creatinine equation, and chronic kidney disease was defined as estimated glomerular filtration rate chronic kidney disease. The relationship persisted even after adjustment for age, sex, body mass index, C-reactive protein, fasting plasma glucose, thyroid stimulating hormone, presence of microalbuminuria, history of renal calculi, history of extracorporeal shockwave lithotripsy, number and location of the stones (odds ratio 1.24, 95% confidence interval 1.02-1.52). The same was not observed for individuals with a cumulative stone size ≥ 20 mm. In kidney stone formers with a cumulative stone size up to 20 mm, estimated glomerular filtration rate linearly declines with increasing cumulative stone size. Additionally, cumulative stone size is an independent predictor of chronic kidney disease in this group of patients. © 2014 The Japanese Urological Association.

  13. Factors influencing level of blood pressure control in chronic kidney disease patients from Ilorin, Nigeria

    Directory of Open Access Journals (Sweden)

    A M Makusidi

    2011-01-01

    Conclusions: Uncontrolled hypertension was unacceptably high among our CKD patients using the newer control guidelines. Ignorance, poverty, advancing age, lack of treatment and poor compliance to treatment were associated with poor BP control. We recommend aggressive management including the use of three or more drugs at increasing doses especially in those having PKD and chronic glomerulonephritis (CGN as aetiology. We also advocate health education with emphasis on compliance with medication in order to forestall socioeconomic burden of end stage renal disease.

  14. Kidney Disease and the Nexus of Chronic Kidney Disease and Acute Kidney Injury: The Role of Novel Biomarkers as Early and Accurate Diagnostics.

    Science.gov (United States)

    Yerramilli, Murthy; Farace, Giosi; Quinn, John; Yerramilli, Maha

    2016-11-01

    Chronic kidney disease (CKD) and acute kidney injury (AKI) are interconnected and the presence of one is a risk for the other. CKD is an important predictor of AKI after exposure to nephrotoxic drugs or major surgery, whereas persistent or repetitive injury could result in the progression of CKD. This brings new perspectives to the diagnosis and monitoring of kidney diseases highlighting the need for a panel of kidney-specific biomarkers that reflect functional as well as structural damage and recovery, predict potential risk and provide prognosis. This article discusses the kidney-specific biomarkers, symmetric dimethylarginine (SDMA), clusterin, cystatin B, and inosine. Copyright © 2016 Elsevier Inc. All rights reserved.

  15. Correlates and management of anaemia of chronic kidney disease ...

    African Journals Online (AJOL)

    Background: Anaemia is a common complication of chronic kidney disease. There is paucity of published local and regional data regarding its associated factors and management. Objective: To assess the correlates and management of anaemia in chronic kidney disease. Design: Cross sectional descriptive study

  16. Frailty in elderly people with chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Maria Eugenia Portilla Franco

    2016-11-01

    Frailty can be reversed, which is why a study of frailty in patients with chronic kidney disease is of particular interest. This article aims to describe the association between ageing, frailty and chronic kidney disease in light of the most recent and relevant scientific publications.

  17. Stage effect of chronic kidney disease in erectile function

    Directory of Open Access Journals (Sweden)

    Márcio Rodrigues Costa

    Full Text Available ABSTRACT Purpose The study aims to assess the influence of the stage of chronic kidney disease and glomerular filtration rate on prevalence and degree of erectile dysfunction. Materials and Methods This transversal study, conducted from May 2013 to December 2015, included patients with chronic kidney disease in conservative treatment, stages III/IV/V. Erectile dysfunction was evaluated by the International Index of Erectile Function. Data classically associated with erectile dysfunction were obtained by medical record review. Erectile dysfunction, degree of erectile dysfunction, and other main variables associated with erectile dysfunction were compared between patients with chronic kidney disease on conservative treatment stages III versus IV/V using the Chi-square test. The relationship between score of the International Index of Erectile Dysfunction and glomerular filtration rate was established by Pearson correlation coefficient. Results Two hundred and forty five patients with chronic kidney disease in conservative treatment participated of the study. The prevalence of erectile dysfunction in patients with chronic kidney disease in stages IV/V was greater than in stage III. Glomerular filtration rate positively correlated with score of the International Index of Erectile Dysfunction. Conclusions The study suggests that chronic kidney disease progression (glomerular filtration rate decrease and advance in chronic kidney disease stages worsen erectile function. Hypothetically, diagnosis and treatment of erectile dysfunction may be anticipated with the analysis of chronic kidney disease progression.

  18. The TRP Channels Pkd2, NompC, and Trpm Act in Cold-Sensing Neurons to Mediate Unique Aversive Behaviors to Noxious Cold in Drosophila.

    Science.gov (United States)

    Turner, Heather N; Armengol, Kevin; Patel, Atit A; Himmel, Nathaniel J; Sullivan, Luis; Iyer, Srividya Chandramouli; Bhattacharya, Surajit; Iyer, Eswar Prasad R; Landry, Christian; Galko, Michael J; Cox, Daniel N

    2016-12-05

    The basic mechanisms underlying noxious cold perception are not well understood. We developed Drosophila assays for noxious cold responses. Larvae respond to near-freezing temperatures via a mutually exclusive set of singular behaviors-in particular, a full-body contraction (CT). Class III (CIII) multidendritic sensory neurons are specifically activated by cold and optogenetic activation of these neurons elicits CT. Blocking synaptic transmission in CIII neurons inhibits CT. Genetically, the transient receptor potential (TRP) channels Trpm, NompC, and Polycystic kidney disease 2 (Pkd2) are expressed in CIII neurons, where each is required for CT. Misexpression of Pkd2 is sufficient to confer cold responsiveness. The optogenetic activation level of multimodal CIII neurons determines behavioral output, and visualization of neuronal activity supports this conclusion. Coactivation of cold- and heat-responsive sensory neurons suggests that the cold-evoked response circuitry is dominant. Our Drosophila model will enable a sophisticated molecular genetic dissection of cold nociceptive genes and circuits. Copyright © 2016 Elsevier Ltd. All rights reserved.

  19. Aberrant Smad3 phosphoisoforms in cyst-lining epithelial cells in the cpk mouse, a model of autosomal recessive polycystic kidney disease.

    Science.gov (United States)

    Hama, Taketsugu; Nakanishi, Koichi; Sato, Masashi; Mukaiyama, Hironobu; Togawa, Hiroko; Shima, Yuko; Miyajima, Masayasu; Nozu, Kandai; Nagao, Shizuko; Takahashi, Hisahide; Sako, Mayumi; Iijima, Kazumoto; Yoshikawa, Norishige; Suzuki, Hiroyuki

    2017-12-01

    Cystic epithelia acquire mesenchymal-like features in polycystic kidney disease (PKD). In this phenotypic alteration, it is well known that transforming growth factor (TGF)-β/Smad3 signaling is involved; however, there is emerging new data on Smad3 phosphoisoforms: Smad3 phosphorylated at linker regions (pSmad3L), COOH-terminal regions (pSmad3C), and both (pSmad3L/C). pSmad3L/C has a pathological role in colorectal cancer. Mesenchymal phenotype-specific cell responses in the TGF-β/Smad3 pathway are implicated in carcinomas. In this study, we confirmed mesenchymal features and examined Smad3 phosphoisoforms in the cpk mouse, a model of autosomal recessive PKD. Kidney sections were stained with antibodies against mesenchymal markers and domain-specific phospho-Smad3. TGF-β, pSmad3L, pSmad3C, JNK, cyclin-dependent kinase (CDK) 4, and c-Myc were evaluated by Western blotting. Cophosphorylation of pSmad3L/C was assessed by immunoprecipitation. α-Smooth muscle actin, which indicates mesenchymal features, was expressed higher in cpk mice. pSmad3L expression was increased in cpk mice and was predominantly localized in the nuclei of tubular epithelial cells in cysts; however, pSmad3C was equally expressed in both cpk and control mice. Levels of pSmad3L, JNK, CDK4, and c-Myc protein in nuclei were significantly higher in cpk mice than in controls. Immunoprecipitation showed that Smad3 was cophosphorylated (pSmad3L/C) in cpk mice. Smad3 knockout/ cpk double-mutant mice revealed amelioration of cpk abnormalities. These findings suggest that upregulating c-Myc through the JNK/CDK4-dependent pSmad3L pathway may be key to the pathophysiology in cpk mice. In conclusion, a qualitative rather than a quantitative abnormality of the TGF-β/Smad3 pathway is involved in PKD and may be a target for disease-specific intervention. Copyright © 2017 the American Physiological Society.

  20. Hormones and arterial stiffness in patients with chronic kidney disease.

    Science.gov (United States)

    Gungor, Ozkan; Kircelli, Fatih; Voroneanu, Luminita; Covic, Adrian; Ok, Ercan

    2013-01-01

    Cardiovascular disease constitutes the major cause of mortality in patients with chronic kidney disease. Arterial stiffness is an important contributor to the occurrence and progression of cardiovascular disease. Various risk factors, including altered hormone levels, have been suggested to be associated with arterial stiffness. Based on the background that chronic kidney disease predisposes individuals to a wide range of hormonal changes, we herein review the available data on the association between arterial stiffness and hormones in patients with chronic kidney disease and summarize the data for the general population.

  1. Gut microbiota in chronic kidney disease.

    Science.gov (United States)

    Cigarran Guldris, Secundino; González Parra, Emilio; Cases Amenós, Aleix

    The intestinal microflora maintains a symbiotic relationship with the host under normal conditions, but its imbalance has recently been associated with several diseases. In chronic kidney disease (CKD), dysbiotic intestinal microflora has been reported with an increase in pathogenic flora compared to symbiotic flora. An enhanced permeability of the intestinal barrier, allowing the passage of endotoxins and other bacterial products to the blood, has also been shown in CKD. By fermenting undigested products that reach the colon, the intestinal microflora produce indoles, phenols and amines, among others, that are absorbed by the host, accumulate in CKD and have harmful effects on the body. These gut-derived uraemic toxins and the increased permeability of the intestinal barrier in CKD have been associated with increased inflammation and oxidative stress and have been involved in various CKD-related complications, including cardiovascular disease, anaemia, mineral metabolism disorders or the progression of CKD. The use of prebiotics, probiotics or synbiotics, among other approaches, could improve the dysbiosis and/or the increased permeability of the intestinal barrier in CKD. This article describes the situation of the intestinal microflora in CKD, the alteration of the intestinal barrier and its clinical consequences, the harmful effects of intestinal flora-derived uraemic toxins, and possible therapeutic options to improve this dysbiosis and reduce CKD-related complications. Copyright © 2016 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.

  2. The link between chronic kidney disease and cardiovascular disease.

    Science.gov (United States)

    Said, Sarmad; Hernandez, German T

    2014-07-01

    It is well known that patients with chronic kidney disease (CKD) have a strong risk of cardiovascular disease (CVD). However, the excess risk of cardiovascular disease in patients with CKD is only partially explained by the presence of traditional risk factors, such as hypertension and diabetes mellitus. Directory of Open Access Journals (DOAJ), Google Scholar, PubMed, EBSCO and Web of Science has been searched. Chronic kidney disease even in its early stages can cause hypertension and potentiate the risk for cardiovascular disease. However, the practice of intensive blood pressure lowering was criticized in recent systematic reviews. Available evidence is inconclusive but does not prove that a blood pressure target of less than 130/80 mmHg as recommended in the guidelines improves clinical outcomes more than a target of less than 140/90 mmHg in adults with CKD. The association between CKD and CVD has been extensively documented in the literature. Both CKD and CVD share common traditional risk factors, such as smoking, obesity, hypertension, diabetes mellitus, and dyslipidemia. However, cardiovascular disease remains often underdiagnosed und undertreated in patients with CKD. It is imperative that as clinicians, we recognize that patients with CKD are a group at high risk for developing CVD and cardiovascular events. Additional studies devoted to further understand the risk factors for CVD in patients with CKD are necessary to develop and institute preventative and treatment strategies to reduce the high morbidity and mortality in patients with CKD.

  3. Resistive index for kidney evaluation in normal and diseased cats.

    Science.gov (United States)

    Tipisca, Vlad; Murino, Carla; Cortese, Laura; Mennonna, Giuseppina; Auletta, Luigi; Vulpe, Vasile; Meomartino, Leonardo

    2016-06-01

    The objectives were to determine the resistive index (RI) in normal cats and in cats with various renal diseases, and to evaluate the effect of age on RI. The subjects were cats that had ultrasonography (US) of the urinary tract and RI measurement at our centre between January 2003 and April 2014. Based on clinical evaluation, biochemical and haematological tests, urinalysis and US, the cats were classified as healthy or diseased. RI measurements were made from the interlobar or arcuate arteries. Data were analysed for differences between the right and the left kidney, the two sexes, different age groups in healthy cats, and between healthy and diseased cats. A total of 116 cats (68 males, 48 females) were included: 24 healthy and 92 diseased. In the healthy cats, RI (mean ± SD) differed significantly (P = 0.02) between the right kidney (0.54 ± 0.07) and the left kidney (0.59 ± 0.08). For the left kidney, RI was significantly higher in cats with chronic kidney disease (0.73 ± 0.12) and acute kidney injury (0.72 ± 0.08) (P = 0.0008). For the right kidney, RI was significantly higher in cats with chronic kidney disease (0.72 ± 0.11), acute kidney injury (0.74 ± 0.08), polycystic kidney disease (0.77 ± 0.11) and renal tumour (0.74 ± 0.001) (P cats, useful in the differential diagnosis of diffuse renal diseases. While it does not change with the age of the cat, ultrasonographers should be aware that RI may differ between the two kidneys. © ISFM and AAFP 2015.

  4. Nutrition for Early Chronic Kidney Disease in Adults

    Science.gov (United States)

    ... Disease (CKD) Eating Right Related Topics English English French Español Section Navigation Chronic Kidney Disease (CKD) What ... foods, instead of deep frying. Cook with nonstick cooking spray or a small amount of olive oil ...

  5. Chronic kidney disease in Chinese postmenopausal women: A ...

    African Journals Online (AJOL)

    2016-07-11

    Jul 11, 2016 ... Data were collected on blood pressure, serum creatinine, urinary albumin, and urinary creatinine. ... onset) have a high risk of developing chronic kidney disease ..... Cardiovascular diseases are the most common causes of.

  6. Association of periodontitis and chronic kidney disease in dogs

    Directory of Open Access Journals (Sweden)

    S. U. Nabi

    2014-06-01

    Full Text Available Aim: The purpose of our study is to study the etiopathogenesis of periodontitis in chronic kidney disease and to identify a correlation between periodontitis and chronic kidney disease, with the help of periodontal exaamination, ultrasonographic and hematobiochemical analysis. Materials and Methods: 46 dogs with renal failure were studied and classified as presenting a slight (56.52%, moderate (36.95% and severe (47.8% degree of periodontal disease. Results: Marked gingival recession involving whole maxillary dental arcade, Oral mucosa ulcers and tissue necrosis and mobility of mandibular incisors was observed in dogs with chronic kidney disease. Dogs with normal renal function were observed to have minimal gingival recession of the mandibular teeth only. Conclusion: In view of the causative association between periodontal infection, generalized inflammation and important systemic diseases like chronic kidney disease, we hypothesize that targeted prophylaxis and careful treatment of oral diseases can prevent the progression of renal failure

  7. Autosomal Recessive Polycystic Kidney Disease: Antenatal Diagnosis and Histopathological Correlation

    Directory of Open Access Journals (Sweden)

    Dayananda Kumar Rajanna

    2013-01-01

    Full Text Available Autosomal recessive polycystic kidney disease (ARPKD is one of the most common inheritable disease manifesting in infancy and childhood with a frequency of 1:6,000 to 1:55,000 births. The patient in her second trimester presented with a history of amenorrhea. Ultrasound examination revealed bilateral, enlarged, hyperechogenic kidneys, placentomegaly, and severe oligohydramnios. The pregnancy was terminated. An autopsy was performed on the fetus. Both the kidneys were found to be enlarged and the cut surface showed numerous cysts. The liver sections showed changes due to fibrosis. The final diagnosis of autosomal recessive polycystic kidney disease was made based on these findings. In this article, we correlate the ante-natal ultrasound and histopathological findings in autosomal recessive polycystic kidney disease.

  8. Bone Marrow and Kidney Transplant for Patients With Chronic Kidney Disease and Blood Disorders

    Science.gov (United States)

    2017-03-21

    Chronic Kidney Disease; Acute Myeloid Leukemia (AML); Acute Lymphoblastic Leukemia (ALL); Chronic Myelogenous Leukemia (CML); Chronic Lymphocytic Leukemia (CLL); Non-Hodgkin's Lymphoma (NHL); Hodgkin Disease; Multiple Myeloma; Myelodysplastic Syndrome (MDS); Aplastic Anemia; AL Amyloidosis; Diamond Blackfan Anemia; Myelofibrosis; Myeloproliferative Disease; Sickle Cell Anemia; Autoimmune Diseases; Thalassemia

  9. Chronic kidney disease among children in Guatemala.

    Science.gov (United States)

    Cerón, Alejandro; Fort, Meredith P; Morine, Chris M; Lou-Meda, Randall

    2014-12-01

    To describe the distribution of pediatric chronic kidney disease (CKD) in Guatemala, estimate incidence and prevalence of pediatric end-stage renal disease (ESRD), and estimate time to progress to ESRD. This study analyzed the registry of the only pediatric nephrology center in Guatemala, from 2004-2013. Incidence and prevalence were calculated for annual periods. Moran's index for spatial autocorrelation was used to determine significance of geographic distribution of incidence. Time to progress to ESRD and associated risk factors were calculated with multivariate Cox regression. Of 1 545 patients from birth to less than 20 years of age, 432 had chronic renal failure (CRF). Prevalence and incidence of ESRD were 4.9 and 4.6 per million age-related population, respectively. Incidence was higher for the Pacific coast and Guatemala City. The cause of CRF was undetermined in 43% of patients. Average time to progress to ESRD was 21.9 months; factors associated with progression were: older age, diagnosis of glomerulopathies, and advanced-stage CKD at consultation. Prevalence and incidence of ESRD in Guatemala are lower than in other countries. This may reflect poor access to diagnosis. Areas with higher incidence and large proportion of CKD of undetermined cause are compatible with other studies from the geographic subregion. Findings on progression to ESRD may reflect delayed referral.

  10. Dietary protein intake and chronic kidney disease.

    Science.gov (United States)

    Ko, Gang Jee; Obi, Yoshitsugu; Tortorici, Amanda R; Kalantar-Zadeh, Kamyar

    2017-01-01

    High-protein intake may lead to increased intraglomerular pressure and glomerular hyperfiltration. This can cause damage to glomerular structure leading to or aggravating chronic kidney disease (CKD). Hence, a low-protein diet (LPD) of 0.6-0.8 g/kg/day is often recommended for the management of CKD. We reviewed the effect of protein intake on incidence and progression of CKD and the role of LPD in the CKD management. Actual dietary protein consumption in CKD patients remains substantially higher than the recommendations for LPD. Notwithstanding the inconclusive results of the 'Modification of Diet in Renal Disease' (MDRD) study, the largest randomized controlled trial to examine protein restriction in CKD, several prior and subsequent studies and meta-analyses appear to support the role of LPD on retarding progression of CKD and delaying initiation of maintenance dialysis therapy. LPD can also be used to control metabolic derangements in CKD. Supplemented LPD with essential amino acids or their ketoanalogs may be used for incremental transition to dialysis especially on nondialysis days. The LPD management in lieu of dialysis therapy can reduce costs, enhance psychological adaptation, and preserve residual renal function upon transition to dialysis. Adherence and adequate protein and energy intake should be ensured to avoid protein-energy wasting. A balanced and individualized dietary approach based on LPD should be elaborated with periodic dietitian counseling and surveillance to optimize management of CKD, to assure adequate protein and energy intake, and to avoid or correct protein-energy wasting.

  11. Chronic kidney disease among children in Guatemala

    Directory of Open Access Journals (Sweden)

    Alejandro Cerón

    2014-12-01

    Full Text Available OBJECTIVE: To describe the distribution of pediatric chronic kidney disease (CKD in Guatemala, estimate incidence and prevalence of pediatric end-stage renal disease (ESRD, and estimate time to progress to ESRD. METHODS: This study analyzed the registry of the only pediatric nephrology center in Guatemala, from 2004-2013. Incidence and prevalence were calculated for annual periods. Moran's index for spatial autocorrelation was used to determine significance of geographic distribution of incidence. Time to progress to ESRD and associated risk factors were calculated with multivariate Cox regression. RESULTS: Of 1 545 patients from birth to less than 20 years of age, 432 had chronic renal failure (CRF. Prevalence and incidence of ESRD were 4.9 and 4.6 per million age-related population, respectively. Incidence was higher for the Pacific coast and Guatemala City. The cause of CRF was undetermined in 43% of patients. Average time to progress to ESRD was 21.9 months; factors associated with progression were: older age, diagnosis of glomerulopathies, and advanced-stage CKD at consultation. CONCLUSIONS: Prevalence and incidence of ESRD in Guatemala are lower than in other countries. This may reflect poor access to diagnosis. Areas with higher incidence and large proportion of CKD of undetermined cause are compatible with other studies from the geographic subregion. Findings on progression to ESRD may reflect delayed referral.

  12. COMORBIDITY OF KIDNEY STONES AND PYCHIATRIC DISEASE

    OpenAIRE

    Bilić, Vedran; Marčinko, Darko

    2010-01-01

    This paper describes a patient who is suffering from PTSD with elements of hypochondria, panic attacks and episodes of 0depression in comorbidity with kidney stones. Kidney stones provoked egzacerbation of psychiatric symptoms. Kidney stones and frustration about them have taken part of provoking factor, the last drop, which led to regression of otherwise precarious, but compensated patient’s mental functioning which resulted in development of psychiatric symptoms.

  13. Laparoscopic assisted percutaneous nephrolithotomy in chronic kidney disease patients with ectopic pelvic kidney

    Directory of Open Access Journals (Sweden)

    Sujata K Patwardhan

    2017-01-01

    Conclusion: Although laparoscopic assisted PCNL is an option in the management of patients with stone disease in ectopic pelvic kidney, prolonged time for healing of tract may increase postoperative morbidity in these patients with impaired renal function.

  14. Bi-allelic Mutations in PKD1L1 Are Associated with Laterality Defects in Humans.

    Science.gov (United States)

    Vetrini, Francesco; D'Alessandro, Lisa C A; Akdemir, Zeynep C; Braxton, Alicia; Azamian, Mahshid S; Eldomery, Mohammad K; Miller, Kathryn; Kois, Chelsea; Sack, Virginia; Shur, Natasha; Rijhsinghani, Asha; Chandarana, Jignesh; Ding, Yan; Holtzman, Judy; Jhangiani, Shalini N; Muzny, Donna M; Gibbs, Richard A; Eng, Christine M; Hanchard, Neil A; Harel, Tamar; Rosenfeld, Jill A; Belmont, John W; Lupski, James R; Yang, Yaping

    2016-10-06

    Disruption of the establishment of left-right (L-R) asymmetry leads to situs anomalies ranging from situs inversus totalis (SIT) to situs ambiguus (heterotaxy). The genetic causes of laterality defects in humans are highly heterogeneous. Via whole-exome sequencing (WES), we identified homozygous mutations in PKD1L1 from three affected individuals in two unrelated families. PKD1L1 encodes a polycystin-1-like protein and its loss of function is known to cause laterality defects in mouse and medaka fish models. Family 1 had one fetus and one deceased child with heterotaxy and complex congenital heart malformations. WES identified a homozygous splicing mutation, c.6473+2_6473+3delTG, which disrupts the invariant splice donor site in intron 42, in both affected individuals. In the second family, a homozygous c.5072G>C (p.Cys1691Ser) missense mutation was detected in an individual with SIT and congenital heart disease. The p.Cys1691Ser substitution affects a highly conserved cysteine residue and is predicted by molecular modeling to disrupt a disulfide bridge essential for the proper folding of the G protein-coupled receptor proteolytic site (GPS) motif. Damaging effects associated with substitutions of this conserved cysteine residue in the GPS motif have also been reported in other genes, namely GPR56, BAI3, and PKD1 in human and lat-1 in C. elegans, further supporting the likely pathogenicity of p.Cys1691Ser in PKD1L1. The identification of bi-allelic PKD1L1 mutations recapitulates previous findings regarding phenotypic consequences of loss of function of the orthologous genes in mice and medaka fish and further expands our understanding of genetic contributions to laterality defects in humans. Copyright © 2016 American Society of Human Genetics. Published by Elsevier Inc. All rights reserved.

  15. Renal angiomyolipoma bleeding in a patient with TSC2/PKD1 contiguous gene syndrome after 17 years of renal replacement therapy.

    Science.gov (United States)

    Furlano, Mónica; Barreiro, Yaima; Martí, Teresa; Facundo, Carme; Ruiz-García, César; DaSilva, Iara; Ayasreh, Nadia; Cabrera-López, Cristina; Ballarín, José; Ars, Elisabet; Torra, Roser

    We report the case of a 32-year-old male diagnosed with TSC2/PKD1 contiguous gene syndrome, presenting with tuberous sclerosis (TS) and autosomal dominant polycystic kidney disease simultaneously. He progressed to end-stage renal disease and received a kidney transplant at the age of 12. The native kidneys presented angiomyolipomas (AML), which are common benign tumours in patients with TS. Seventeen years after transplantation, he presented with abdominal pain, anaemia and a retroperitoneal haematoma, the latter caused by renal AML bleeding. Selective embolisation was performed. Our patient could have benefited from the administration of mTOR inhibitors at transplant. This therapy is immunosuppressive and reduces the size of benign tumours in TS as well as the risk of rupture and bleeding. This patient did not receive mTOR inhibitors at the time of the transplant because the relationship between mTOR inhibitors and TS was unknown at that time. This case confirms the persistent risk of renal AML bleeding for both transplanted patients and patients on dialysis. As a result, we would recommend routine check-ups of native kidneys and nephrectomy assessment. Copyright © 2017 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.

  16. Chronic kidney disease and the skeleton

    Institute of Scientific and Technical Information of China (English)

    Paul D Miller

    2014-01-01

    Fractures across the stages of chronic kidney disease (CKD) could be due to osteoporosis, some form of renal osteodystrophy defined by specific quantitative histomorphometry or chronic kidney disease–mineral and bone disorder (CKD–MBD). CKD–MBD is a systemic disease that links disorders of mineral and bone metabolism due to CKD to either one or all of the following:abnormalities of calcium, phosphorus, parathyroid hormone or vitamin D metabolism;abnormalities in bone turnover, mineralization, volume, linear growth or strength;or vascular or other soft-tissue calcification. Osteoporosis, as defined by the National Institutes of Health, may coexist with renal osteodystrophy or CKD–MBD. Differentiation among these disorders is required to manage correctly the correct disorder to reduce the risk of fractures. While the World Health Organization (WHO) bone mineral density (BMD) criteria for osteoporosis can be used in patients with stages 1–3 CKD, the disorders of bone turnover become so aberrant by stages 4 and 5 CKD that neither the WHO criteria nor the occurrence of a fragility fracture can be used for the diagnosis of osteoporosis. The diagnosis of osteoporosis in stages 4 and 5 CKD is one of the exclusion—excluding either renal osteodystrophy or CKD–MBD as the cause of low BMD or fragility fractures. Differentiations among the disorders of renal osteodystrophy, CKD–MBD or osteoporosis are dependent on the measurement of specific biochemical markers, including serum parathyroid hormone (PTH) and/or quantitative bone histomorphometry. Management of fractures in stages 1–3 CKD does not differ in persons with or without CKD with osteoporosis assuming that there is no evidence for CKD–MBD, clinically suspected by elevated PTH, hyperphosphatemia or fibroblast growth factor 23 due to CKD. Treatment of fractures in persons with osteoporosis and stages 4 and 5 CKD is not evidence-based, with the exception of post-hoc analysis suggesting efficacy and

  17. Kidney disease and aging: A reciprocal relation.

    Science.gov (United States)

    Kooman, Jeroen P; van der Sande, Frank M; Leunissen, Karel M L

    2017-01-01

    Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are overrepresented in elderly patients. This provides specific challenges for the treatment, as the start of dialysis in vulnerable elderly patients may be associated with a rapid decline in functional performance. However, prognosis in elderly patients with ESRD is quite variable and related to the presence of comorbidity and geriatric impairments. The decision to start dialysis in elderly patients should always be based on shared decision making, which may be aided by the use of prediction models which should however not be used to withhold dialysis treatment. The treatment of ESRD in elderly patients should be based on a multidimensional treatment plan with a role for active rehabilitation. Moreover, there also appears to be a reciprocal relationship between aging and CKD, as the presence of geriatric complications is also high in younger patients with ESRD. This has led to the hypothesis of a premature aging process associated with CKD, resulting in different phenotypes such as premature vascular aging, muscle wasting, bone disease, cognitive dysfunction and frailty. Prevention and treatment of this phenotype is based on optimal treatment of CKD, associated comorbidities, and lifestyle factors by established treatments. For the future, interventions, which are developed to combat the aging process in general, might also have relevance for the treatment of patients with CKD, but their role should always be investigated in adequately powered clinical trials, as results obtained in experimental trials may not be directly translatable to the clinical situation of elderly patients. In the meantime, physical exercise is a very important intervention, by improving both physical capacity and functional performance, as well as by a direct effect on the aging process. Copyright © 2016 Elsevier Inc. All rights reserved.

  18. Cardiovascular Disease and Chronic Inflammation in End Stage Kidney Disease

    Directory of Open Access Journals (Sweden)

    Sofia Zyga

    2013-01-01

    Full Text Available Background: Chronic Kidney Disease (CKD is one of the most severe diseases worldwide. In patients affected by CKD, a progressive destruction of the nephrons is observed not only in structuralbut also in functional level. Atherosclerosis is a progressive disease of large and medium-sized arteries. It is characterized by the deposition of lipids and fibrous elements and is a common complication of the uremic syndrome because of the coexistence of a wide range of risk factors. High blood pressure, anaemia, insulin resistance, inflammation, high oxidative stress are some of the most common factors that cause cardiovascular disease and atherogenesis in patients suffering from End Stage Kidney Disease (ESRD. At the same time, the inflammatory process constitutes a common element in the apparition and development of CKD. A wide range of possible causes can justify the development of inflammation under uremic conditions. Such causes are oxidative stress, oxidation, coexistentpathological conditions as well as factors that are due to renal clearance techniques. Patients in ESRD and coronary disease usually show increased acute phase products. Pre-inflammatory cytokines, such as IL-6 and TNF-a, and acute phase reactants, such as CRP and fibrinogen, are closely related. The treatment of chronic inflammation in CKD is of high importance for the development ofthe disease as well as for the treatment of cardiovascular morbidity.Conclusions: The treatment factors focus on the use of renin-angiotensic system inhibitors, acetylsalicylic acid, statins and anti-oxidant treatment in order to prevent the action of inflammatorycytokines that have the ability to activate the mechanisms of inflammation.

  19. Chronic kidney disease in Nigeria: primary care physicians must ...

    African Journals Online (AJOL)

    Chronic Kidney disease (CKD) is one of the world's major public health problems and the prevalence of Kidney failure is rising steadily. ... Only thirty percent (30%) of the doctors tested for proteinuria in thirty nine percent (39%) of those they were treating for Diabetes Mellitus and only thirty five percent (35%) of the doctors ...

  20. Obesity and kidney disease: hidden consequences of the epidemic

    African Journals Online (AJOL)

    for chronic kidney disease (CKD), like diabetes and hypertension, and it has a direct impact .... meta-analysis, kidney cancers had the third highest risk associated with obesity (relative ..... Ellington AA, Malik AR, Klee GG, et al. Association of ...

  1. Awareness, knowledge and perception of chronic kidney disease in ...

    African Journals Online (AJOL)

    2015-06-29

    Jun 29, 2015 ... Abdominal obesity and cigarette smoking were seen in 14.6% and 16.6% respectively. Hypertension was ... Chronic kidney disease (CKD) is defined as abnormalities of kidney structure ... majority affected are unable to sustain hemodialysis and ..... knowledge and then probably took measures to prevent.

  2. Noninvasive diagnosis of chronic kidney diseases using urinary proteome analysis

    DEFF Research Database (Denmark)

    Siwy, Justyna; Zürbig, Petra; Argilés, Angel

    2017-01-01

    BACKGROUND: In spite of its invasive nature and risks, kidney biopsy is currently required for precise diagnosis of many chronic kidney diseases (CKDs). Here, we explored the hypothesis that analysis of the urinary proteome can discriminate different types of CKD irrespective of the underlying me...

  3. Periodontitis associated with chronic kidney disease among Mexican Americans.

    Science.gov (United States)

    Ioannidou, Effie; Hall, Yoshio; Swede, Helen; Himmelfarb, Jonathan

    2013-01-01

    In comparison to non-Hispanic whites, a number of health-care disparities, including poor oral health, have been identified among Hispanics in general and Mexican Americans in particular. We hypothesized that Mexican Americans with chronic kidney disease (CKD) would have higher prevalence of chronic periodontitis compared with Mexican Americans with normal kidney function, and that the level of kidney function would be inversely related to the prevalence of periodontal disease. We examined this hypothesis using the National Health and Nutrition Examination Survey 1988-1994 (NHANES III) data set. We followed the American Academy of Periodontology/Center for Disease Control and Prevention case definition for periodontitis. Glomerular filtration rate was estimated using the CKD-Epidemiology equation for Hispanic populations. The classification to CKD stages was based on the National Kidney Foundation Kidney Disease Outcomes Quality Initiative. Periodontitis prevalence increased across the kidney function groups showing a statistically significant dose-response association (Pperiodontitis compared with Mexican Americans with normal kidney function after adjusting for potential confounders such as smoking, diabetes, and socioeconomic status. Multivariate adjusted odds ratio for periodontitis significantly increased with 1, 5, and 10 mL/minute estimated glomerular filtration rate reduction from the mean. This is the first report, to the best our knowledge, that showed an increase of periodontitis prevalence with decreased kidney function in this population. © 2012 American Association of Public Health Dentistry.

  4. The role of the immune system in kidney disease.

    Science.gov (United States)

    Tecklenborg, J; Clayton, D; Siebert, S; Coley, S M

    2018-05-01

    The immune system and the kidneys are closely linked. In health the kidneys contribute to immune homeostasis, while components of the immune system mediate many acute forms of renal disease and play a central role in progression of chronic kidney disease. A dysregulated immune system can have either direct or indirect renal effects. Direct immune-mediated kidney diseases are usually a consequence of autoantibodies directed against a constituent renal antigen, such as collagen IV in anti-glomerular basement membrane disease. Indirect immune-mediated renal disease often follows systemic autoimmunity with immune complex formation, but can also be due to uncontrolled activation of the complement pathways. Although the range of mechanisms of immune dysregulation leading to renal disease is broad, the pathways leading to injury are similar. Loss of immune homeostasis in renal disease results in perpetual immune cell recruitment and worsening damage to the kidney. Uncoordinated attempts at tissue repair, after immune-mediated disease or non-immune mediated injury, result in fibrosis of structures important for renal function, leading eventually to kidney failure. As renal disease often manifests clinically only when substantial damage has already occurred, new diagnostic methods and indeed treatments must be identified to inhibit further progression and promote appropriate tissue repair. Studying cases in which immune homeostasis is re-established may reveal new treatment possibilities. © 2018 British Society for Immunology.

  5. Pregnancy in autosomal recessive polycystic kidney disease.

    Science.gov (United States)

    Banks, Nicole; Bryant, Joy; Fischer, Roxanne; Huizing, Marjan; Gahl, William A; Gunay-Aygun, Meral

    2015-03-01

    Autosomal recessive polycystic kidney disease (ARPKD) is the most common childhood-onset ciliopathy. As treatments improve, more women are reaching reproductive age, but little is known about ARPKD and pregnancy. In our ongoing study on ARPKD and other ciliopathies, 12 females over 18 years of age were identified and systematically evaluated. Six had children; four carried pregnancies and delivered, one used assisted reproductive technology and had a surrogate carry the pregnancy, and one adopted. We report the outcomes of four pregnancies with live birth deliveries and two women who chose alternate family building options. Patient one was diagnosed at 6 months, and at age 21 had a pregnancy complicated by transient worsening of renal function (creatinine increase from 1.15 to 1.78 mg/dL). Patient two was diagnosed with ARPKD at age seven and had an uncomplicated pregnancy at age 23. Patient three was diagnosed incidentally with ARPKD at age 23, 3 months after completion of an uncomplicated pregnancy. Patient four who had an uncomplicated pregnancy at age 33 was diagnosed with ARPKD at age 46. Women with ARPKD face reproductive decisions largely bereft of information about the pregnancies of other ARPKD patients. We report four cases of pregnancy and ARPKD to expand current knowledge and encourage further research.

  6. Dietary Metabolites and Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Sho Hasegawa

    2017-04-01

    Full Text Available Dietary contents and their metabolites are closely related to chronic kidney disease (CKD progression. Advanced glycated end products (AGEs are a type of uremic toxin produced by glycation. AGE accumulation is not only the result of elevated glucose levels or reduced renal clearance capacity, but it also promotes CKD progression. Indoxyl sulfate, another uremic toxin derived from amino acid metabolism, accumulates as CKD progresses and induces tubulointerstitial fibrosis and glomerular sclerosis. Specific types of amino acids (d-serine or fatty acids (palmitate are reported to be closely associated with CKD progression. Promising therapeutic targets associated with nutrition include uremic toxin absorbents and inhibitors of AGEs or the receptor for AGEs (RAGE. Probiotics and prebiotics maintain gut flora balance and also prevent CKD progression by enhancing gut barriers and reducing uremic toxin formation. Nrf2 signaling not only ameliorates oxidative stress but also reduces elevated AGE levels. Bardoxolone methyl, an Nrf2 activator and NF-κB suppressor, has been tested as a therapeutic agent, but the phase 3 clinical trial was terminated owing to the high rate of cardiovascular events. However, a phase 2 trial has been initiated in Japan, and the preliminary analysis reveals promising results without an increase in cardiovascular events.

  7. Central Blood Pressure and Chronic Kidney Disease Progression

    Directory of Open Access Journals (Sweden)

    Debbie L. Cohen

    2011-01-01

    Full Text Available Hypertension, diabetes, and proteinuria are well-recognized risk factors for progressive kidney function loss. However, despite excellent antihypertensive and antidiabetic drug therapies, which also often lower urinary protein excretion, there remains a significant reservoir of patients with chronic kidney disease who are at high risk for progression to end-stage kidney disease. This has led to the search for less traditional cardiovascular risk factors that will help stratify patients at risk for more rapid kidney disease progression. Among these are noninvasive estimates of vascular structure and function. Arterial stiffness, manifested by the pulse wave velocity in the aorta, has been established in a number of studies as a significant risk factor for kidney disease progression and cardiovascular endpoints. Much less well studied in chronic kidney disease are measures of central arterial pressures. In this paper we cover the physiology behind the generation of the central pulse wave contour and the studies available using these approaches and conclude with some speculations on the rationale for why measurements of central pressure may be informative for the study of chronic kidney disease progression.

  8. Clinico-pathological features of kidney disease in diabetic cases.

    Science.gov (United States)

    Furuichi, Kengo; Shimizu, Miho; Okada, Hirokazu; Narita, Ichiei; Wada, Takashi

    2018-03-21

    Diabetic kidney disease is the major cause of end-stage kidney disease in developed countries. However, the onset of kidney disorder and the progression pattern of kidney dysfunction and proteinuria greatly vary cases by cases. Therefore, risk classification with clinical data and pathological findings is important. Recent clinico-pathological study with kidney biopsy samples from diabetic patients revealed that pathological changes of diabetic nephropathy are characteristic and have special impacts on prognosis in each clinical stage. Moreover, comparison of the clinico-pathological findings of diabetic nephropathy with hypertensive nephrosclerosis revealed that there are few differences in their pathological findings in cases with low albuminuria and preserved estimated glomerular filtration rate (eGFR). Because it is so difficult to clearly distinguish pure kidney lesions caused by diabetes and kidney lesions due to effects other than diabetes, it is vital that these overlapped pathological findings be confirmed on kidney biopsy in cases of early stage diabetes. Further research is warranted regarding the pathogenesis of diabetic nephropathy and indication of kidney biopsy in diabetic cases.

  9. Vascular cognitive impairments in chronic kidney disease

    Directory of Open Access Journals (Sweden)

    I. V. Rogova

    2015-01-01

    Full Text Available Objective: to study the specific features of development of cognitive impairments (CIs, the role of traditional cardiovascular risk factors and renal failure-induced factors in patients with Stages I–IV chronic kidney disease (CKD and to assess an association of CIs with the signs of vascular wall remodeling in them. Patients and methods. Fifty-one patients aged 53±10 years with CKD were examined. Among them, there were 20 patients with Stages I–II CKD: a glomerular filtration rate (GFR of і60 ml/min/1.73 m2, signs of renal lesion; 20 with Stages III CKD: a GFR of <60–30 ml/min/1.73 m2, and 11 with Stages VI CKD: a GFR of <30–15 ml/min/1.73 m2. Results and discussion. CIs were more common in the patients with Stages III–IV than in those with Stages I–II, as shown by the scores of the mini-mental state examination (p<0.001, the frontal assessment battery (p=0.001, and the regulatory function test (p<0.001. These tests showed that the magnitude of CIs increased with the higher stage of CKD. Stages III–IV CKD is an independent predictor of CIs in persons with predialysis-stage kidney lesion. CIs were found to be related to hyperhomocysteinemia, anemia, abdominal obesity, left ventricular hypertrophy, and patient age. The signs of atherosclerotic lesion of the common carotid arteries and the indicators of arterial stiffness were also associated with the incidence and magnitude of CIs in CKD. The detection of CIs in patients with early CKD allows one to timely initiate adequate therapy aimed particularly at improving cerebral circulation, eliminating the impact of risk factors, and slowing down the vascular remodeling. The management tactics for patients with CKD must involve the identification and correction of cardiovascular risk factors, and duplex scanning of the wall of the common carotid arteries may be used as a noninvasive method to assess the risk of the development and progression of CIs in predialysis CKD. 

  10. Dietary Protein Intake and Chronic Kidney Disease

    Science.gov (United States)

    Ko, Gang Jee; Obi, Yoshitsugu; Tortoricci, Amanda R.; Kalantar-Zadeh, Kamyar

    2018-01-01

    Purpose of review High protein intake may lead to increased intraglomerular pressure and glomerular hyperfiltration. This can cause damage to glomerular structure leading to or aggravating chronic kidney disease (CKD). Hence, a low protein diet (LPD) of 0.6–0.8 g/kg/day is often recommended for the management of CKD. We reviewed the effect of protein intake on incidence and progression of CKD and the role of LPD the CKD management. Recent findings Actual dietary protein consumption in CKD patients remain substantially higher than the recommendations for LPD. Notwithstanding the inconclusive results of the Modification of Diet in Renal Disease (MDRD) study, the largest randomized controlled trial to examine protein restriction in CKD, several prior and subsequent studies and meta-analyses including secondary analyses of the MDRD data appear to support the role of LPD on retarding progression of CKD and delaying initiation of maintenance dialysis therapy. LPD can also be used to control metabolic derangements in CKD. Supplemented LPD with essential amino acids or their keto-analogs may be used for incremental transition to dialysis especially in non-dialysis days. An LPD management in lieu of dialysis therapy can reduce costs, enhance psychological adaptation, and preserve residual renal function upon transition to dialysis. Adherence and adequate protein and energy intake should be ensured to avoid protein-energy wasting. Summary A balanced and individualized dietary approach based on LPD should be elaborated with periodic dietitian counselling and surveillance to optimize management of CKD, to assure adequate protein and energy intake and to avoid or correct protein-energy wasting. PMID:27801685

  11. Polycystic kidney disease in a patient with achondroplasia ...

    African Journals Online (AJOL)

    Autosomal dominant polycystic kidney disease is a multisystem disease involving many organs. An association with other diseases such as tuberous sclerosis, von Hippel-Lindau disease and Marfan syndrome have been previously described. We describe a 35 year old female with achondroplasia who developed ...

  12. Low Phosphorus Diet: Best for Kidney Disease?

    Science.gov (United States)

    ... cereal, rice and pasta White bread, crackers, cereals, rice and pasta Quick breads, biscuits, cornbread, muffins, pancakes or waffles White dinner rolls, bread, bagels or English muffins Dried peas (split, black-eyed), beans (black, garbanzo, lima, kidney, navy, pinto) ...

  13. Pregnancy across the spectrum of chronic kidney disease.

    Science.gov (United States)

    Hladunewich, Michelle A; Melamad, Nir; Bramham, Kate

    2016-05-01

    Management of the pregnant woman with chronic kidney disease is difficult for both nephrologists and obstetricians. Prepregnancy counselling with respect to risk stratification, optimization of maternal health prior to pregnancy, as well as management of the many potential pregnancy-associated complications in this complex patient population remains challenging due to the paucity of large, well-designed clinical studies. Furthermore, the heterogeneity of disease and the relative infrequency of pregnancy, particularly in more advanced stages of chronic kidney disease, leaves many clinicians feeling ill prepared to manage these pregnancies. As such, counselling is imprecise and management varies substantially across centers. All pregnancies in women with chronic kidney disease can benefit from a collaborative multidisciplinary approach with a team that consists of nephrologists experienced in the management of kidney disease in pregnancy, maternal-fetal medicine specialists, high-risk pregnancy nursing staff, dieticians, and pharmacists. Further access to skilled neonatologists and neonatal intensive care unit support is essential given the risks for preterm delivery in this patient population. The goal of this paper is to highlight some of the data that currently exist in the literature, provide management strategies for the practicing nephrologist at all stages of chronic kidney disease, and explore some of the knowledge gaps where future multinational collaborative research efforts should concentrate to improve pregnancy outcomes in women with kidney disease across the globe. Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

  14. Systematic kidney disease management in a population with diabetes mellitus: turning the tide of kidney failure.

    Science.gov (United States)

    Rayner, Hugh C; Hollingworth, Lee; Higgins, Robert; Dodds, Simon

    2011-10-01

    A significant proportion of patients with diabetes mellitus do not get the benefit of treatment that would reduce their risk of progressive kidney disease and reach a nephrologist once significant loss of kidney function has already occurred. Systematic disease management of patients with diabetes and kidney disease. Diverse population (approximately 800,000) in and around Birmingham, West Midlands, UK. Number of outpatient appointments, estimated glomerular filtration rate (eGFR) at first contact with nephrologist, number of patients starting kidney replacement therapy (KRT) and mode of KRT at start. Identification of patients with low or deteriorating trend in eGFR from weekly database review, specialist diabetes-kidney clinic, self-management of blood pressure and transfer to multidisciplinary clinic >12 months before end-stage kidney disease. New patients increased from 62 in 2003 to 132 in 2010; follow-ups fell from 251 to 174. Median eGFR at first clinic visit increased from 28.8 ml/min/1.73 m(2) (range 6.1-67.0) in 2000/2001 to 35.0 (11.1-147.5) in 2010 (pmanagement across a large population significantly improves patient outcomes, increases the productivity of a specialist service and could reduce healthcare costs compared with the current model of care.

  15. Diagnostic approach to chronic kidney disease | Naiker | South ...

    African Journals Online (AJOL)

    Chronic kidney disease (CKD) can be considered to be present if a patient has a glomerular filtration rate 3 months. These include proteinuria, haematuria and radiological abnormalities. Regardless of the stage of CKD, the approach is mainly similar.

  16. Impaired vascular reactivity in patients with chronic kidney disease

    DEFF Research Database (Denmark)

    Tetzner, Fabian; Scholze, Alexandra; Wittstock, Antje

    2008-01-01

    Patients with chronic kidney disease (CKD) show increased cardiovascular morbidity. We hypothesized that vascular properties which can be routinely evaluated noninvasively are related to different stages of CKD and their clinical and biochemical characteristics....

  17. [Phosphate binders in chronic kidney disease: the positions of sevelamer].

    Science.gov (United States)

    Fomin, V V; Shilov, E M; Svistunov, A A; Milovanov, Iu S

    2013-01-01

    The paper shows the role of phosphate binders in the correction of phosphorus and calcium metabolic disturbances in chronic kidney disease. The results of clinical trials demonstrating the efficacy and safety of sevelamer are discussed.

  18. Obesity and kidney disease: hidden consequences of the epidemic

    African Journals Online (AJOL)

    factors for Chronic Kidney Disease (CKD), like diabetes and hypertension, and it ... Epidemiology of obesity in adults and children. Over the last 3 .... Table 1. Studies examining the association of obesity with various measures of CKD. Study.

  19. Genetics Home Reference: REN-related kidney disease

    Science.gov (United States)

    ... 2 Related Information How are genetic conditions and genes named? Additional Information & Resources MedlinePlus (5 links) Encyclopedia: Hyperkalemia Encyclopedia: Renin Health Topic: Anemia Health Topic: Gout Health Topic: Kidney Diseases Additional NIH Resources (2 ...

  20. When Your Child Has a Chronic Kidney Disease

    Science.gov (United States)

    ... Kidney Diseases Treatment begins with dietary changes and medicines. Your child may need to take several medicines, including vitamins, ... be set to remind kids to take their medicine. If your child must take so much medicine that it affects ...

  1. A Soft Computing Approach to Kidney Diseases Evaluation.

    Science.gov (United States)

    Neves, José; Martins, M Rosário; Vilhena, João; Neves, João; Gomes, Sabino; Abelha, António; Machado, José; Vicente, Henrique

    2015-10-01

    Kidney renal failure means that one's kidney have unexpectedly stopped functioning, i.e., once chronic disease is exposed, the presence or degree of kidney dysfunction and its progression must be assessed, and the underlying syndrome has to be diagnosed. Although the patient's history and physical examination may denote good practice, some key information has to be obtained from valuation of the glomerular filtration rate, and the analysis of serum biomarkers. Indeed, chronic kidney sickness depicts anomalous kidney function and/or its makeup, i.e., there is evidence that treatment may avoid or delay its progression, either by reducing and prevent the development of some associated complications, namely hypertension, obesity, diabetes mellitus, and cardiovascular complications. Acute kidney injury appears abruptly, with a rapid deterioration of the renal function, but is often reversible if it is recognized early and treated promptly. In both situations, i.e., acute kidney injury and chronic kidney disease, an early intervention can significantly improve the prognosis. The assessment of these pathologies is therefore mandatory, although it is hard to do it with traditional methodologies and existing tools for problem solving. Hence, in this work, we will focus on the development of a hybrid decision support system, in terms of its knowledge representation and reasoning procedures based on Logic Programming, that will allow one to consider incomplete, unknown, and even contradictory information, complemented with an approach to computing centered on Artificial Neural Networks, in order to weigh the Degree-of-Confidence that one has on such a happening. The present study involved 558 patients with an age average of 51.7 years and the chronic kidney disease was observed in 175 cases. The dataset comprise twenty four variables, grouped into five main categories. The proposed model showed a good performance in the diagnosis of chronic kidney disease, since the

  2. A modified elliptical formula to estimate kidney collagen content in a model of chronic kidney disease.

    Science.gov (United States)

    Nieto, Jake A; Zhu, Janice; Duan, Bin; Li, Jingsong; Zhou, Ping; Paka, Latha; Yamin, Michael A; Goldberg, Itzhak D; Narayan, Prakash

    2018-01-01

    The extent of scarring or renal interstitial collagen deposition in chronic kidney disease (CKD) can only be ascertained by highly invasive, painful and sometimes risky, tissue biopsy. Interestingly, while CKD-related abnormalities in kidney size can often be visualized using ultrasound, not only does the ellipsoid formula used today underestimate true renal size, but the calculated renal size does not inform tubulointerstitial collagen content. We used coronal kidney sections from healthy mice and mice with kidney disease to develop a new formula for estimating renal parenchymal area. While treating the kidney as an ellipse with the major axis (a) the polar distance, this technique involves extending the minor axis (b) into the renal pelvis to obtain a new minor axis, be. The calculated renal parenchymal area is remarkably similar to the true or measured area. Biochemically determined kidney collagen content revealed a strong and positive correlation with the calculated renal parenchymal area. Picrosirius red staining for tubulointerstitial collagen also correlated with calculated renal parenchymal area. The extent of renal scarring, i.e. kidney interstitial collagen content, can now be computed by making just two axial measurements which can easily be accomplished via noninvasive imaging of this organ.

  3. Renal oxygenation and hemodynamics in acute kidney injury and chronic kidney disease

    Science.gov (United States)

    Singh, Prabhleen; Ricksten, Sven-Erik; Bragadottir, Gudrun; Redfors, Bengt; Nordquist, Lina

    2013-01-01

    Summary 1. Acute kidney injury (AKI) puts a major burden on health systems that may arise from multiple initiating insults, including ischemia-reperfusion injury, cardiovascular surgery, radio-contrast administration as well as sepsis. Similarly, the incidence and prevalence of chronic kidney disease (CKD) continues to increase with significant morbidity and mortality. Moreover, an increasing number of AKI patients survive to develop CKD and end-stage kidney disease (ESRD). 2. Although the mechanisms for development of AKI and progression of CKD remain poorly understood, initial impairment of oxygen balance is likely to constitute a common pathway, causing renal tissue hypoxia and ATP starvation that will in turn induce extracellular matrix production, collagen deposition and fibrosis. Thus, possible future strategies for one or both conditions may involve dopamine, loop-diuretics, inducible nitric oxide synthase inhibitors and atrial natriuretic peptide, substances that target kidney oxygen consumption and regulators of renal oxygenation such as nitric oxide and heme oxygenase-1. PMID:23360244

  4. Urea and impairment of the Gut-Kidney axis in Chronic Kidney Disease.

    Science.gov (United States)

    Di Iorio, Biagio Raffaele; Marzocco, Stefania; Nardone, Luca; Sirico, Marilisa; De Simone, Emanuele; Di Natale, Gabriella; Di Micco, Lucia

    2017-12-05

    Gut microbiota can be considered a real organ coordinating health and wellness of our body. It is made of more than 100 trillions of microorganisms, thus about 3 times higher than the number of human body cells and more than 150 times than human genes containing 1000 different microbe species. It has been described a symbiotic relationship between gut and kidney, confirmed by several observations. This is a bi-directional relation with a mutual influence, even when kidney disease occurs, and consequent alterations of intestinal microbiota and production of uremic toxins, that in turn worsens kidney disease and its progression. Our review analyzes the components of gut-kidney axis and relative clinical consequences. Copyright by Società Italiana di Nefrologia SIN, Rome, Italy.

  5. Pharmacological management of acute kidney injury and chronic kidney disease in neonates.

    Science.gov (United States)

    Jetton, Jennifer G; Sorenson, Mark

    2017-04-01

    Both acute kidney injury (AKI) and chronic kidney disease (CKD) are seen more frequently in the neonatal intensive care unit (NICU) as advances in supportive care improve the survival of critically ill infants as well as those with severe, congenital kidney and urinary tract anomalies. Many aspects of the infant's care, including fluid balance, electrolyte and mineral homeostasis, acid-base balance, and growth and nutrition require close monitoring by and collaboration among neonatologists, nephrologists, dieticians, and pharmacologists. This educational review summarizes the therapies widely used for neonates with AKI and CKD. Use of these therapies is extrapolated from data in older children and adults or based on clinical experience and case series. There is a critical need for more research on the use of therapies in infants with kidney disease as well as for the development of drug delivery systems and preparations scaled more appropriately for these small patients. Copyright © 2016 Elsevier Ltd. All rights reserved.

  6. Inhaling Difluoroethane Computer Cleaner Resulting in Acute Kidney Injury and Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Kristen Calhoun

    2018-01-01

    Full Text Available Difluoroethane is the active ingredient in various computer cleaners and is increasingly abused by teenagers due to its ease of access, quick onset of euphoric effects, and lack of detectability on current urine drug screens. The substance has detrimental effects on various organ systems; however, its effects on the kidneys remain largely unreported. The following case report adds new information to the developing topic of acute kidney injury in patients abusing difluoroethane inhalants. In addition, it is one of the first to show a possible relationship between prolonged difluoroethane abuse and the development of chronic kidney disease in the absence of other predisposing risk factors.

  7. Stroke and bleeding in atrial fibrillation with chronic kidney disease

    DEFF Research Database (Denmark)

    Olesen, Jonas Bjerring; Lip, Gregory Y.H.; Kamper, Anne-Lise

    2012-01-01

    Both atrial fibrillation and chronic kidney disease increase the risk of stroke and systemic thromboembolism. However, these risks, and the effects of antithrombotic treatment, have not been thoroughly investigated in patients with both conditions.......Both atrial fibrillation and chronic kidney disease increase the risk of stroke and systemic thromboembolism. However, these risks, and the effects of antithrombotic treatment, have not been thoroughly investigated in patients with both conditions....

  8. [Vitamins and microelements in patients with chronic kidney disease].

    Science.gov (United States)

    Małgorzewicz, Sylwia; Jankowska, Magdalena; Kaczkan, Małgorzata; Czajka, Beata; Rutkowski, Bolesław

    2014-01-01

    The supply of vitamins and microelements in patients with chronic kidney disease (CKD) is very important and requires special attention. CKD patients presented deficiency of these substances in the diet and in organism, but also excess of fat-soluble vitamins or trace elements is observed. Studies indicate that deficiency of vitamins and antioxidants in diet and also enhanced oxidative stress are cause of many complications for example: accelerated process of arteriosclerosis in patients with chronic kidney disease.

  9. Managing Fluid and Electrolyte Disorders in Kidney Disease.

    Science.gov (United States)

    Langston, Cathy

    2017-03-01

    Because of the role of the kidneys in maintaining homeostasis in the body, kidney disease leads to derangements of fluid, electrolyte, and acid-base balance. The most effective therapy of a uremic crisis is careful management of fluid balance, which involves thoughtful assessment of hydration, a fluid treatment plan personalized for the specific patient, and repeated and frequent reassessment of fluid and electrolyte balance. Disorders of sodium, chloride, potassium, calcium, and phosphorus are commonly encountered in kidney disease and some may be life-threatening. Treatment of metabolic acidosis and nutritional support is frequently needed. Copyright © 2016 Elsevier Inc. All rights reserved.

  10. Management of adynamic bone disease in chronic kidney disease: A brief review

    Directory of Open Access Journals (Sweden)

    Swathi K. Sista

    2016-09-01

    Full Text Available The Kidney Disease: Improving Global Outcomes (KDIGO work group released recommendations in 2006 to define the bone-related pathology associated with chronic kidney disease as renal osteodystrophy. In 2009, KDIGO released revised clinical practice guidelines which redefined systemic disorders of bone and mineral metabolism due to chronic kidney disease as chronic kidney disease-mineral and bone disorders. Conditions under this overarching term include osteitis fibrosa cystica, osteomalacia, and adynamic bone disease. We aim to provide a brief review of the histopathology, pathophysiology, epidemiology, and diagnostic features of adynamic bone disease, focusing on current trends in the management of this complex bone disorder.

  11. Triumph and tragedy: anemia management in chronic kidney disease.

    Science.gov (United States)

    Novak, James E; Szczech, Lynda A

    2008-11-01

    Recent trial data have resulted in a reevaluation of the management of anemia in chronic kidney disease, including the use of erythropoiesis-stimulating agents, intravenous iron, and novel pharmaceuticals. In this review, we evaluate the latest research on anemia management in chronic kidney disease. Clinical trials of erythropoiesis-stimulating agents indicate that targeting the complete correction of anemia in patients with chronic kidney disease results in a greater risk of morbidity and mortality despite improved hemoglobin and quality of life. Conversely, intravenous iron has been found effective and relatively well tolerated in treating anemia in chronic kidney disease, even in patients with elevated ferritin. New agents to manage anemia, including long-acting erythropoietin derivatives, are also in active development. Erythropoiesis-stimulating agents should be used to target hemoglobin 11-12 g/dl in patients with chronic kidney disease. Intravenous iron may be beneficial for patients with hemoglobin less than 11 g/dl and transferrin saturation less than 25% despite elevated ferritin (500-1200 ng/ml). An upcoming placebo-controlled trial of darbepoetin should help to define the role of erythropoiesis-stimulating agents in chronic kidney disease.

  12. Chronic kidney disease: an inherent risk factor for acute kidney injury?

    Science.gov (United States)

    Singh, Prabhleen; Rifkin, Dena E; Blantz, Roland C

    2010-09-01

    Epidemiologic evidence suggests that chronic kidney disease (CKD) is a risk factor for acute kidney injury (AKI) due to the prevalence of CKD in patients who have episodes of AKI. However, the high burden of comorbidities such as age, diabetes, peripheral vascular, cardiovascular, and liver disease accompanying CKD, and the difficulties of defining AKI in the setting of CKD make these observations difficult to interpret. These comorbidities not only could alter the course of AKI but also may be the driving force behind the epidemiologic association between CKD and AKI because of systemic changes and/or increased exposure to potential nephrotoxic risks. Here, we contend that studies suggesting that CKD is a risk factor for AKI may suffer from residual confounding and reflect an overall susceptibility to illness rather than biologic susceptibility of the kidney parenchyma to injury. In support of our argument, we discuss the clinical evidence from epidemiologic studies, and the knowledge obtained from animal models on the pathophysiology of AKI and CKD, demonstrating a preconditioning influence of the previously impaired kidneys against subsequent injury. We conclude that, under careful analysis, factors apart from the inherent pathophysiology of the diseased kidney may be responsible for the increased frequency of AKI in CKD patients, and the impact of CKD on the risk and severity of AKI needs further investigation. Moreover, certain elements in the pathophysiology of a previously injured kidney may, surprisingly, bear out to be protective against AKI.

  13. Functional genomics in renal transplantation and chronic kidney disease

    International Nuclear Information System (INIS)

    Wilflingseder, J.

    2010-01-01

    For the past decade, the development of genomic technology has revolutionized modern biological research. Functional genomic analyses enable biologists to study genetic events on a genome wide scale. Examples of applications are gene discovery, biomarker determination, disease classification, and drug target identification. Global expression profiles performed with microarrays enable a better understanding of molecular signature of human disease, including acute and chronic kidney disease. About 10 % of the population in western industrialized nations suffers from chronic kidney disease (CKD). Treatment of end stage renal disease, the final stage of CKD is performed by either hemo- or peritoneal dialysis or renal transplantation. The preferred treatment is renal transplantation, because of the higher quality of life. But the pathophysiology of the disease on a molecular level is not well enough understood and early biomarkers for acute and chronic kidney disease are missing. In my studies I focused on genomics of allograft biopsies, prevention of delayed graft function after renal transplantation, anemia after renal transplantation, biocompatibility of hemodialysis membranes and peritoneal dialysis fluids and cardiovascular diseases and bone disorders in CKD patients. Gene expression profiles, pathway analysis and protein-protein interaction networks were used to elucidate the underlying pathophysiological mechanism of the disease or phenomena, identifying early biomarkers or predictors of disease state and potentially drug targets. In summery my PhD thesis represents the application of functional genomic analyses in chronic kidney disease and renal transplantation. The results provide a deeper view into the molecular and cellular mechanisms of kidney disease. Nevertheless, future multicenter collaborative studies, meta-analyses of existing data, incorporation of functional genomics into large-scale prospective clinical trials are needed and will give biomedical

  14. Salt intake in kidney disease-a missed therapeutic opportunity?

    NARCIS (Netherlands)

    Lambers Heerspink, Hiddo J.; Navis, Gerjan; Ritz, Eberhard

    Although significant progress has been made in the treatment of chronic kidney disease (CKD), treatment is not yet satisfactory, particularly when it is started in the late stages of the disease. Novel modes of intervention to mitigate the burden of disease are required. The reduction of dietary

  15. MicroRNAs in the pathogenesis of cystic kidney disease.

    Science.gov (United States)

    Phua, Yu Leng; Ho, Jacqueline

    2015-04-01

    Cystic kidney diseases are common renal disorders characterized by the formation of fluid-filled epithelial cysts in the kidneys. The progressive growth and expansion of the renal cysts replace existing renal tissue within the renal parenchyma, leading to reduced renal function. While several genes have been identified in association with inherited causes of cystic kidney disease, the molecular mechanisms that regulate these genes in the context of post-transcriptional regulation are still poorly understood. There is increasing evidence that microRNA (miRNA) dysregulation is associated with the pathogenesis of cystic kidney disease. In this review, recent studies that implicate dysregulation of miRNA expression in cystogenesis will be discussed. The relationship of specific miRNAs, such as the miR-17∼92 cluster and cystic kidney disease, miR-92a and von Hippel-Lindau syndrome, and alterations in LIN28-LET7 expression in Wilms tumor will be explored. At present, there are no specific treatments available for patients with cystic kidney disease. Understanding and identifying specific miRNAs involved in the pathogenesis of these disorders may have the potential to lead to the development of novel therapies and biomarkers.

  16. Chronic Kidney Disease Awareness Among Individuals with Clinical Markers of Kidney Dysfunction

    Science.gov (United States)

    Plantinga, Laura C.; Hsu, Chi-yuan; Jordan, Regina; Burrows, Nilka Ríos; Hedgeman, Elizabeth; Yee, Jerry; Saran, Rajiv; Powe, Neil R.

    2011-01-01

    Summary Background and objectives Awareness of chronic kidney disease (CKD) among providers and patients is low. Whether clinical cues prompt recognition of CKD is unknown. We examined whether markers of kidney disease that should trigger CKD recognition among providers are associated with higher individual CKD awareness. Design, setting, participants, & measurements CKD awareness was assessed in 1852 adults with an estimated GFR kidneys?” Participants were grouped by distribution of the following abnormal markers of CKD: hyperkalemia, acidosis, hyperphosphatemia, elevated blood urea nitrogen, anemia, albuminuria, and uncontrolled hypertension. Odds of CKD awareness associated with each abnormal marker and groupings of markers were estimated by multivariable logistic regression. Results Among individuals with kidney disease, only those with albuminuria had greater odds of CKD awareness (adjusted odds ratio, 4.0, P disease. Conclusions Although individuals who manifest many markers of kidney dysfunction are more likely to be aware of their CKD, their CKD awareness remains low. A better understanding of mechanisms of awareness is required to facilitate earlier detection of CKD and implement therapy to minimize associated complications. PMID:21784832

  17. Correlation of Point Shear Wave Velocity and Kidney Function in Chronic Kidney Disease.

    Science.gov (United States)

    Grosu, Iulia; Bob, Flaviu; Sporea, Ioan; Popescu, Alina; Şirli, Roxana; Schiller, Adalbert

    2018-04-24

    Point shear wave elastography is a quantitative ultrasound-based imaging method used in the assessment of renal disease. Among point shear wave elastographic options, 2 techniques have been studied considerably: Virtual Touch quantification (VTQ; Siemens AG, Erlangen, Germany) and ElastPQ (EPQ; Philips Healthcare, Bothell, WA). Both rely on the tissue response to an acoustic beam generated by the ultrasound transducer. The data on renal VTQ are more extensive, whereas EPQ has been used less thus far in the assessment of the kidneys. This study aimed to evaluate the performance of EPQ in the kidney and compare it with VTQ. We studied 124 participants using EPQ: 22 with no renal disease and 102 with chronic kidney disease (CKD). Ninety-one were studied with both the EPQ and VTQ methods. We obtained 5 valid measurements in each kidney, expressed in meters per second. The mean kidney stiffness measurements ± SD obtained with EPQ in the healthy control group were as follows: right kidney, 1.23 ± 0.33 m/s; and left kidney, 1.26 ± 0.32 m/s (P = .6). In the patients with CKD (all stages), the mean kidney stiffness measurements obtained were significantly lower: right kidney, 1.09 ± 0.39 m/s; and left kidney, 1.04 ± 0.38 m/s (P = .4). We observed that, similar to VTQ, EPQ values decreased with CKD progression, based on analysis of variance results using different CKD stages. From a receiver operating characteristic curve analysis, the cutoff value for an estimated glomerular filtration rate of less than 45 mL/min was 1.24 m/s, and the value for an estimated glomerular filtration rate of less than 30 mL/min was 1.07 m/s. When using EPQ, the kidney shear wave velocity is decreased in patients with CKD, an observation similar to that obtained by using the VTQ method. © 2018 by the American Institute of Ultrasound in Medicine.

  18. Bicarbonate therapy for prevention of chronic kidney disease progression.

    Science.gov (United States)

    Łoniewski, Igor; Wesson, Donald E

    2014-03-01

    Kidney injury in chronic kidney disease (CKD) is likely multifactorial, but recent data support that a component is mediated by mechanisms used by the kidney to increase acidification in response to an acid challenge to systemic acid-base status. If so, systemic alkalization might attenuate this acid-induced component of kidney injury. An acid challenge to systemic acid-base status increases nephron acidification through increased production of endothelin, aldosterone, and angiotensin II, each of which can contribute to kidney inflammation and fibrosis that characterizes CKD. Systemic alkalization that ameliorates an acid challenge might attenuate the contributions of angiotensin II, endothelin, and aldosterone to kidney injury. Some small clinical studies support the efficacy of alkalization in attenuating kidney injury and slowing glomerular filtration rate decline in CKD. This review focuses on the potential that orally administered NaHCO₃ prevents CKD progression and additionally addresses its mechanism of action, side effects, possible complications, dosage, interaction, galenic form description, and contraindications. Current National Kidney Foundation guidelines recommend oral alkali, including NaHCO₃(-), in CKD patients with serum HCO₃(-) <22 mmol/l. Although oral alkali can be provided by other medications and by base-inducing dietary constituents, oral NaHCO₃ will be the focus of this review because of its relative safety and apparent efficacy, and its comparatively low cost.

  19. Dietary management of chronic kidney disease: protein restriction and beyond.

    Science.gov (United States)

    Goraya, Nimrit; Wesson, Donald E

    2012-11-01

    More kidney protective strategies are needed to reduce the burden of complete kidney failure from chronic kidney disease (CKD). Clinicians sometimes use protein restriction as kidney protection despite its demonstrated lack of effectiveness in the only large-scale study. Small-scale studies support that dietary acid reduction is kidney-protective, including when done with base-inducing foods like fruits and vegetables. We review these studies in light of current kidney-protective recommendations. Animal models of CKD show that acid-inducing dietary protein exacerbates and base-inducing protein ameliorates nephropathy progression, and that increased intake of acid-inducing but not base-inducing dietary protein exacerbates progression. Clinical studies show that dietary acid reduction with Na-based alkali reduces kidney injury and slows nephropathy progression in patients with CKD and reduced glomerular filtration rate (GFR); base-inducing fruits and vegetables reduce kidney injury in patients with reduced GFR; and base-inducing fruits and vegetables improve metabolic acidosis in CKD. Protein type rather than amount might more importantly affect nephropathy progression. Base-inducing foods might be another way to reduce dietary acid, a strategy shown in small studies to slow nephropathy progression. Further studies will determine if CKD patients should be given base-inducing food as part of their management.

  20. Linking acute kidney injury to chronic kidney disease: the missing links.

    Science.gov (United States)

    Kaballo, Mohammed A; Elsayed, Mohamed E; Stack, Austin G

    2017-08-01

    Acute kidney injury (AKI) is considered to be a major public health problem around the globe, and it is associated with major adverse clinical outcomes and significant health care costs. There is growing evidence suggesting that AKI is associated with the subsequent development of chronic kidney disease (CKD). While recovery of kidney function occurs in the majority of patients surviving an AKI episode, a large number of patients do not recover completely. Similarly, CKD is a well-known risk factor for the development of AKI. Recent studies suggest that both AKI and CKD are not separate disease entities but are in fact components of a far more closely interconnected disease continuum. However, the true nature of this relationship is complex and poorly understood. This review explores potential relationships between AKI and CKD, and seeks to uncover a number of "missing links" in this tentative emerging relationship.

  1. Chronic kidney disease of unknown etiology in agricultural communities.

    Science.gov (United States)

    Almaguer, Miguel; Herrera, Raúl; Orantes, Carlos M

    2014-04-01

    In recent years, Central America, Egypt, India and Sri Lanka have reported a high prevalence of chronic kidney disease of unknown etiology in agricultural communities, predominantly among male farmworkers. This essay examines the disease's case definitions, epidemiology (disease burden, demographics, associated risk factors) and causal hypotheses, by reviewing published findings from El Salvador, Nicaragua, Costa Rica, Sri Lanka, Egypt and India. The range of confirmed chronic kidney disease prevalence was 17.9%-21.1%. Prevalence of reduced glomerular filtration (homemade alcohol use and family history of chronic kidney disease. There is no strong evidence for a single cause, and multiple environmental, occupational and social factors are probably involved. Further etiological research is needed, plus interventions to reduce preventable risk factors.

  2. Autosomal Dominant Polycystic Kidney Disease, incidental finding ...

    African Journals Online (AJOL)

    N.J. Gildenhuys

    2016-06-30

    Jun 30, 2016 ... This case study serves as a learning opportunity and future reference in the cases and management of ... sentation, special investigations, and treatment. The table ... trauma to an abnormal kidney is still a controversial topic. .... running into fence. AP ... He does not have any prior medical or surgical history.

  3. Histone deacetylase 6 inhibition reduces cysts by decreasing cAMP and Ca2+ in knock-out mouse models of polycystic kidney disease.

    Science.gov (United States)

    Yanda, Murali K; Liu, Qiangni; Cebotaru, Valeriu; Guggino, William B; Cebotaru, Liudmila

    2017-10-27

    Autosomal dominant polycystic kidney disease (ADPKD) is associated with progressive enlargement of multiple renal cysts, often leading to renal failure that cannot be prevented by a current treatment. Two proteins encoded by two genes are associated with ADPKD: PC1 ( pkd1 ), primarily a signaling molecule, and PC2 ( pkd2 ), a Ca 2+ channel. Dysregulation of cAMP signaling is central to ADPKD, but the molecular mechanism is unresolved. Here, we studied the role of histone deacetylase 6 (HDAC6) in regulating cyst growth to test the possibility that inhibiting HDAC6 might help manage ADPKD. Chemical inhibition of HDAC6 reduced cyst growth in PC1-knock-out mice. In proximal tubule-derived, PC1-knock-out cells, adenylyl cyclase 6 and 3 (AC6 and -3) are both expressed. AC6 protein expression was higher in cells lacking PC1, compared with control cells containing PC1. Intracellular Ca 2+ was higher in PC1-knock-out cells than in control cells. HDAC inhibition caused a drop in intracellular Ca 2+ and increased ATP-simulated Ca 2+ release. HDAC6 inhibition reduced the release of Ca 2+ from the endoplasmic reticulum induced by thapsigargin, an inhibitor of endoplasmic reticulum Ca 2+ -ATPase. HDAC6 inhibition and treatment of cells with the intracellular Ca 2+ chelator 1,2-bis(2-aminophenoxy)ethane- N , N , N ', N '-tetraacetic acid tetrakis(acetoxymethyl ester) reduced cAMP levels in PC1-knock-out cells. Finally, the calmodulin inhibitors W-7 and W-13 reduced cAMP levels, and W-7 reduced cyst growth, suggesting that AC3 is involved in cyst growth regulated by HDAC6. We conclude that HDAC6 inhibition reduces cell growth primarily by reducing intracellular cAMP and Ca 2+ levels. Our results provide potential therapeutic targets that may be useful as treatments for ADPKD. © 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

  4. MicroRNAs as potential therapeutic targets in kidney disease

    Science.gov (United States)

    Gomez, Ivan G; Grafals, Monica; Portilla, Didier; Duffield, Jeremy S

    2014-01-01

    One cornerstone of Chronic Kidney Disease (CKD) is fibrosis, as kidneys are susceptible due to their high vascularity and predisposition to ischemia. Presently, only therapies targeting the angiotensin receptor are used in clinical practice to retard the progression of CKD. Thus, there is a pressing need for new therapies designed to treat the damaged kidney. Several independent laboratories have identified a number of microRNAs that are dysregulated in human and animal models of CKD. We will explore the evidence suggesting that by blocking the activity of such dysregulated microRNAs, new therapeutics could be developed to treat the progression of CKD. PMID:23660218

  5. Biomarker for early renal microvascular and diabetic kidney diseases.

    Science.gov (United States)

    Futrakul, Narisa; Futrakul, Prasit

    2017-11-01

    Recognition of early stage of diabetic kidney disease, under common practice using biomarkers, namely microalbuminuria, serum creatinine level above 1 mg/dL and accepted definition of diabetic kidney disease associated with creatinine clearance value below 60 mL/min/1.73 m 2 , is unlikely. This would lead to delay treatment associated with therapeutic resistance to vasodilator due to a defective vascular homoeostasis. Other alternative biomarkers related to the state of microalbuminuria is not sensitive to screen for early diabetic kidney disease (stages I, II). In this regard, a better diagnostic markers to serve for this purpose are creatinine clearance, fractional excretion of magnesium (FE Mg), cystatin C. Recently, renal microvascular disease and renal ischemia have been demonstrated to correlate indirectly with the development of diabetic kidney disease and its function. Among these are angiogenic and anti-angiogenic factors, namely VEGF, VEGF receptors, angiopoietins and endostatin. With respect to therapeutic prevention, implementation of treatment at early stage of diabetic and nondiabetic kidney disease is able to restore renal perfusion and function.

  6. Chronic kidney disease, severe arterial and arteriolar sclerosis and kidney neoplasia: on the spectrum of kidney involvement in MELAS syndrome.

    Science.gov (United States)

    Piccoli, Giorgina Barbara; Bonino, Laura Davico; Campisi, Paola; Vigotti, Federica Neve; Ferraresi, Martina; Fassio, Federica; Brocheriou, Isabelle; Porpiglia, Francesco; Restagno, Gabriella

    2012-02-21

    MELAS syndrome (MIM ID#540000), an acronym for Mitochondrial Encephalopathy, Lactic Acidosis and Stroke-like episodes, is a genetically heterogeneous mitochondrial disorder with protean manifestations and occasional kidney involvement. Interest in the latter is rising due to the identification of cases with predominant kidney involvement and to the hypothesis of a link between mitochondrial DNA and kidney neoplasia. We report the case of a 41-year-old male with full blown MELAS syndrome, with lactic acidosis and neurological impairment, affected by the "classic" 3243A > G mutation of mitochondrial DNA, with kidney cancer. After unilateral nephrectomy, he rapidly developed severe kidney functional impairment, with nephrotic proteinuria. Analysis of the kidney tissue at a distance from the two tumor lesions, sampled at the time of nephrectomy was performed in the context of normal blood pressure, recent onset of diabetes and before the appearance of proteinuria. The morphological examination revealed a widespread interstitial fibrosis with dense inflammatory infiltrate and tubular atrophy, mostly with thyroidization pattern. Vascular lesions were prominent: large vessels displayed marked intimal fibrosis and arterioles had hyaline deposits typical of hyaline arteriolosclerosis. These severe vascular lesions explained the different glomerular alterations including ischemic and obsolescent glomeruli, as is commonly observed in the so-called "benign" arteriolonephrosclerosis. Some rare glomeruli showed focal segmental glomerulosclerosis; as the patient subsequently developed nephrotic syndrome, these lesions suggest that silent ischemic changes may result in the development of focal segmental glomerulosclerosis secondary to nephron loss. Nephron loss may trigger glomerular sclerosis, at least in some cases of MELAS-related nephropathy. Thus the incidence of kidney disease in the "survivors" of MELAS syndrome may increase as the support therapy of these patients improves.

  7. The definition, classification, and prognosis of chronic kidney disease : a KDIGO Controversies Conference report

    NARCIS (Netherlands)

    Levey, Andrew S.; de Jong, Paul E.; Coresh, Josef; El Nahas, Meguid; Astor, Brad C.; Matsushita, Kunihiro; Gansevoort, Ron T.; Kasiske, Bertram L.; Eckardt, Kai-Uwe

    The definition and classification for chronic kidney disease was proposed by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF-KDOQI) in 2002 and endorsed by the Kidney Disease: Improving Global Outcomes (KDIGO) in 2004. This framework promoted increased attention to

  8. Protein kinase D1 (PKD1) influences androgen receptor (AR) function in prostate cancer cells

    International Nuclear Information System (INIS)

    Mak, Paul; Jaggi, Meena; Syed, Viqar; Chauhan, Subhash C.; Hassan, Sazzad; Biswas, Helal; Balaji, K.C.

    2008-01-01

    Protein kinase D1 (PKD1), founding member of PKD protein family, is down-regulated in advanced prostate cancer (PCa). We demonstrate that PKD1 and androgen receptor (AR) are present as a protein complex in PCa cells. PKD1 is associated with a transcriptional complex which contains AR and promoter sequence of the Prostate Specific Antigen (PSA) gene. Ectopic expression of wild type PKD1 and the kinase dead mutant PKD1 (K628W) attenuated the ligand-dependent transcriptional activation of AR in prostate cancer cells and yeast cells indicating that PKD1 can affect AR transcription activity, whereas knocking down PKD1 enhanced the ligand-dependent transcriptional activation of AR. Co-expression of kinase dead mutant with AR significantly inhibited androgen-mediated cell proliferation in both LNCaP and DU145 PC cells. Our data demonstrate for the first time that PKD1 can influence AR function in PCa cells

  9. A qualitative assessment of personal and social responsibility for kidney disease: the Increasing Kidney Disease Awareness Network Transplant Project.

    Science.gov (United States)

    Spigner, Clarence; Lyles, Courtney Rees; Galvin, Georgia; Sabin, Janice; Davis, Connie; Dick, Andre; Young, Bessie A

    2011-01-01

    Limited qualitative research has explored opinions of kidney disease health care providers regarding racial and ethnic disparities in access to and receipt of kidney transplantation. Key informant interviews were conducted among transplant nephrologists, nephrologists, transplant social workers, and transplant coordinators to determine barriers to transplantation among African Americans compared to whites with end-stage renal disease (ESRD). Thirty-eight interviews were audio recorded and transcribed to hardcopy for content analysis. Grounded theory was used to determine dominant themes within the interviews. Reliability and validity were ensured by several coinvestigators independently sorting verbatim responses used for generating themes and subsequent explanations. Several major categories arose from analysis of the transcripts. Under the category of personal and social responsibility for kidney transplantation, interviews revealed 4 major themes: negative personal behaviors, acquisition of and lack of self-treatment of comorbid conditions, lack of individual responsibility, and the need for more social responsibility. Many providers perceived patients as being largely responsible for the development of ESRD, while some providers expressed the idea that more social responsibility was needed to improve poor health status and disparities in kidney transplantation rates. Kidney disease health providers seemed torn between notions of patients' accountability and social responsibility for racial disparities in chronic kidney disease and ESRD. Further research is needed to clarify which aspects contribute most to disparities in access to transplantation.

  10. Role of the Immune System in Diabetic Kidney Disease.

    Science.gov (United States)

    Hickey, Fionnuala B; Martin, Finian

    2018-03-12

    The purpose of this review is to examine the proposed role of immune modulation in the development and progression of diabetic kidney disease (DKD). Diabetic kidney disease has not historically been considered an immune-mediated disease; however, increasing evidence is emerging in support of an immune role in its pathophysiology. Both systemic and local renal inflammation have been associated with DKD. Infiltration of immune cells, predominantly macrophages, into the kidney has been reported in a number of both experimental and clinical studies. In addition, increased levels of circulating pro-inflammatory cytokines have been linked to disease progression. Consequently, a variety of therapeutic strategies involving modulation of the immune response are currently being investigated in diabetic kidney disease. Although no current therapies for DKD are directly based on immune modulation many of the therapies in clinical use have anti-inflammatory effects along with their primary actions. Macrophages emerge as the most likely beneficial immune cell target and compounds which reduce macrophage infiltration to the kidney have shown potential in both animal models and clinical trials.

  11. Tolvaptan and Kidney Pain in Patients With Autosomal Dominant Polycystic Kidney Disease : Secondary Analysis From a Randomized Controlled Trial

    NARCIS (Netherlands)

    Casteleijn, Niek F.; Blais, Jaime D.; Chapman, Arlene B.; Czerwiec, Frank S.; Devuyst, Olivier; Higashihara, Eiji; Leliveld, Anna M.; Ouyang, John; Perrone, Ronald D.; Torres, Vicente E.; Gansevoort, Ron T.

    Background: Kidney pain is a common complication in patients with autosomal dominant polycystic kidney disease (ADPKD), and data from the TEMPO 3: 4 trial suggested that tolvaptan, a vasopressin V2 receptor antagonist, may have a positive effect on kidney pain in this patient group. Because pain is

  12. Rare inherited kidney diseases: challenges, opportunities, and perspectives.

    NARCIS (Netherlands)

    Devuyst, O.; Knoers, N.V.A.M.; Remuzzi, G.; Schaefer, F.; Bindels, R.J.; et al.,

    2014-01-01

    At least 10% of adults and nearly all children who receive renal-replacement therapy have an inherited kidney disease. These patients rarely die when their disease progresses and can remain alive for many years because of advances in organ-replacement therapy. However, these disorders substantially

  13. a potential cause of cardiovascular diseases in chronic kidney ...

    African Journals Online (AJOL)

    Fibroblast growth factor 23 (FGF-23) has been identified as one of the risk factors for the development of cardiovascular diseases (CVDs) in chronic kidney disease (CKD) patients. Although FGF-23 is necessary for the maintenance of phosphate balance, it has been implicated in the pathogenesis of left ventricular ...

  14. Chronic kidney disease: sonographic/clinical findings at the ...

    African Journals Online (AJOL)

    Introduction: Kidney disease arises from various causes which can lead to death, especially if it progresses to chronic renal disease. Some of these patients can be managed by the use of conservative management, drugs, dialysis or renal transplantation depending on several factors. Amongst several investigative methods ...

  15. Obesity and kidney disease: hidden consequences of the epidemic ...

    African Journals Online (AJOL)

    Obesity has become a worldwide epidemic, and its prevalence has been projected to grow by 40% in the next decade. This increasing prevalence has implications for the risk of diabetes, cardiovascular disease and also for Chronic Kidney Disease. A high body mass index is one of the strongest risk factors for new-onset ...

  16. Development of a vaccine for bacterial kidney disease in salmon

    International Nuclear Information System (INIS)

    Kaatari, S.; Turaga, P.; Wiens, G.

    1989-08-01

    This document is the executive summary and background review for the final report of ''Development of a Vaccine for Bacterial Kidney Disease in Salmon''. A description of the disease is provided, with microbiological characterization of the infective agent. A brief discussion of attempts to eradicate the disease is included. Recent progress in vaccine development and attempts to control the disease through pharmacological means are described, along with potential ways to break the cycle of infection. 80 refs

  17. Diffusion-weighted MR imaging of kidneys in patients with chronic kidney disease: initial study

    Energy Technology Data Exchange (ETDEWEB)

    Xu, Xueqin; Fang, Wenqiang; Ling, Huawei; Chai, Weimin; Chen, Kemin [Ruijin Hospital Shanghai, Jiaotong University School of Medicine, Department of Radiology, Shanghai (China)

    2010-04-15

    To prospectively evaluate the feasibility of diffusion-weighted (DW) magnetic resonance (MR) imaging in the assessment of renal function in patients with chronic kidney disease (CKD). Seventy-two healthy volunteers and 43 patients underwent coronal echo-planar DW MR imaging of the kidneys with a single breath-hold time of 16 s. The patients were grouped according to five stages as indicated by the K/DOQI CKD (kidney disease outcome quality initiative). The apparent diffusion coefficient (ADC) value of the kidneys was calculated with high b values (b = 500 s/mm{sup 2}). The ADC values were compared between patients and healthy volunteers, and among different stages. For statistical analysis, Student's t tests, ANOVA, Pearson's correlation tests, and Spearman's correlation tests were used. No difference between the cortex and medulla could be observed on DW images of all volunteers. Patients with CKD had significantly lower renal ADC (t = -4.383, P = 0.000) than volunteers. The ADC values of kidneys were significantly lower than normal at most stages of CKD, except CKD1. There was a negative correlation between the ADCs and serum creatinine (sCr) level (P = 0.000) amongst the patients. Diffusion-weighted MR imaging is feasible in the assessment of renal function, especially in the detection of early stage renal failure of CKD. (orig.)

  18. Diffusion-weighted MR imaging of kidneys in patients with chronic kidney disease: initial study

    International Nuclear Information System (INIS)

    Xu, Xueqin; Fang, Wenqiang; Ling, Huawei; Chai, Weimin; Chen, Kemin

    2010-01-01

    To prospectively evaluate the feasibility of diffusion-weighted (DW) magnetic resonance (MR) imaging in the assessment of renal function in patients with chronic kidney disease (CKD). Seventy-two healthy volunteers and 43 patients underwent coronal echo-planar DW MR imaging of the kidneys with a single breath-hold time of 16 s. The patients were grouped according to five stages as indicated by the K/DOQI CKD (kidney disease outcome quality initiative). The apparent diffusion coefficient (ADC) value of the kidneys was calculated with high b values (b = 500 s/mm 2 ). The ADC values were compared between patients and healthy volunteers, and among different stages. For statistical analysis, Student's t tests, ANOVA, Pearson's correlation tests, and Spearman's correlation tests were used. No difference between the cortex and medulla could be observed on DW images of all volunteers. Patients with CKD had significantly lower renal ADC (t = -4.383, P = 0.000) than volunteers. The ADC values of kidneys were significantly lower than normal at most stages of CKD, except CKD1. There was a negative correlation between the ADCs and serum creatinine (sCr) level (P = 0.000) amongst the patients. Diffusion-weighted MR imaging is feasible in the assessment of renal function, especially in the detection of early stage renal failure of CKD. (orig.)

  19. Recent developments in epigenetics of acute and chronic kidney diseases.

    Science.gov (United States)

    Reddy, Marpadga A; Natarajan, Rama

    2015-08-01

    The growing epidemic of obesity and diabetes, the aging population as well as prevalence of drug abuse has led to significant increases in the rates of the closely associated acute and chronic kidney diseases, including diabetic nephropathy. Furthermore, evidence shows that parental behavior and diet can affect the phenotype of subsequent generations via epigenetic transmission mechanisms. These data suggest a strong influence of the environment on disease susceptibility and that, apart from genetic susceptibility, epigenetic mechanisms need to be evaluated to gain critical new information about kidney diseases. Epigenetics is the study of processes that control gene expression and phenotype without alterations in the underlying DNA sequence. Epigenetic modifications, including cytosine DNA methylation and covalent post-translational modifications of histones in chromatin, are part of the epigenome, the interface between the stable genome and the variable environment. This dynamic epigenetic layer responds to external environmental cues to influence the expression of genes associated with disease states. The field of epigenetics has seen remarkable growth in the past few years with significant advances in basic biology, contributions to human disease, as well as epigenomics technologies. Further understanding of how the renal cell epigenome is altered by metabolic and other stimuli can yield novel new insights into the pathogenesis of kidney diseases. In this review, we have discussed the current knowledge on the role of epigenetic mechanisms (primarily DNAme and histone modifications) in acute and chronic kidney diseases, and their translational potential to identify much needed new therapies.

  20. Treatment and Prevention of Common Complications of Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Sheikh Salahuddin Ahmed

    2014-01-01

    Full Text Available Chronic kidney disease (CKD is a worldwide public health problem with an increasing incidence and prevalence. Outcomes of CKD include not only complications of decreased kidney function and cardiovascular disease but also kidney failure causing increased morbidity and mortality. Unfortunately, CKD is often undetected and undertreated because of its insidious onset, variable progression, and length of time to overt kidney failure. Diabetes is now the leading cause of CKD requiring renal replacement therapy in many parts of the world, and its prevalence is increasing disproportionately in the developing countries. This review article outlines the current recommendations from various clinical guidelines and research studies for treatment, prevention and delaying the progression of both CKD and its common complications such as hypertension, anemia, renal osteodystrophy, electrolyte and acid-base imbalance, and hyperlipidemia. Recommendations for nutrition in CKD and measures adopted for early diabetic kidney disease to prevent further progression have also been reviewed. There is strong evidence that early detection and management of CKD can prevent or reduce disease progression, decrease complications and improve outcomes. Evidence supports that achieving optimal glucose control, blood pressure, reduction in albuminuria with a multifactorial intervention slows the progression of CKD. Angiotensin-converting enzyme inhibitors and angiotensin-II receptor antagonists are most effective because of their unique ability to decrease proteinuria, a factor important for the progression of CKD.

  1. Mechanisms by Which Dehydration May Lead to Chronic Kidney Disease.

    Science.gov (United States)

    Roncal-Jimenez, C; Lanaspa, M A; Jensen, T; Sanchez-Lozada, L G; Johnson, R J

    2015-01-01

    Dehydration, a condition that characterizes excessive loss of body water, is well known to be associated with acute renal dysfunction; however, it has largely been considered reversible and to be associated with no long-term effects on the kidney. Recently, an epidemic of chronic kidney disease has emerged in Central America in which the major risk factor seems to be recurrent heat-associated dehydration. This has led to studies investigating whether recurrent dehydration may lead to permanent kidney damage. Three major potential mechanisms have been identified, including the effects of vasopressin on the kidney, the activation of the aldose reductase-fructokinase pathway, and the effects of chronic hyperuricemia. The discovery of these pathways has also led to the recognition that mild dehydration may be a risk factor in progression of all types of chronic kidney diseases. Furthermore, there is some evidence that increasing hydration, particularly with water, may actually prevent CKD. Thus, a whole new area of investigation is developing that focuses on the role of water and osmolarity and their influence on kidney function and health. © 2015 S. Karger AG, Basel.

  2. Cannabinoids and the kidney: effects in health and disease.

    Science.gov (United States)

    Park, Frank; Potukuchi, Praveen K; Moradi, Hamid; Kovesdy, Csaba P

    2017-11-01

    Consumption of cannabis and various related products (cannabinoids) for both medicinal and recreational use is gaining popularity. Furthermore, regulatory changes are fostering a cultural shift toward increasing liberalization of cannabis use, thereby increasing the likelihood of even larger numbers of individuals being exposed in the future. The two different types of receptors (CB 1 and CB 2 ) that are activated by the pharmacologically active ingredients of cannabis are found in numerous tissues, including the kidneys. Experimental studies suggest that stimulation of these receptors using pharmacologic agents or their naturally occurring ligands could have both deleterious and beneficial effects on the kidneys, depending on receptor distribution, type of renal insult, or the timing of the activation during acute or chronic states of kidney injury. To date, the mechanisms by which the CB 1 or CB 2 receptors are involved in the pathology of these renal conditions remain to be fully described. Furthermore, a better understanding of the impact of exocannabinoids and endocannabinoids on the renal system may lead to the development of new drugs to treat kidney disease and its complications. Given the increasing public health relevance of cannabis exposure, it is clear that more research is necessary to clarify the various physiological and pathophysiological effects of cannabis and related analogs on the kidney. This will help limit the deleterious effects of these substances while promoting their potential beneficial impact on renal function in various types of kidney diseases.

  3. Endocrine Abnormalities in Patients with Chronic Kidney Disease.

    Science.gov (United States)

    Kuczera, Piotr; Adamczak, Marcin; Wiecek, Andrzej

    2015-01-01

    In patients with chronic kidney disease the alterations of the endocrine system may arise from several causes. The kidney is the site of degradation as well as synthesis of many different hormones. Moreover, a number of concomitant pathological conditions such as inflammation, metabolic acidosis and malnutrition may participate in the pathogenesis of endocrine abnormalities in this group of patients. The most pronounced endocrine abnormalities in patients with chronic kidney disease are the deficiencies of: calcitriol, testosterone, insulin-like growth factor and, erythropoietin (EPO). Additionally accumulation of several hormones, such as: prolactin, growth hormone and insulin frequently also occur. The clinical consequences of the abovementioned endocrine abnormalities are among others: anemia, infertility and bone diseases.

  4. Better recovery of kidney function in patients with de novo chronic kidney disease after partial nephrectomy compared with those with pre-existing chronic kidney disease.

    Science.gov (United States)

    Takagi, Toshio; Kondo, Tsunenori; Iizuka, Junpei; Omae, Kenji; Kobayashi, Hirohito; Hashimoto, Yasunobu; Yoshida, Kazuhiko; Tanabe, Kazunari

    2014-06-01

    We compared kidney functional recovery between patients with pre-existing chronic kidney disease, those with de novo chronic kidney disease and those with normal kidney function, after partial nephrectomy. A total of 311 patients who underwent partial nephrectomy at Tokyo Women's Medical University Hospital, Tokyo, Japan, between January 2004 and July 2011 with sufficient kidney functional data participated in the study. Patients with pre-existing chronic kidney disease (group1: 78 patients) were defined as those with estimated glomerular filtration rate under 60 mL/min/m(2) before partial nephrectomy. Patients with de novo chronic kidney disease (group 2: 49) were defined as those with estimated glomerular filtration rate over 60 mL/min/m(2) before surgery and who developed estimated glomerular filtration rate under 60 mL/min/m(2) 3 months after partial nephrectomy. Normal patients (group 3: 184) were defined as those with estimated glomerular filtration rate over 60 mL/min/m(2) both before and after partial nephrectomy. Group 1 was associated with older age and higher comorbidity, including hypertension and diabetes mellitus, compared with other groups. R.E.N.A.L. score was not significantly different between the groups. Although the percent change of estimated glomerular filtration rate between the preoperative period and 3 months after partial nephrectomy in group 2 was significantly decreased compared with that in other groups (group 1: -6.8%, group 2: -18%, group 3: -7.3%), the renal functional recovery between 3 and 12 months after partial nephrectomy in group 2 was better than that in other groups (group 1: -0.5%, group 2: 5.6%, group 3: -0.4%). Patients with de novo chronic kidney disease had better kidney functional recovery than the other two groups, which might suggest that they were surgically assaulted and developed chronic kidney disease in the early postoperative period, and were essentially different from those with pre-existing chronic kidney

  5. Cell cycle arrest and the evolution of chronic kidney disease from acute kidney injury.

    Science.gov (United States)

    Canaud, Guillaume; Bonventre, Joseph V

    2015-04-01

    For several decades, acute kidney injury (AKI) was generally considered a reversible process leading to complete kidney recovery if the individual survived the acute illness. Recent evidence from epidemiologic studies and animal models, however, have highlighted that AKI can lead to the development of fibrosis and facilitate the progression of chronic renal failure. When kidney injury is mild and baseline function is normal, the repair process can be adaptive with few long-term consequences. When the injury is more severe, repeated, or to a kidney with underlying disease, the repair can be maladaptive and epithelial cell cycle arrest may play an important role in the development of fibrosis. Indeed, during the maladaptive repair after a renal insult, many tubular cells that are undergoing cell division spend a prolonged period in the G2/M phase of the cell cycle. These tubular cells recruit intracellular pathways leading to the synthesis and the secretion of profibrotic factors, which then act in a paracrine fashion on interstitial pericytes/fibroblasts to accelerate proliferation of these cells and production of interstitial matrix. Thus, the tubule cells assume a senescent secretory phenotype. Characteristic features of these cells may represent new biomarkers of fibrosis progression and the G2/M-arrested cells may represent a new therapeutic target to prevent, delay or arrest progression of chronic kidney disease. Here, we summarize recent advances in our understanding of the biology of the cell cycle and how cell cycle arrest links AKI to chronic kidney disease. © The Author 2014. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

  6. Derivation and External Validation of Prediction Models for Advanced Chronic Kidney Disease Following Acute Kidney Injury.

    Science.gov (United States)

    James, Matthew T; Pannu, Neesh; Hemmelgarn, Brenda R; Austin, Peter C; Tan, Zhi; McArthur, Eric; Manns, Braden J; Tonelli, Marcello; Wald, Ron; Quinn, Robert R; Ravani, Pietro; Garg, Amit X

    2017-11-14

    Some patients will develop chronic kidney disease after a hospitalization with acute kidney injury; however, no risk-prediction tools have been developed to identify high-risk patients requiring follow-up. To derive and validate predictive models for progression of acute kidney injury to advanced chronic kidney disease. Data from 2 population-based cohorts of patients with a prehospitalization estimated glomerular filtration rate (eGFR) of more than 45 mL/min/1.73 m2 and who had survived hospitalization with acute kidney injury (defined by a serum creatinine increase during hospitalization > 0.3 mg/dL or > 50% of their prehospitalization baseline), were used to derive and validate multivariable prediction models. The risk models were derived from 9973 patients hospitalized in Alberta, Canada (April 2004-March 2014, with follow-up to March 2015). The risk models were externally validated with data from a cohort of 2761 patients hospitalized in Ontario, Canada (June 2004-March 2012, with follow-up to March 2013). Demographic, laboratory, and comorbidity variables measured prior to discharge. Advanced chronic kidney disease was defined by a sustained reduction in eGFR less than 30 mL/min/1.73 m2 for at least 3 months during the year after discharge. All participants were followed up for up to 1 year. The participants (mean [SD] age, 66 [15] years in the derivation and internal validation cohorts and 69 [11] years in the external validation cohort; 40%-43% women per cohort) had a mean (SD) baseline serum creatinine level of 1.0 (0.2) mg/dL and more than 20% had stage 2 or 3 acute kidney injury. Advanced chronic kidney disease developed in 408 (2.7%) of 9973 patients in the derivation cohort and 62 (2.2%) of 2761 patients in the external validation cohort. In the derivation cohort, 6 variables were independently associated with the outcome: older age, female sex, higher baseline serum creatinine value, albuminuria, greater severity of acute kidney injury, and higher

  7. What is the impact of chronic kidney disease stage and cardiovascular disease on the annual cost of hospital care in moderate-to-severe kidney disease?

    NARCIS (Netherlands)

    Kent, Seamus; Schlackow, Iryna; Lozano-Kuehne, Jingky; Reith, Christina; Emberson, Jonathan; Haynes, Richard; Gray, Alastair; Cass, Alan; Baigent, Colin; Landray, Martin J.; Herrington, William; Mihaylova, Borislava; de Zeeuw, Dick; Navis, Gerjan

    2015-01-01

    Background: Reliable estimates of the impacts of chronic kidney disease (CKD) stage, with and without cardiovascular disease, on hospital costs are needed to inform health policy. Methods: The Study of Heart and Renal Protection (SHARP) randomized trial prospectively collected information on kidney

  8. The Role of MicroRNAs in Kidney Disease

    Directory of Open Access Journals (Sweden)

    Sydwell Mukhadi

    2015-11-01

    Full Text Available MicroRNAs (miRNAs are short noncoding RNAs that regulate pathophysiological processes that suppress gene expression by binding to messenger RNAs. These biomolecules can be used to study gene regulation and protein expression, which will allow better understanding of many biological processes such as cell cycle progression and apoptosis that control the fate of cells. Several pathways have also been implicated to be involved in kidney diseases such as Transforming Growth Factor-β, Mitogen-Activated Protein Kinase signaling, and Wnt signaling pathways. The discovery of miRNAs has provided new insights into kidney pathologies and may provide new innovative and effective therapeutic strategies. Research has demonstrated the role of miRNAs in a variety of kidney diseases including renal cell carcinoma, diabetic nephropathy, nephritic syndrome, renal fibrosis, lupus nephritis and acute pyelonephritis. MiRNAs are implicated as playing a role in these diseases due to their role in apoptosis, cell proliferation, differentiation and development. As miRNAs have been detected in a stable condition in different biological fluids, they have the potential to be tools to study the pathogenesis of human diseases with a great potential to be used in disease prognosis and diagnosis. The purpose of this review is to examine the role of miRNA in kidney disease.

  9. Coronary heart disease is not significantly linked to acute kidney injury identified using Acute Kidney Injury Group criteria.

    Science.gov (United States)

    Yayan, Josef

    2012-01-01

    Patients with unstable angina or myocardial infarction are at risk of acute kidney injury, which may be aggravated by the iodine-containing contrast agent used during coronary angiography; however, the relationship between these two conditions remains unclear. The current study investigated the relationship between acute kidney injury and coronary heart disease prior to coronary angiography. All patients were evaluated after undergoing coronary angiography in the cardiac catheterization laboratory of the Vinzentius Hospital in Landau, Germany, in 2011. The study group included patients with both acute coronary heart disease and acute kidney injury (as defined according to the classification of the Acute Kidney Injury Group); the control group included patients without acute coronary heart disease. Serum creatinine profiles were evaluated in all patients, as were a variety of demographic and health characteristics. Of the 303 patients examined, 201 (66.34%) had coronary artery disease. Of these, 38 (18.91%) also had both acute kidney injury and acute coronary heart disease prior to and after coronary angiography, and of which in turn 34 (16.91%) had both acute kidney injury and acute coronary heart disease only prior to the coronary angiography. However, the occurrence of acute kidney injury was not significantly related to the presence of coronary heart disease (P = 0.95, Chi-square test). The results of this study indicate that acute kidney injury is not linked to acute coronary heart disease. However, physicians should be aware that many coronary heart patients may develop kidney injury while hospitalized for angiography.

  10. Dietary sodium in chronic kidney disease: a comprehensive approach.

    Science.gov (United States)

    Wright, Julie A; Cavanaugh, Kerri L

    2010-01-01

    Despite existing guidelines, dietary sodium intake among people worldwide often exceeds recommended limits. Research evidence is growing in both animal and human studies showing indirect and direct adverse consequences of high dietary sodium on the kidney. In patients with kidney disease, dietary sodium may have important effects on proteinuria, efficacy of antiproteinuric pharmacologic therapy, hypertension control, maintaining an optimal volume status, and immunosuppressant therapy. Dietary sodium intake is an important consideration in patients with all stages of chronic kidney disease, including those receiving dialysis therapy or those who have received a kidney transplant. We review in detail the dietary sodium recommendations suggested by various organizations for patients with kidney disease. Potential barriers to successfully translating current sodium intake guidelines into practice include poor knowledge about the sodium content of food among both patients and providers, complex labeling information, patient preferences related to taste, and limited support for modifications in public policy. Finally, we offer existing and potential solutions that may assist providers in educating and empowering patients to effectively manage their dietary sodium intake.

  11. Telomere attrition, kidney function, and prevalent chronic kidney disease in the United States.

    Science.gov (United States)

    Mazidi, Moshen; Rezaie, Peyman; Covic, Adriac; Malyszko, Jolanta; Rysz, Jacek; Kengne, Andre Pascal; Banach, Maciej

    2017-10-06

    Telomere length is an emerging novel biomarker of biologic age, cardiovascular risk and chronic medical conditions. Few studies have focused on the association between telomere length (TL) and kidney function. We investigated the association between TL and kidney function/prevalent chronic kidney disease (CKD) in US adults. The National Health and Nutrition Examination Survey (NHANES) participants with measured data on kidney function and TL from 1999 to 2002 were included. Estimated glomerular filtration rate (eGFR) was based on CKD Epidemiology Collaboration (CKD-EPI) equation. Urinary albumin excretion was assessed using urinary albumin-creatinine ratio (ACR). We used multivariable adjusted linear and logistic regression models, accounting for the survey design and sample weights. Of the 10568 eligible participants, 48.0% ( n =5020) were men. Their mean age was 44.1 years. eGFR significantly decreased and ACR significantly increased across increasing quarters of TL (all p function remained robust even after adjusting for potential confounding factors, but the association between TL and ACR was only borderline significant (β-coefficient= -0.012, p =0.056). The association of kidney function with a marker of cellular senescence suggests an underlying mechanism influencing the progression of nephropathy.

  12. Effects of Lowering LDL Cholesterol on Progression of Kidney Disease

    DEFF Research Database (Denmark)

    Haynes, Richard; Lewis, David; Emberson, Jonathan

    2014-01-01

    Lowering LDL cholesterol reduces the risk of developing atherosclerotic events in CKD, but the effects of such treatment on progression of kidney disease remain uncertain. Here, 6245 participants with CKD (not on dialysis) were randomly assigned to simvastatin (20 mg) plus ezetimibe (10 mg) daily...... or matching placebo. The main prespecified renal outcome was ESRD (defined as the initiation of maintenance dialysis or kidney transplantation). During 4.8 years of follow-up, allocation to simvastatin plus ezetimibe resulted in an average LDL cholesterol difference (SEM) of 0.96 (0.02) mmol/L compared...... with placebo; rate ratio, 0.93; 95% CI, 0.86 to 1.01; P=0.09). Exploratory analyses also showed no significant effect on the rate of change in eGFR. Lowering LDL cholesterol by 1 mmol/L did not slow kidney disease progression within 5 years in a wide range of patients with CKD....

  13. [Horseshoe kidney, stone disease and prostate cancer: a case presentation].

    Science.gov (United States)

    Hermida Pérez, J A; Bermejo Hernández, A; Hernández Guerra, J S; Sobenes Gutierrez, R J

    2013-01-01

    The horseshoe kidney is the most common congenital renal fusion anomalies. It occurs in 0.25% of the population, or 1 in every 400 people. It is more frequent in males (ratio 2:1). The most observed complication of horseshoe kidney is stone disease, although there may be others such as, abdominal pain, urinary infections, haematuria, hydronephrosis, trauma and tumours (most commonly associated with hypernephroma and Wilms tumour). We describe a case of a male patient with horseshoe kidney, stone disease and adenocarcinoma of the prostate. One carrier of this condition who suffered a transitional cell carcinoma of the prostate was found in a review of the literature. Copyright © 2012 Sociedad Española de Médicos de Atención Primaria (SEMERGEN). Publicado por Elsevier España. All rights reserved.

  14. [Type 2 diabetes mellitus and chronic kidney disease].

    Science.gov (United States)

    Ponťuch, Peter

    The number of type 2 diabetic patients is increasing world-wide and a prediction of prevalence of chronic kidney disease up to 2025 in European diabetic population is alarming. Albuminuria and estimated glomerular filtration rate are cardinal biochemical parameters in diagnostics of diabetic nephropathy. Following diagnostic methods are also used: renal ultrasonography, ophthalmoscopy and in not clarified cases renal biopsy. Long-term optimal glycemic control, efficient antihypertensive treatment by angiotensin converting enzyme inhibitor, or angiotensin receptor blocker and recommended protein intake is a cornerstone of therapy. The research is presently focused on new pathophysiological mechanisms, as analysis of genome, microRNA, kidney injury biomarkers and proteomes.Key words: chronic kidney disease - type 2 diabetes mellitus.

  15. 76 FR 36931 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2011-06-23

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Liver Disease and Transplantation... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the... of Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Urinary Tract Dysfunction P01...

  16. Genetic basis of kidney cancer: Role of genomics for the development of disease-based therapeutics

    OpenAIRE

    Linehan, W. Marston

    2012-01-01

    Kidney cancer is not a single disease; it is made up of a number of different types of cancer, including clear cell, type 1 papillary, type 2 papillary, chromophobe, TFE3, TFEB, and oncocytoma. Sporadic, nonfamilial kidney cancer includes clear cell kidney cancer (75%), type 1 papillary kidney cancer (10%), papillary type 2 kidney cancer (including collecting duct and medullary RCC) (5%), the microphalmia-associated transcription (MiT) family translocation kidney cancers (TFE3, TFEB, and MITF...

  17. Association Between Newborn Metabolic Profiles and Pediatric Kidney Disease

    Directory of Open Access Journals (Sweden)

    Manish M. Sood

    2018-05-01

    Full Text Available Introduction: Metabolomics offers considerable promise in early disease detection. We set out to test the hypothesis that routine newborn metabolic profiles at birth, obtained through screening for inborn errors of metabolism, would be associated with kidney disease and add incremental information to known clinical risk factors. Methods: We conducted a population-level cohort study in Ontario, Canada, using metabolic profiles from 1,288,905 newborns from 2006 to 2015. The primary outcome was chronic kidney disease (CKD or dialysis. Individual metabolites and their ratio combinations were examined by logistic regression after adjustment for established risk factors for kidney disease and incremental risk prediction measured. Results: CKD occurred in 2086 (0.16%, median time 612 days and dialysis in 641 (0.05%, median time 99 days infants and children. Individual metabolites consisted of amino acids, acylcarnitines, markers of fatty acid oxidation, and others. Base models incorporating clinical risk factors only provided c-statistics of 0.61 for CKD and 0.70 for dialysis. The addition of identified metabolites to risk prediciton models resulted in significant incremental improvement in the performance of both models (CKD model: c-statistic 0.66 NRI 0.36 IDI 0.04, dialysis model: c-statistic 0.77 NRI 0.57 IDI 0.09. This was consistent after internal validation using bootstrapping and a sensitivity analysis excluding outcomes within the first 30 days. Conclusion: Routinely collected screening metabolites at birth are associated with CKD and the need for dialytic therapies in infants and children, and add incremental information to traditional clinical risk factors. Keywords: chronic kidney disease, dialysis, end-stage kidney disease, metabolomics, newborn screening, pediatric, renal failure

  18. Modeling Kidney Disease with iPS Cells

    Science.gov (United States)

    Freedman, Benjamin S.

    2015-01-01

    Induced pluripotent stem cells (iPSCs) are somatic cells that have been transcriptionally reprogrammed to an embryonic stem cell (ESC)-like state. iPSCs are a renewable source of diverse somatic cell types and tissues matching the original patient, including nephron-like kidney organoids. iPSCs have been derived representing several kidney disorders, such as ADPKD, ARPKD, Alport syndrome, and lupus nephritis, with the goals of generating replacement tissue and ‘disease in a dish’ laboratory models. Cellular defects in iPSCs and derived kidney organoids provide functional, personalized biomarkers, which can be correlated with genetic and clinical information. In proof of principle, disease-specific phenotypes have been described in iPSCs and ESCs with mutations linked to polycystic kidney disease or focal segmental glomerulosclerosis. In addition, these cells can be used to model nephrotoxic chemical injury. Recent advances in directed differentiation and CRISPR genome editing enable more specific iPSC models and present new possibilities for diagnostics, disease modeling, therapeutic screens, and tissue regeneration using human cells. This review outlines growth opportunities and design strategies for this rapidly expanding and evolving field. PMID:26740740

  19. Paediatric chronic kidney disease | van Biljon | South African ...

    African Journals Online (AJOL)

    Doctors use various guidelines on paediatric chronic kidney disease (CKD) for managing their patients according to the availability of resources. As with adolescent and adult patients, CKD in children can also progress to end-stage renal failure – the time course being influenced by several modifiable factors. Decline in ...

  20. Clinical Course of Acute Pancreatitis in Chronic Kidney Disease ...

    African Journals Online (AJOL)

    Introduction: The aim of this study was to assess the clinical course, etiology and complications of acute pancreatitis among chronic kidney disease (CKD) patients in a tertiary care renal center in Karachi. Methods: We retrospectively evaluated the clinical course of CKD patients who presented to our emergency room with ...

  1. Left ventricular hypertrophy among chronic kidney disease patients ...

    African Journals Online (AJOL)

    Introduction: The presence of left ventricular hypertrophy (LVH) in patients with Chronic Kidney Disease (CKD) is associated with worsening cardiovascular outcomes. There is a dearth of data on LVH in Ghanaian CKD patients. Methods: This was a cross sectional study carried out at the Komfo Anokye Teaching Hospital ...

  2. Guest Editorial: Chronic kidney disease | Motsoaledi | South African ...

    African Journals Online (AJOL)

    South African Medical Journal. Journal Home · ABOUT · Advanced Search · Current Issue · Archives · Journal Home > Vol 105, No 4 (2015) >. Log in or Register to get access to full text downloads. Username, Password, Remember me, or Register. Guest Editorial: Chronic kidney disease. A Motsoaledi. Abstract. No abstract ...

  3. Guest Editorial: Chronic kidney disease | Meyers | South African ...

    African Journals Online (AJOL)

    South African Medical Journal. Journal Home · ABOUT · Advanced Search · Current Issue · Archives · Journal Home > Vol 105, No 3 (2015) >. Log in or Register to get access to full text downloads. Username, Password, Remember me, or Register. Guest Editorial: Chronic kidney disease. AM Meyers. Abstract. No abstract.

  4. Chronic kidney disease in sub-Saharan Africa: Hypothesis for ...

    African Journals Online (AJOL)

    The world's disease profile is changing and chronic ... morbidity and mortality in the world, accounts for ... contribute substantially to the disparate burden ... the year 2030, more than 70% of patients with ... 2002. New York: National Kidney Foundation; 2002. 7. Pugsley D, Norris KC, ... and projections to the year 2010.

  5. Cell-based therapies for chronic kidney disease

    NARCIS (Netherlands)

    van Koppen, A.N.

    2013-01-01

    Chronic kidney disease (CKD) may lead to end-stage renal failure, requiring renal replacement strategies. Development of new therapies to reduce progression of CKD is therefore a major global public health target. The aim of this thesis was to investigate whether cell-based therapies have the

  6. Skin autofluorescence associates with vascular calcification in chronic kidney disease.

    Science.gov (United States)

    Wang, Angela Yee-Moon; Wong, Chun-Kwok; Yau, Yat-Yin; Wong, Sharon; Chan, Iris Hiu-Shuen; Lam, Christopher Wai-Kei

    2014-08-01

    This study aims to evaluate the relationship between tissue advanced glycation end products, as reflected by skin autofluorescence, and vascular calcification in chronic kidney disease. Three hundred patients with stage 3 to 5 chronic kidney disease underwent multislice computed tomography to estimate total coronary artery calcium score (CACS) and had tissue advanced glycation end product assessed using a skin autofluorescence reader. Intact parathyroid hormone (Pskin autofluorescence after age (Pskin autofluorescence was associated with a 7.43-fold (95% confidence intervals, 3.59-15.37; PSkin autofluorescence retained significance in predicting CACS ≥400 (odds ratio, 3.63; 95% confidence intervals, 1.44-9.18; P=0.006) when adjusting for age, sex, serum calcium, phosphate, albumin, C-reactive protein, lipids, blood pressure, estimated glomerular filtration rate, and intact parathyroid hormone but marginally lost significance when additionally adjusting for diabetes mellitus (odds ratio, 2.23; 95% confidence intervals, 0.81-6.14; P=0.1). Combination of diabetes mellitus and higher intact parathyroid hormone was associated with greater skin autofluorescence and CACS versus those without diabetes mellitus and having lower intact parathyroid hormone. Tissue advanced glycation end product, as reflected by skin autofluorescence, showed a significant novel association with vascular calcification in chronic kidney disease. These data suggest that increased tissue advanced glycation end product may contribute to vascular calcification in chronic kidney disease and diabetes mellitus and warrant further experimental investigation. © 2014 American Heart Association, Inc.

  7. Effect of chronic kidney disease on serum resistin level | Dan ...

    African Journals Online (AJOL)

    ... between two groups was statistically significant. Conclusion: Our study is probably the first study in India comparing serum resistin levels of CKD patients vis-à-vis control subjects. Further cellular research may be needed to explore this relation. Key words: Chronic kidney disease, HOMA-IR, insulin resistance, resistin ...

  8. Epidemiology of chronic kidney disease in northern region of Senegal

    African Journals Online (AJOL)

    Introduction: Chronic kidney disease (CKD) is an emerging worldwide epidemic but few data are available in African populations. We aimed to assess prevalence of CKD in adult populations of Saint-Louis (northern Senegal). Methods: In a population-based survey between January and May 2012, we included 1,037 adults ...

  9. Chronic kidney disease screening: Results of the 2013 World ...

    African Journals Online (AJOL)

    Background: Chronic kidney disease (CKD) is on the rise globally due to the increase in prevalence of common risk factors. Screening for CKD risk factors is important for early detection and institution of measures to retard its progression. This study aimed to determine the markers of CKD and its risk factors in a selected ...

  10. Prevalence of chronic kidney disease in a Nigerian family practice ...

    African Journals Online (AJOL)

    (p = 0.002) and age group (p = 0.0027) were true predictors of CKD among the study subjects. ... from intrinsic kidney and urinary tract disease was one million in the .... tract infections or acute illness with fever, and those who refused to.

  11. Elevated potassium levels in patients with chronic kidney disease

    DEFF Research Database (Denmark)

    Thomsen, Reimar W; Nicolaisen, Sia K; Hasvold, Pål

    2018-01-01

    Background: Data on the true burden of hyperkalemia (HK) in patients with chronic kidney disease (CKD) in a real-world setting are scarce. Methods: The incidence rate of HK [first blood test with an elevated blood potassium level level >5.0 mmol/L] in primary or hospital care was assessed...

  12. Hyperparathyroidism in chronic kidney disease: complexities within the commonplace.

    Science.gov (United States)

    Cai, Michael M; McMahon, Lawrence P; Smith, Edward R; Williams, David S; Holt, Stephen G

    2012-08-01

    Secondary hyperparathyroidism in patients with chronic kidney disease (CKD) is common and usually caused by associated metabolic abnormalities, in particular, hypocalcaemia and hyperphosphataemia. Nevertheless, other causes of hyperparathyroidism can exist concurrently with CKD, challenging diagnostic interpretation and therapeutic intervention. We present four cases of hyperparathyroidism in patients with CKD that highlight some of these dilemmas.

  13. Chronic kidney disease in rheumatoid arthritis at Kenyatta National ...

    African Journals Online (AJOL)

    Objective: To determine the prevalence of chronic kidney disease among patients with rheumatoid arthritis on follow up at the rheumatology outpatient clinic at Kenyatta National Hospital. Design: Descriptive, cross-sectional study. Setting: Rheumatology outpatient clinic at the Kenyatta National Hospital, a public national ...

  14. Polycystic Kidney Disease In Pregnancy In A Nigerian Woman ...

    African Journals Online (AJOL)

    Adult Polycystic Kidney disease (ADPKD) is a known but uncommon cause of haematuria in pregnancy in this environment. Other causes include, haemaglobinopathies, calculi, pyelonephritis, schistosomiasis, haemangiomata and neoplasms. Although ADPKD is the commonest single gene disorder of man affecting both ...

  15. [Chronic kidney disease - The relevant information for an occupational physician].

    Science.gov (United States)

    Renke, Marcin; Parszuto, Jacek; Rybacki, Marcin; Wołyniec, Wojciech; Rutkowski, Przemysław; Rutkowski, Bolesław; Walusiak-Skorupa, Jolanta; Dębska-Ślizień, Alicja

    2018-01-01

    For a number of years chronic kidney disease (CKD) has been listed in the group of lifestyle diseases, such as obesity, diabetes, cardiovascular disease and hypertension. It is estimated that in Poland more than 4 million people may suffer from various stages of CKD. Chronic kidney disease may also be a consequence of all the other civilization diseases. At the same time it is worth noting that nephrological problems are increasingly being taken into account in modern medical certification. The aim of this work is, among other things, to improve safe access to the labor for patients with kidney diseases. In the legislation existing in our country since 2014 it is stated that chronic renal failure is a potential health contraindication to driving. Also in the annex to the Regulation of the Minister of Health dated 9 December 2015 on health conditions required for seafarers to work on a seagoing ship, it is said that ICD-10 codes (International Classification of Diseases) corresponding to acute and chronic renal failure (N17-N19) should be taken into account when qualifying employees to work at sea. Med Pr 2018;69(1):67-75. This work is available in Open Access model and licensed under a CC BY-NC 3.0 PL license.

  16. Advances in genetic detection of kidney disease

    International Nuclear Information System (INIS)

    Dosekun, Akinsan K.; Foringer, John R.; Kone, Bruce C.

    2003-01-01

    The Human Genome Project has provided a vast amount of molecular genetic information for the analysis of normal and diseased genes. This new information provides new opportunities for precise diagnosis, assessment of predisposition and risk factors and novel therapeutic strategies. At the same time, this constantly expanding knowledge base represents on e of the most difficult challenges in molecular medicine. For monogenic disease nearly 2000 human disease genes have thus for been identified. Most of these conditions are characterized by large mutational variation and even greater phenotypic variation. In nephrology, several genetic diseases have been elucidated that provide new insight into the structure, function and developmental biology of the glomerulus, tubules and urogenital tracts, as well as renal cell tumors. Great improvements in the diagnostic resolution of genetic diseases have been achieved, such that single base pair mutations can be readily detected. Because of accurate diagnosis and risk assessment, genetic testing may be valuable in improving disease management and preventive care when genotype-specific therapies are available. Moreover, such testing may identify de novo mutations and potentially aid in understanding the disease process. This review summarizes recent advances in the renal genetic database and methods for genetic testing of renal diseases. (author)

  17. Oxidative Stress in Kidney Diseases: The Cause or the Consequence?

    Science.gov (United States)

    Krata, Natalia; Zagożdżon, Radosław; Foroncewicz, Bartosz; Mucha, Krzysztof

    2018-06-01

    Exaggerated oxidative stress (OS) is usually considered as a disturbance in regular function of an organism. The excessive levels of OS mediators may lead to major damage within the organism's cells and tissues. Therefore, the OS-associated biomarkers may be considered as new diagnostic tools of various diseases. In nephrology, researchers are looking for alternative methods replacing the renal biopsy in patients with suspicion of chronic kidney disease (CKD). Currently, CKD is a frequent health problem in world population, which can lead to progressive loss of kidney function and eventually to end-stage renal disease. The course of CKD depends on the primary disease. It is assumed that one of the factors influencing the course of CKD might be OS. In the current work, we review whether monitoring the OS-associated biomarkers in nephrology patients can support the decision-making process regarding diagnosis, prognostication and treatment initiation.

  18. Chronic Kidney Disease and Exposure to Nephrotoxic Metals

    Science.gov (United States)

    Orr, Sarah E.; Bridges, Christy C.

    2017-01-01

    Chronic kidney disease (CKD) is a common progressive disease that is typically characterized by the permanent loss of functional nephrons. As injured nephrons become sclerotic and die, the remaining healthy nephrons undergo numerous structural, molecular, and functional changes in an attempt to compensate for the loss of diseased nephrons. These compensatory changes enable the kidney to maintain fluid and solute homeostasis until approximately 75% of nephrons are lost. As CKD continues to progress, glomerular filtration rate decreases, and remaining nephrons are unable to effectively eliminate metabolic wastes and environmental toxicants from the body. This inability may enhance mortality and/or morbidity of an individual. Environmental toxicants of particular concern are arsenic, cadmium, lead, and mercury. Since these metals are present throughout the environment and exposure to one or more of these metals is unavoidable, it is important that the way in which these metals are handled by target organs in normal and disease states is understood completely. PMID:28498320

  19. Cadmium, diabetes and chronic kidney disease

    International Nuclear Information System (INIS)

    Edwards, Joshua R.; Prozialeck, Walter C.

    2009-01-01

    Recent epidemiological studies suggest a positive association between exposure to the environmental pollutant cadmium (Cd) and the incidence and severity of diabetes. In this review, we examine the literature suggesting a relationship between Cd exposure, elevated blood glucose levels, and the development of diabetes. In addition we review human and animal studies indicating that Cd potentiates or exacerbates diabetic nephropathy. We also review the various possible cellular mechanisms by which Cd may alter blood glucose levels. In addition, we present some novel findings from our own laboratories showing that Cd elevates fasting blood glucose levels in an animal model of subchronic Cd exposure before overt signs of renal dysfunction are evident. These studies also show that Cd reduces insulin levels and has direct cytotoxic effects on the pancreas. Together, these findings indicate that Cd may be a factor in the development of some types of diabetes and they raise the possibility that Cd and diabetes-related hyperglycemia may act synergistically to damage the kidney.

  20. Kidney Problems

    Science.gov (United States)

    ... our e-newsletter! Aging & Health A to Z Kidney Problems Basic Facts & Information The kidneys are two ... kidney (renal) diseases are called nephrologists . What are Kidney Diseases? For about one-third of older people, ...

  1. Diabetic kidney disease: a report from an ADA Consensus Conference.

    Science.gov (United States)

    Tuttle, Katherine R; Bakris, George L; Bilous, Rudolf W; Chiang, Jane L; de Boer, Ian H; Goldstein-Fuchs, Jordi; Hirsch, Irl B; Kalantar-Zadeh, Kamyar; Narva, Andrew S; Navaneethan, Sankar D; Neumiller, Joshua J; Patel, Uptal D; Ratner, Robert E; Whaley-Connell, Adam T; Molitch, Mark E

    2014-10-01

    The incidence and prevalence of diabetes mellitus have grown significantly throughout the world, due primarily to the increase in type 2 diabetes. This overall increase in the number of people with diabetes has had a major impact on development of diabetic kidney disease (DKD), one of the most frequent complications of both types of diabetes. DKD is the leading cause of end-stage renal disease (ESRD), accounting for approximately 50% of cases in the developed world. Although incidence rates for ESRD attributable to DKD have recently stabilized, these rates continue to rise in high-risk groups such as middle-aged African Americans, Native Americans, and Hispanics. The costs of care for people with DKD are extraordinarily high. In the Medicare population alone, DKD-related expenditures among this mostly older group were nearly $25 billion in 2011. Due to the high human and societal costs, the Consensus Conference on Chronic Kidney Disease and Diabetes was convened by the American Diabetes Association in collaboration with the American Society of Nephrology and the National Kidney Foundation to appraise issues regarding patient management, highlighting current practices and new directions. Major topic areas in DKD included (1) identification and monitoring, (2) cardiovascular disease and management of dyslipidemia, (3) hypertension and use of renin-angiotensin-aldosterone system blockade and mineralocorticoid receptor blockade, (4) glycemia measurement, hypoglycemia, and drug therapies, (5) nutrition and general care in advanced-stage chronic kidney disease, (6) children and adolescents, and (7) multidisciplinary approaches and medical home models for health care delivery. This current state summary and research recommendations are designed to guide advances in care and the generation of new knowledge that will meaningfully improve life for people with DKD. Copyright © 2014 American Diabetes Association and the National Kidney Foundation. Published by Elsevier Inc

  2. Metformin in Patients With Type 2 Diabetes and Kidney Disease

    Science.gov (United States)

    Inzucchi, Silvio E.; Lipska, Kasia J.; Mayo, Helen; Bailey, Clifford J.; McGuire, Darren K.

    2015-01-01

    IMPORTANCE Metformin is widely viewed as the best initial pharmacological option to lower glucose concentrations in patients with type 2 diabetes mellitus. However, the drug is contraindicated in many individuals with impaired kidney function because of concerns of lactic acidosis. OBJECTIVE To assess the risk of lactic acidosis associated with metformin use in individuals with impaired kidney function. EVIDENCE ACQUISITION In July 2014, we searched the MEDLINE and Cochrane databases for English-language articles pertaining to metformin, kidney disease, and lactic acidosis in humans between 1950 and June 2014. We excluded reviews, letters, editorials, case reports, small case series, and manuscripts that did not directly pertain to the topic area or that met other exclusion criteria. Of an original 818 articles, 65 were included in this review, including pharmacokinetic/metabolic studies, large case series, retrospective studies, meta-analyses, and a clinical trial. RESULTS Although metformin is renally cleared, drug levels generally remain within the therapeutic range and lactate concentrations are not substantially increased when used in patients with mild to moderate chronic kidney disease (estimated glomerular filtration rates, 30-60 mL/min per 1.73 m2). The overall incidence of lactic acidosis in metformin users varies across studies from approximately 3 per 100 000 person-years to 10 per 100 000 person-years and is generally indistinguishable from the background rate in the overall population with diabetes. Data suggesting an increased risk of lactic acidosis in metformin-treated patients with chronic kidney disease are limited, and no randomized controlled trials have been conducted to test the safety of metformin in patients with significantly impaired kidney function. Population-based studies demonstrate that metformin may be prescribed counter to prevailing guidelines suggesting a renal risk in up to 1 in 4 patients with type 2 diabetes mellitus

  3. Inflammation and nutrition in children with chronic kidney disease

    OpenAIRE

    Tu, Juan; Cheung, Wai W; Mak, Robert H

    2016-01-01

    Chronic inflammation and nutritional imbalance are important comorbid conditions that correlate with poor clinical outcomes in children with chronic kidney disease (CKD). Nutritional disorders such as cachexia/protein energy wasting, obesity and growth retardation negatively impact the quality of life and disease progression in children with CKD. Inadequate nutrition has been associated with growth disturbances in children with CKD. On the other hand, over-nutrition and obesity are associated...

  4. Diet in chronic kidney disease in a Mediterranean African country

    OpenAIRE

    Kammoun, Khawla; Chaker, Hanen; Mahfoudh, Hichem; Makhlouf, Nouha; Jarraya, Faical; Hachicha, Jamil

    2017-01-01

    Background Mediterranean diet is characterized by low to moderate consumption of animal protein and high consumption of fruits, vegetables, bread, beans, nuts, seeds and other cereals. It has been associated with reduced risk of cardiovascular disease. However, it is not suitable for chronic kidney disease because of high potassium intake. Discussion Tunisia is an emerging Mediterranean country with limited resources, a high prevalence of chronic hemodialysis treatment and high dialysis expen...

  5. Aging and the Kidneys: Anatomy, Physiology and Consequences for Defining Chronic Kidney Disease.

    Science.gov (United States)

    Glassock, Richard J; Rule, Andrew D

    2016-01-01

    The varied functions of the kidneys are influenced by the complex process of aging. The glomerular filtration rate (GFR) steadily declines with normal aging, and the progress of this process can be influenced by superimposed diseases. Microscopically, nephron numbers decrease as global glomerulosclerosis becomes more evident. The precise mechanisms underlying nephron loss with aging are not well understood, but derangements in podocyte biology appear to be involved. Classifications of chronic kidney disease (CKD) incorporate GFR values and attendant risk of adverse events. Arbitrary and fixed thresholds of GFR for defining CKD have led to an overdiagnosis of CKD in the elderly. An age-sensitive definition of CKD could offer a solution to this problem and more meaningfully capture the prognostic implications of CKD. © 2016 S. Karger AG, Basel.

  6. 78 FR 6123 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2013-01-29

    ... Digestive and Kidney Diseases Special Emphasis Panel; Host Innate Immune Microbial Interactions in... Kidney Diseases Special Emphasis Panel; DDK-D Members Conflict SEP. Date: March 13, 2013. Time: 10:10 a.m...

  7. Hospital specific factors affect quality of blood pressure treatment in chronic kidney disease

    NARCIS (Netherlands)

    Zuilen, A.D. van; Blankestijn, P.J.; Buren, M. van; Dam, M.A. ten; Kaasjager, K.A.; Ligtenberg, G.; Sijpkens, Y.W.; Sluiter, H.E.; Ven, P.J. van der; Vervoort, G.M.M.; Vleming, L.; Bots, M.L.; Wetzels, J.F.M.

    2011-01-01

    BACKGROUND: Blood pressure (BP) is the most important modifiable risk factor for cardiovascular (CV) disease and progression of kidney dysfunction in patients with chronic kidney disease. Despite extensive antihypertensive treatment possibilities, adequate control is notoriously hard to achieve.

  8. Predialytic treatment of chronic kidney disease

    African Journals Online (AJOL)

    2007-08-16

    Aug 16, 2007 ... Diabetic nephropathy is a condition where tight control of blood sugar slows the ... patients with renal disease, obesity per se has been shown to aggravate .... supplemented with essential amino acids. In my opinion the ...

  9. Exploring sleep disorders in patients with chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Nigam G

    2018-01-01

    Full Text Available Gaurav Nigam,1 Macario Camacho,2 Edward T Chang,2 Muhammad Riaz3 1Division of Sleep Medicine, Clay County Hospital, Flora, IL, 2Division of Otolaryngology, Sleep Surgery and Sleep Medicine, Tripler Army Medical Center, Honolulu, HI, 3Division of Sleep Medicine, Astria Health Center, Grandview, WA, USA Abstract: Kidney disorders have been associated with a variety of sleep-related disorders. Therefore, researchers are placing greater emphasis on finding the role of chronic kidney disease (CKD in the development of obstructive sleep apnea and restless legs syndrome. Unfortunately, the presence of other sleep-related disorders with CKDs and non-CKDs has not been investigated with the same clinical rigor. Recent studies have revealed that myriad of sleep disorders are associated with CKDs. Furthermore, there are a few non-CKD-related disorders that are associated with sleep disorders. In this narrative review, we provide a balanced view of the spectrum of sleep disorders (as identified in International Classification of Sleep disorders-3 related to different types of renal disorders prominently including but not exclusively limited to CKD. Keywords: kidney disease, sleep disorders, obstructive sleep apnea, parasomnias, restless legs syndrome, chronic kidney disease, insomnia

  10. Autosomal-dominant polycystic kidney disease (ADPKD) : executive summary from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

    NARCIS (Netherlands)

    Chapman, Arlene B.; Devuyst, Olivier; Eckardt, Kai-Uwe; Gansevoort, Ron T.; Harris, Tess; Horie, Shigeo; Kasiske, Bertram L.; Odland, Dwight; Pei, York; Perrone, Ronald D.; Pirson, Yves; Schrier, Robert W.; Torra, Roser; Torres, Vicente E.; Watnick, Terry; Wheeler, David C.

    Autosomal-dominant polycystic kidney disease (ADPKD) affects up to 12 million individuals and is the fourth most common cause for renal replacement therapy worldwide. There have been many recent advances in the understanding of its molecular genetics and biology, and in the diagnosis and management

  11. Role of leptin in reverse epidemiology in chronic kidney disease

    DEFF Research Database (Denmark)

    Scholze, Alexandra; Tepel, Martin

    2007-01-01

    Leptin is mainly produced by adipocytes and metabolized in the kidney. Leptin is taken up into the central nervous system by a saturable transport system, and controls appetite in rodents and in healthy subjects. Leptin acts on peripheral tissue and increases the inflammatory response by stimulat......Leptin is mainly produced by adipocytes and metabolized in the kidney. Leptin is taken up into the central nervous system by a saturable transport system, and controls appetite in rodents and in healthy subjects. Leptin acts on peripheral tissue and increases the inflammatory response......, indicating leptin resistance. In healthy subjects increased leptin concentration constitutes a biomarker for increased cardiovascular risk. On the other hand, a recent prospective long-term study in patients with chronic kidney disease stage 5 on hemodialysis therapy showed that reduced serum leptin...... concentration is an independent risk factor for mortality in these patients....

  12. Optimum nutrition for kidney stone disease.

    Science.gov (United States)

    Heilberg, Ita P; Goldfarb, David S

    2013-03-01

    We summarize the data regarding the associations of individual dietary components with kidney stones and the effects on 24-hour urinary profiles. The therapeutic recommendations for stone prevention that result from these studies are applied where possible to stones of specific composition. Idiopathic calcium oxalate stone-formers are advised to reduce ingestion of animal protein, oxalate, and sodium while maintaining intake of 800 to 1200 mg of calcium and increasing consumption of citrate and potassium. There are few data regarding dietary therapy of calcium phosphate stones. Whether the inhibitory effect of citrate sufficiently counteracts increasing urine pH to justify more intake of potassium and citrate is not clear. Reduction of sodium intake to decrease urinary calcium excretion would also be expected to decrease calcium phosphate stone recurrence. Conversely, the most important urine variable in the causation of uric acid stones is low urine pH, linked to insulin resistance as a component of obesity and the metabolic syndrome. The mainstay of therapy is weight loss and urinary alkalinization provided by a more vegetarian diet. Reduction in animal protein intake will reduce purine ingestion and uric acid excretion. For cystine stones, restriction of animal protein is associated with reduction in intake of the cystine precursor methionine as well as cystine. Reduction of urine sodium results in less urine cystine. Ingestion of vegetables high in organic anion content, such as citrate and malate, should be associated with higher urine pH and fewer stones because the amino acid cystine is soluble in more alkaline urine. Because of their infectious origin, diet has no definitive role for struvite stones except for avoiding urinary alkalinization, which may worsen their development. Published by Elsevier Inc.

  13. Basement Membrane Defects in Genetic Kidney Diseases

    Directory of Open Access Journals (Sweden)

    Christine Chew

    2018-01-01

    Full Text Available The glomerular basement membrane (GBM is a specialized structure with a significant role in maintaining the glomerular filtration barrier. This GBM is formed from the fusion of two basement membranes during development and its function in the filtration barrier is achieved by key extracellular matrix components including type IV collagen, laminins, nidogens, and heparan sulfate proteoglycans. The characteristics of specific matrix isoforms such as laminin-521 (α5β2γ1 and the α3α4α5 chain of type IV collagen are essential for the formation of a mature GBM and the restricted tissue distribution of these isoforms makes the GBM a unique structure. Detailed investigation of the GBM has been driven by the identification of inherited abnormalities in matrix proteins and the need to understand pathogenic mechanisms causing severe glomerular disease. A well-described hereditary GBM disease is Alport syndrome, associated with a progressive glomerular disease, hearing loss, and lens defects due to mutations in the genes COL4A3, COL4A4, or COL4A5. Other proteins associated with inherited diseases of the GBM include laminin β2 in Pierson syndrome and LMX1B in nail patella syndrome. The knowledge of these genetic mutations associated with GBM defects has enhanced our understanding of cell–matrix signaling pathways affected in glomerular disease. This review will address current knowledge of GBM-associated abnormalities and related signaling pathways, as well as discussing the advances toward disease-targeted therapies for patients with glomerular disease.

  14. Urinary endotrophin predicts disease progression in patients with chronic kidney disease

    DEFF Research Database (Denmark)

    Rasmussen, Daniel Guldager Kring; Fenton, Anthony; Jesky, Mark

    2017-01-01

    Renal fibrosis is the central pathogenic process in progression of chronic kidney disease (CKD). Collagen type VI (COL VI) is upregulated in renal fibrosis. Endotrophin is released from COL VI and promotes pleiotropic pro-fibrotic effects. Kidney disease severity varies considerably and accurate...... information regarding CKD progression may improve clinical decisions. We tested the hypothesis that urinary endotrophin derived during COL VI deposition in fibrotic human kidneys is a marker for progression of CKD in the Renal Impairment in Secondary Care (RIISC) cohort, a prospective observational study...... of 499 CKD patients. Endotrophin localised to areas of increased COL VI deposition in fibrotic kidneys but was not present in histologically normal kidneys. The third and fourth quartiles of urinary endotrophin:creatinine ratio (ECR) were independently associated with one-year disease progression after...

  15. Genetics of kidney disease and related cardiometabolic phenotypes in Zuni Indians: The Zuni Kidney Project

    Directory of Open Access Journals (Sweden)

    Sandra L Laston

    2015-01-01

    Full Text Available The objective of this study is to identify genetic factors associated with chronic kidney disease (CKD and related cardiometabolic phenotypes among participants of the Genetics of Kidney Disease in Zuni Indians study. The study was conducted as a community-based participatory research project in the Zuni Indians, a small endogamous tribe in rural New Mexico. We recruited 998 members from 28 extended multigenerational families, ascertained through probands with CKD who had at least one sibling with CKD. We used the Illumina Infinium Human1M-Duo v3.0 BeadChips to type 1.1 million single nucleotide polymorphisms (SNPs. Prevalence estimates for CKD, hyperuricemia, diabetes and hypertension were 24%, 30%, 17% and 34%, respectively. We found a significant (p<1.58 × 10-7 association for a SNP in a novel gene for serum creatinine (PTPLAD2. We replicated significant associations for genes with serum uric acid (SLC2A9, triglyceride levels (APOA1, BUD13, ZNF259, and total cholesterol (PVRL2. We found novel suggestive associations (p<1.58 × 10-6 for SNPs in genes with systolic (OLFML2B, and diastolic blood pressure (NFIA. We identified a series of genes associated with CKD and related cardiometabolic phenotypes among Zuni Indians, a population with a high prevalence of kidney disease. Illuminating genetic variations that modulate the risk for these disorders may ultimately provide a basis for novel preventive strategies and therapeutic interventions.

  16. Platelet thromboxane B2-formation in end-stage kidney disease and after kidney transplantation

    International Nuclear Information System (INIS)

    Stefanovic, V.; Lecic, N.

    1986-01-01

    The aim of this work was to analyse TxB 2 formation by platelets in endstage kidney disease patients and in kidney graft recipients. Four groups of patients were studied: 12 preterminal chronic renal failure patients, 42 patients on maintenance hemodialysis, 8 patients on CAPD and 11 grafted patients. TxB 2 production by platelets was determined in serum following spontaneous blood clotting for 1/2 h at 37 0 C. Hemodialysis patients generated 80.7 ± 9.6 ng/ml (mean ± S.E.M.) of TxB 2 which was significantly (p 2 formation in hemodialysis patients had no relationship with the residual kidney function. Patients on CAPD produced 65.0 ± 12.7 ng/ml of TxB 2 . Very low TxB 2 generation was obtained also in preterminal chronic renal failure patients (57.0 ± 11.8 ng/ml). Kidney graft recipients had a mean TxB 2 production of 81.6 ± 24.2 ng/ml with a range from 12.5-200 ng/ml. Very low TxB 2 was formed in grafted patients with renal failure. (orig.) [de

  17. Political Economy of Epidemic Kidney Disease in Sri Lanka

    Directory of Open Access Journals (Sweden)

    Asoka Bandarage

    2013-10-01

    Full Text Available The Chronic Kidney Disease (CKD, taking the lives of thousands in poor farming communities in Sri Lanka, is commonly seen as a problem peculiar to the island’s north central dry zone agricultural region. The prevailing bio-medical focus is on identifying one or more “environmental nephrotoxins.” While delineating important controversies on the etiology of the disease, this article seeks to broaden the discourse on the hitherto neglected political economy of CKD in Sri Lanka. In so doing, it seeks to bring together the bio-medical debate on the impact of widespread and unregulated use of agrochemicals on public health and kidney disease with broader global interdisciplinary perspectives on the industrialization of agriculture and the consolidation of food production by transnational agribusiness corporations. The article concludes pointing out environmentally sustainable and socially equitable development and organic agriculture as the long-term solutions to CKD in Sri Lanka and elsewhere.

  18. 75 FR 61766 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2010-10-06

    ... Institute of Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, Liver PPG Application. Date... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the...: National Institute of Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, Nutrition Obesity...

  19. 75 FR 69685 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2010-11-15

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Liver Ancillary Studies. Date: December... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Special Emphasis Panel for R01...

  20. 78 FR 50428 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2013-08-19

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; NIDDK Ancillary R01 Studies on Liver... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Diabetic Ketoacidosis. Date: September...

  1. 78 FR 9401 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2013-02-08

    ... Institute of Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Liver Related Ancillary... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Beta-Cell Function and Cognition. Date...

  2. 75 FR 4830 - National Institute of Diabetes and Digestive and Kidney Diseases;

    Science.gov (United States)

    2010-01-29

    ... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel. Predictors of Genitourinary Disorders... Digestive and Kidney Diseases Special Emphasis Panel; Small Grant Program. Date: March 12, 2010. Time: 2 p.m...

  3. Familial polycystic kidney disease in Nigeria: A report of two cases ...

    African Journals Online (AJOL)

    A case of familial polycystic kidney disease is reported. Although isolated cases of adult polycystic kidney disease have been reported in our environment, no case to our knowledge has been reported with a familial link. Polycystic kidney disease is said to be rare in Africans. Although it commonly terminates in chronic renal ...

  4. Common acquired kidney diseases in children

    African Journals Online (AJOL)

    2012-02-01

    Feb 1, 2012 ... salt and water retention. Volume overload may also cause acute left-heart failure and pulmonary oedema. Atypical presentations of APSGN include those with subclinical disease and those presenting with acute complications of hypertension in the absence of overtly abnormal urine. Special investigations.

  5. POLYCYSTIC KIDNEY DISEASE IN A PATIENT WITH ...

    African Journals Online (AJOL)

    hi-tech

    2003-01-01

    Jan 1, 2003 ... bossing with a depressed nasal bridge, bowing of the lower extremeties, trident hands, lumbar lordosis, ... cystic enlargement, is one of the most common dominantly inherited conditions and is an important ... addition to other autosomal dominant inherited diseases like tuberous sclerosis and von Hippel- ...

  6. Predialytic treatment of chronic kidney disease

    African Journals Online (AJOL)

    2007-08-16

    Aug 16, 2007 ... in high turnover bone disease. Note the poor outline of the femurs. Fig. 4. Severe calciphylaxis in a patient with CKD. Note the extensive skin and subcutaneous infarc- tion with underlying muscle clearly visible. Predialytic treatment of CKD. 392. CME August 2007 Vol.25 No.8 pg389-394.indd 392. 8/16/07 ...

  7. Management of patients with chronic kidney disease

    African Journals Online (AJOL)

    This article deals with these aspects, including follow-up guidelines and management and treatment ... those with ischaemic heart disease also require cardiac review at least once a year. .... doses when fluid losses are high, e.g. sweating in hot environments, ... dried beans, lentils, offal, salmon, chocolate, cola drinks and.

  8. Vitamin D deficiency aggravates chronic kidney disease progression after ischemic acute kidney injury.

    Directory of Open Access Journals (Sweden)

    Janaína Garcia Gonçalves

    Full Text Available Despite a significant improvement in the management of chronic kidney disease (CKD, its incidence and prevalence has been increasing over the years. Progressive renal fibrosis is present in CKD and involves the participation of several cytokines, including Transforming growth factor-β1 (TGF-β1. Besides cardiovascular diseases and infections, several studies show that Vitamin D status has been considered as a non-traditional risk factor for the progression of CKD. Given the importance of vitamin D in the maintenance of essential physiological functions, we studied the events involved in the chronic kidney disease progression in rats submitted to ischemia/reperfusion injury under vitamin D deficiency (VDD.Rats were randomized into four groups: Control; VDD; ischemia/reperfusion injury (IRI; and VDD+IRI. At the 62 day after sham or IRI surgery, we measured inulin clearance, biochemical variables and hemodynamic parameters. In kidney tissue, we performed immunoblotting to quantify expression of Klotho, TGF-β, and vitamin D receptor (VDR; gene expression to evaluate renin, angiotensinogen, and angiotensin-converting enzyme; and immunohistochemical staining for ED1 (macrophages, type IV collagen, fibronectin, vimentin, and α-smooth mucle actin. Histomorphometric studies were performed to evaluate fractional interstitial area.IRI animals presented renal hypertrophy, increased levels of mean blood pressure and plasma PTH. Furthermore, expansion of the interstitial area, increased infiltration of ED1 cells, increased expression of collagen IV, fibronectin, vimentin and α-actin, and reduced expression of Klotho protein were observed. VDD deficiency contributed to increased levels of plasma PTH as well as for important chronic tubulointerstitial changes (fibrosis, inflammatory infiltration, tubular dilation and atrophy, increased expression of TGF-β1 and decreased expression of VDR and Klotho protein observed in VDD+IRI animals.Through inflammatory

  9. Renal resistive index and mortality in chronic kidney disease.

    Science.gov (United States)

    Toledo, Clarisse; Thomas, George; Schold, Jesse D; Arrigain, Susana; Gornik, Heather L; Nally, Joseph V; Navaneethan, Sankar D

    2015-08-01

    Renal resistive index (RRI) measured by Doppler ultrasonography is associated with cardiovascular events and mortality in hypertensive, diabetic, and elderly patients. We studied the factors associated with high RRI (≥0.70) and its associations with mortality in chronic kidney disease patients without renal artery stenosis. We included 1962 patients with an estimated glomerular filtration rate of 15 to 59 mL/min per 1.73 m(2) who also had RRI measured (January 1, 2005, to October 2011) from an existing chronic kidney disease registry. Participants with renal artery stenosis (60%-99% or renal artery occlusion) were excluded. Multivariable logistic regression model was used to study factors associated with high RRI (≥0.70), and its association with mortality was studied using Kaplan-Meier plots and Cox proportional hazards model. Hypertension was prevalent in >90% of the patients. In the multivariable logistic regression, older age, female sex, diabetes mellitus, coronary artery disease, peripheral vascular disease, higher systolic blood pressure, and the use of β blockers were associated with higher odds of having RRI≥0.70. During a median follow-up of 2.2 years, 428 patients died. After adjusting for covariates, RRI≥0.70 was associated with increased mortality (adjusted hazard ratio, 1.29; 95% confidence interval, 1.02-1.65; Pchronic kidney disease. Noncardiovascular/non-malignancy-related deaths were higher in those with RRI≥0.70. RRI≥0.70 is associated with higher mortality in hypertensive chronic kidney disease patients without clinically significant renal artery stenosis after accounting for other significant risk factors. Its evaluation may allow early identification of those who are at risk thereby potentially preventing or delaying adverse outcomes. © 2015 American Heart Association, Inc.

  10. Diet in chronic kidney disease in a Mediterranean African country.

    Science.gov (United States)

    Kammoun, Khawla; Chaker, Hanen; Mahfoudh, Hichem; Makhlouf, Nouha; Jarraya, Faical; Hachicha, Jamil

    2017-01-23

    Mediterranean diet is characterized by low to moderate consumption of animal protein and high consumption of fruits, vegetables, bread, beans, nuts, seeds and other cereals. It has been associated with reduced risk of cardiovascular disease. However, it is not suitable for chronic kidney disease because of high potassium intake. Tunisia is an emerging Mediterranean country with limited resources, a high prevalence of chronic hemodialysis treatment and high dialysis expenditures. In order to limit dialysis cost, primary and secondary prevention of chronic renal disease are of paramount importance. In addition to drugs, secondary prevention includes diet measures (e.g. salt diet, protein diet). The aims of diet practice in chronic kidney disease are to slow chronic renal failure progression and to prevent its complications like hyperphosphatemia and hyperkaliemiae. A few decades ago, a Tunisian diet was exclusively Mediterranean, and protein consumption was not excessive. However, today, protein consumption is more comparable to western countries. Salt consumption is also excessive. Some Tunisian diets still include food with high potassium intake, which are not suitable for patients with chronic kidney disease. Therefore, the role of the dietician is extremely important to help calculate and create a dietary regimen tailored to each of our patients. Advice about diets should be adapted to both the patient and population habits to improve adherence rate. As such, the purpose of this article is to provide our own experience regarding medical nutrition therapy in patients with chronic kidney disease in Tunisia, with some changes in food habits. Prevention is far better than treatment. In this perspective, dietary measures must be at the core of our intervention.

  11. Asian Leadership in Chronic Kidney Disease

    OpenAIRE

    Becker, Gavin J

    2009-01-01

    Asian Pacific countries include those with the highest incidence of renal failure in the world, the richest and poorest economies and unparalleled diversity of economy, culture and geography. From this come many challenges, but also a strong basis for the introduction of strategies to combat renal diseases. With a rapidly developing scientific community, Asia needs to accept the challenge of becoming a global leader in nephrology in the near future.

  12. Insulin Resistance in Patients with Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Min-Tser Liao

    2012-01-01

    Full Text Available Metabolic syndrome and its components are associated with chronic kidney disease (CKD development. Insulin resistance (IR plays a central role in the metabolic syndrome and is associated with increased risk for CKD in nondiabetic patients. IR is common in patients with mild-to-moderate stage CKD, even when the glomerular filtration rate is within the normal range. IR, along with oxidative stress and inflammation, also promotes kidney disease. In patients with end stage renal disease, IR is an independent predictor of cardiovascular disease and is linked to protein energy wasting and malnutrition. Systemic inflammation, oxidative stress, elevated serum adipokines and fetuin-A, metabolic acidosis, vitamin D deficiency, depressed serum erythropoietin, endoplasmic reticulum stress, and suppressors of cytokine signaling all cause IR by suppressing insulin receptor-PI3K-Akt pathways in CKD. In addition to adequate renal replacement therapy and correction of uremia-associated factors, thiazolidinedione, ghrelin, protein restriction, and keto-acid supplementation are therapeutic options. Weight control, reduced daily prednisolone dosage, and the use of cyclosporin decrease the risk of developing new-onset diabetes after kidney transplantation. Improved understanding of the pathogenic mechanisms underlying IR in CKD may lead to more effective therapeutic strategies to reduce uremia-associated morbidity and mortality.

  13. RESEARCH ARTICLE Mutational screening of PKD2 gene in north ...

    Indian Academy of Sciences (India)

    2017-01-12

    Jan 12, 2017 ... Results: Two associated symptoms, hypertension (19%) and liver cyst (31%) have major contribution to PKD. Gender based analysis reveled that familial female patients (27%) and familial male patients (33%) are more hypertensive. Liver cyst, the second major contributing symptom presented by large.

  14. Sexual and gonadal dysfunction in chronic kidney disease: Pathophysiology

    Directory of Open Access Journals (Sweden)

    Manish Rathi

    2012-01-01

    Full Text Available Sexual and gonadal dysfunction/infertility are quite common in patients with chronic kidney disease. Forty percent of male and 55% of female dialysis patients do not achieve orgasm. The pathophysiology of gonadal dysfunction is multifactorial. It is usually a combination of psychological, physiological, and other comorbid factors. Erectile dysfunction in males is mainly due to arterial factors, venous leakage, psychological factors, neurogenic factors, endocrine factors, and drugs. Sexual dysfunction in females is mainly due to hormonal factors and manifests mainly as menstrual irregularities, amenorrhea, lack of vaginal lubrication, and failure to conceive. Treatment of gonadal dysfunction in chronic kidney disease is multipronged and an exact understanding of underlying pathology is essential in proper management of these patients.

  15. The role of SIRT1 in diabetic kidney disease

    Directory of Open Access Journals (Sweden)

    Rabi eYacoub

    2014-10-01

    Full Text Available Sirtuins (SIRTs are members of the silent information regulator 2 (Sir2 family. In mammals, of the seven known SIRTs, SIRT1 function is most studied and has been shown to regulate wide range of cellular functions that affect metabolic homeostasis and aging. SIRT1 exerts anti-apoptotic, anti-oxidative, and anti-inflammatory effects against cellular injury, and protects the cells through the regulation of mitochondrial biogenesis, autophagy, and metabolism in response to the cellular energy and redox status. SIRT1 also promotes vasodilation and protects vascular tissues. In humans and animal models with diabetic kidney disease, its expression tends to be decreased in renal cells, and increased expression of SIRT1 was found to play a renal protective role in animal models with diabetic kidney disease. In this review we discuss the role and potential mechanisms by which SIRT1 protects against DKD.

  16. Continuation of lithium after a diagnosis of chronic kidney disease

    DEFF Research Database (Denmark)

    Kessing, L V; Feldt-Rasmussen, B; Andersen, P K

    2017-01-01

    OBJECTIVE: To investigate whether continued lithium or anticonvulsant treatment after a first diagnosis of chronic kidney disease (CKD) was associated with progression to irreversible end-stage kidney disease. METHODS: Nationwide cohort study including all individuals in Denmark in a period from...... 1995 to 2012 with a diagnosis of CKD and (i) a history of lithium treatment (N = 754, among whom 238 patients had a diagnosis of bipolar disorder) or (ii) a history of anticonvulsant treatment (N = 5.004, among whom 199 patients had a diagnosis of bipolar disorder). End-stage CKD was defined as chronic...... dialysis or renal transplantation. RESULTS: Continuing lithium (HR = 0.58 (95% CI: 0.37-0.90) and continuing anticonvulsants (HR = 0.53 (95% CI: 0.44-0.64) were associated with decreased rates of end-stage CKD. In the subcohorts of patients with a diagnosis of bipolar disorder, continuing lithium...

  17. Bisphenol A in Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Emilio González-Parra

    2013-01-01

    Full Text Available Phenols are uremic toxins of intestinal origin formed by bacteria during protein metabolism. Of these molecules, p-cresol is the most studied and has been associated with renal function impairment and vascular damage. Bisphenol A (BPA is a molecule with structural similarity with phenols found in plastic food and beverage containers as well as in some dialyzers. BPA is considered an environmental toxicant based on animal and cell culture studies. Japanese authorities recently banned BPA use in baby bottles based on observational association studies in newborns. BPA is excreted in urine and uremic patients present higher serum levels, but there is insufficient evidence to set cut-off levels or to link BPA to any harmful effect in CKD. However, the renal elimination and potential exposure during dialysis warrant the monitoring of BPA exposure and the design of observational studies in which the potential health risks of BPA for end-stage renal disease patients are evaluated.

  18. Important causes of chronic kidney disease in South Africa | Moosa ...

    African Journals Online (AJOL)

    In hypertensive patients without chronic kidney disease (CKD) the goal is to keep blood pressure (BP) at ≤140/90 mmHg. When CKD is present, especially where there is proteinuria of ≥0.5 g/day, the goal is a BP of ≤130/80 mmHg. Lifestyle measures are mandatory, especially limitation of salt intake, ingestion of ...

  19. Assessment of diet in chronic kidney disease female predialysis patients

    OpenAIRE

    Dariusz Włodarek; Dominika Głąbska; Jadwiga Rojek-Trębicka

    2014-01-01

    [b]introduction and objective[/b]. Nutrition is important in the therapy of predialysis patients. The aim of the presented single-centre descriptive study was to assess the diet in chronic kidney disease female predialysis patients with no previous dietary intervention, in comparison with recommendations, as well as the analysis of the energy, protein and phosphate intake in correlation with chosen laboratory measurements. [b]materials and methods.[/b] The research was carried out in 31...

  20. Using digital media to promote kidney disease education.

    Science.gov (United States)

    Goldstein, Karen; Briggs, Michael; Oleynik, Veronica; Cullen, Mac; Jones, Jewel; Newman, Eileen; Narva, Andrew

    2013-07-01

    Health-care providers and patients increasingly turn to the Internet-websites as well as social media platforms-for health-related information and support. Informed by research on audience behaviors and preferences related to digital health information, the National Kidney Disease Education Program (NKDEP) developed a comprehensive and user-friendly digital ecosystem featuring content and platforms relevant for each audience. NKDEP's analysis of website metrics and social media conversation mapping related to CKD revealed gaps and opportunities, informing the development of a digital strategy to position NKDEP as a trustworthy digital source for evidence-based kidney disease information. NKDEP launched a redesigned website (www.nkdep.nih.gov) with enhanced content for multiple audiences as well as a complementary social media presence on Twitter and Facebook serving to drive traffic to the website as well as actively engage target audiences in conversations about kidney disease. The results included improved website metrics and increasing social media engagement among consumers and health-care providers. NKDEP will continue to monitor trends, explore new directions, and work to improve communication across digital platforms. Published by Elsevier Inc.

  1. Effect of mineralocorticoid receptor antagonists on proteinuria and progression of chronic kidney disease: A systematic review and meta-analysis

    NARCIS (Netherlands)

    Currie, G. (Gemma); Taylor, A.H.M. (Alison H. M.); Fujita, T. (Toshiro); Ohtsu, H. (Hiroshi); Lindhardt, M. (Morten); K. Rossing; Boesby, L. (Lene); Edwards, N.C. (Nicola C.); Ferro, C.J. (Charles J.); J. Townend (Jonathan); A.H. van den Meiracker (Anton); Saklayen, M.G. (Mohammad G.); Oveisi, S. (Sonia); Jardine, A.G. (Alan G.); C. Delles (Christian); Preiss, D.J. (David J.); Mark, P.B. (Patrick B.)

    2016-01-01

    textabstractBackground: Hypertension and proteinuria are critically involved in the progression of chronic kidney disease. Despite treatment with renin angiotensin system inhibition, kidney function declines in many patients. Aldosterone excess is a risk factor for progression of kidney disease.

  2. Vasopressin, Copeptin, and Renal Concentrating Capacity in Patients with Autosomal Dominant Polycystic Kidney Disease without Renal Impairment

    NARCIS (Netherlands)

    Zittema, Debbie; Boertien, Wendy E.; van Beek, Andre P.; Dullaart, Robin P. F.; Franssen, Casper F. M.; de Jong, Paul E.; Meijer, Esther; Gansevoort, Ron T.

    Background and objectives Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent hereditary renal disease, characterized by cyst formation in the kidneys leading to end stage kidney failure. It is clinically acknowledged that ADPKD patients have impaired urine concentrating

  3. 75 FR 57971 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting

    Science.gov (United States)

    2010-09-23

    ... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting Pursuant to section 10(d) of the... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, Central Repositories Non-Renewable Sample Access (PAR-10-90)--Liver, Kidney, Urological Sciences. Date: October 12, 2010. Time: 2 p.m. to 4...

  4. K/DOQI clinical practice guidelines for chronic kidney disease: Evaluation, classification, and stratification

    NARCIS (Netherlands)

    Levey, Andrew S.; Coresh, Josef; Bolton, Kline; Culleton, Bruce; Harvey, Kathy Schiro; Ikizler, T. Alp; Johnson, Cynda Ann; Kausz, Annamaria; Kimmel, Paul L.; Kusek, John; Levin, Adeera; Minaker, Kenneth L.; Nelson, Robert; Rennke, Helmut; Steffes, Michael; Witten, Beth; Hogg, Ronald J.; Furth, Susan; Lemley, Kevin V.; Portman, Ronald J.; Schwartz, George; Lau, Joseph; Balk, Ethan; Perrone, Ronald D.; Karim, Tauqeer; Rayan, Lara; Al-Massry, Inas; Chew, Priscilla; Astor, Brad C.; De Vine, Deirdre; Eknoyan, Garabed; Levin, Nathan; Burrows-Hudson, Sally; Keane, William; Kliger, Alan; Latos, Derrick; Mapes, Donna; Oberley, Edith; Willis, Kerry; Bailie, George; Becker, Gavin; Burrowes, Jerrilynn; Churchill, David; Collins, Allan; Couser, William; de Zeeuw, Dick; Garber, Alan; Golper, Thomas; Gotch, Frank; Gotto, Antonio; Greer, Joel W.; Grimm Jr., Richard; Hannah, Ramon G.; Acosta, Jaime Herrera; Hogg, Ronald; Hunsicker, Lawrence; Klag, Michael; Klahr, Saulo; Lewis, Caya; Lowrie, Edmund; Matas, Arthur; McCulloch, Sally; Michael, Maureen; Nally, Joseph V.; Newmann, John M.; Nissenson, Allen; Norris, Keith; Owen Jr., William; Patel, Thakor G.; Payne, Glenda; Rivera-Mizzoni, Rosa A.; Smith, David; Star, Robert; Steinman, Theodore; Valderrabano, Fernando; Walls, John; Wauters, Jean-Pierre; Wenger, Nanette; Briggs, Josephine

    2002-01-01

    Introduction: Chronic kidney disease as a public health problem. Chronic kidney disease is a worldwide public health problem. In the United States, there is a rising incidence and prevalence of kidney failure, with poor outcomes and high cost. There is an even higher prevalence of earlier stages of

  5. Effect of mineralocorticoid receptor antagonists on proteinuria and progression of chronic kidney disease

    DEFF Research Database (Denmark)

    Currie, Gemma; Taylor, Alison H M; Fujita, Toshiro

    2016-01-01

    BACKGROUND: Hypertension and proteinuria are critically involved in the progression of chronic kidney disease. Despite treatment with renin angiotensin system inhibition, kidney function declines in many patients. Aldosterone excess is a risk factor for progression of kidney disease. Hyperkalaemi...... pressure and urinary protein/albumin excretion with a quantifiable risk of hyperkalaemia above predefined study upper limit....

  6. Subclinical chronic kidney disease modifies the diagnosis of experimental acute kidney injury.

    Science.gov (United States)

    Succar, Lena; Pianta, Timothy J; Davidson, Trent; Pickering, John W; Endre, Zoltán H

    2017-09-01

    Extensive structural damage within the kidney must be present before serum creatinine increases. However, a subclinical phase of chronic kidney disease (CKD) usually goes undetected. Here we tested whether experimental subclinical CKD would modify functional and damage biomarker profiles of acute kidney injury (AKI). Subclinical CKD was induced in rats by adenine or aristolochic acid models but without increasing serum creatinine. After prolonged recovery (three to six weeks), AKI was induced with a subnephrotoxic dose of cisplatin. Urinary levels of kidney injury molecule-1 (KIM-1), cytochrome C, monocyte chemotactic protein-1 (MCP-1), clusterin, and interleukin-18 increased during CKD induction, without an increase in serum creatinine. After AKI in adenine-induced CKD, serum creatinine increased more rapidly, while increased urinary KIM-1, clusterin, and MCP-1 were delayed and reduced. Increased serum creatinine and biomarker excretion were associated with diffuse tubulointerstitial injury in the outer stripe of outer medulla coupled with over 50% cortical damage. Following AKI in aristolochic acid-induced CKD, increased serum creatinine, urinary KIM-1, clusterin, MCP-1, cytochrome C, and interleukin-18 concentrations and excretion were greater at day 21 than day 42 and inversely correlated with cortical injury. Subclinical CKD modified functional and damage biomarker profiles in diametrically opposite ways. Functional biomarker profiles were more sensitive, while damage biomarker diagnostic thresholds and increases were diminished and delayed. Damage biomarker concentrations and excretion were inversely linked to the extent of prior cortical damage. Thus, thresholds for AKI biomarkers may need to be lower or sampling delayed in the known presence of CKD. Crown Copyright © 2017. Published by Elsevier Inc. All rights reserved.

  7. Osteoblast-specific deletion of Pkd2 leads to low-turnover osteopenia and reduced bone marrow adiposity.

    Directory of Open Access Journals (Sweden)

    Zhousheng Xiao

    Full Text Available Polycystin-1 (Pkd1 interacts with polycystin-2 (Pkd2 to form an interdependent signaling complex. Selective deletion of Pkd1 in the osteoblast lineage reciprocally regulates osteoblastogenesis and adipogenesis. The role of Pkd2 in skeletal development has not been defined. To this end, we conditionally inactivated Pkd2 in mature osteoblasts by crossing Osteocalcin (Oc-Cre;Pkd2+/null mice with floxed Pkd2 (Pkd2flox/flox mice. Oc-Cre;Pkd2flox/null (Pkd2Oc-cKO mice exhibited decreased bone mineral density, trabecular bone volume, cortical thickness, mineral apposition rate and impaired biomechanical properties of bone. Pkd2 deficiency resulted in diminished Runt-related transcription factor 2 (Runx2 expressions in bone and impaired osteoblastic differentiation ex vivo. Expression of osteoblast-related genes, including, Osteocalcin, Osteopontin, Bone sialoprotein (Bsp, Phosphate-regulating gene with homologies to endopeptidases on the X chromosome (Phex, Dentin matrix protein 1 (Dmp1, Sclerostin (Sost, and Fibroblast growth factor 23 (FGF23 were reduced proportionate to the reduction of Pkd2 gene dose in bone of Oc-Cre;Pkd2flox/+ and Oc-Cre;Pkd2flox/null mice. Loss of Pkd2 also resulted in diminished peroxisome proliferator-activated receptor γ (PPARγ expression and reduced bone marrow fat in vivo and reduced adipogenesis in osteoblast culture ex vivo. Transcriptional co-activator with PDZ-binding motif (TAZ and Yes-associated protein (YAP, reciprocally acting as co-activators and co-repressors of Runx2 and PPARγ, were decreased in bone of Oc-Cre;Pkd2flox/null mice. Thus, Pkd1 and Pkd2 have coordinate effects on osteoblast differentiation and opposite effects on adipogenesis, suggesting that Pkd1 and Pkd2 signaling pathways can have independent effects on mesenchymal lineage commitment in bone.

  8. Vitamin D, Phosphate and Fibroblast Growth Factor 23: A role in the pathogenesis and management of Chronic Kidney Disease and Chronic Kidney Disease Mineral and Bone Disorder

    OpenAIRE

    Damasiewicz, Matthew John

    2017-01-01

    Chronic kidney disease (CKD) is defined by the presence of proteinuria or decreased kidney function, with a prevalence of 10-15% in the adult population. CKD can progress to end-stage kidney disease (ESKD) and is associated with progressive abnormalities of bone and mineral metabolism, defined as CKD mineral and bone disorder (CKD-MBD). The use of vitamin D in CKD, the optimal level for initiating treatment and the use of current and novel biomarkers in the management of ...

  9. Epithelial hyperplasia in human polycystic kidney diseases. Its role in pathogenesis and risk of neoplasia.

    OpenAIRE

    Bernstein, J.; Evan, A. P.; Gardner, K. D.

    1987-01-01

    The importance of tubular epithelial hyperplasia in polycystic kidney diseases has become apparent during the last decade. Micropapillary hyperplasia occurs in autosomal dominant polycystic kidney disease, in localized cystic disease, and in acquired cystic disease. Neoplastic or severely dysplastic epithelial hyperplasia occurs in von Hippel-Lindau disease. A histopathologically distinctive epithelial hyperplasia occurs in tuberous sclerosis. In each of these conditions, epithelial hyperplas...

  10. The therapeutic use of mesenchymal stem cells for treating kidney disease

    OpenAIRE

    Wise, Andrea Frances

    2017-01-01

    A surge in the prevalence of chronic diseases, including chronic kidney disease (CKD), has caused a major shift in the developed world’s disease profile. The increasing incidence of CKD is in part due to the escalating incidence of type 2 diabetes. For end-stage renal disease (ESRD) patients, the only renal replacement therapy options for kidney disease patients are dialysis and kidney transplantation. However, dialysis places a substantial burden on patient quality of life and the global hea...

  11. On the occasion of world kidney day 2017; obesity and its relationship with chronic kidney disease.

    Science.gov (United States)

    Mahmoodnia, Leila; Tamadon, Mohammad Reza

    2017-07-01

    Numerous studies have reported the impact of obesity in the incidence of chronic kidney disease (CKD). Some studies have suggested the direct role of obesity in the incidence of CKD, while some other studies suggest an indirect effect caused by the effects of obesity on blood pressure and diabetes. PubMed, EBSCO, Web of Science, directory of open access journals (DOAJ), EMBASE, and Google Scholar have been searched. Recent studies have presented more strong evidences on the role of obesity on the incidence of CKD. The double role of obesity in the incidence of CKD has also been mentioned in some studies. Such an additional effect arises from the impact of obesity on the incidence of some conditions and diseases such as cardiovascular disease, hypertension, and diabetes, which in turn are involved in the incidence of CKD and are considered as its risk factors.

  12. Murine nephrotoxic nephritis as a model of chronic kidney disease

    DEFF Research Database (Denmark)

    Ougaard, M. K.E.; Kvist, P. H.; Jensen, H. E.

    2018-01-01

    Using the nonaccelerated murine nephrotoxic nephritis (NTN) as a model of chronic kidney disease (CKD) could provide an easily inducible model that enables a rapid test of treatments. Originally, the NTN model was developed as an acute model of glomerulonephritis, but in this study we evaluate...... progressive mesangial expansion and significant renal fibrosis within three weeks suggesting CKD development. CD1 and C57BL/6 females showed a similar disease progression, but female mice seemed more susceptible to NTS compared to male mice. The presence of albuminuria, GFR decline, mesangial expansion...

  13. The increasing financial impact of chronic kidney disease in australia.

    Science.gov (United States)

    Tucker, Patrick S; Kingsley, Michael I; Morton, R Hugh; Scanlan, Aaron T; Dalbo, Vincent J

    2014-01-01

    The aim of this investigation was to determine and compare current and projected expenditure associated with chronic kidney disease (CKD), renal replacement therapy (RRT), and cardiovascular disease (CVD) in Australia. Data published by Australia and New Zealand Dialysis and Transplant Registry, Australian Institute of Health and Welfare, and World Bank were used to compare CKD-, RRT-, and CVD-related expenditure and prevalence rates. Prevalence and expenditure predictions were made using a linear regression model. Direct statistical comparisons of rates of annual increase utilised indicator variables in combined regressions. Statistical significance was set at P Australia's healthcare system, compared to CVD. Research focusing on novel preventative/therapeutic interventions is warranted.

  14. 78 FR 43214 - Proposed Collection; 60-day Comment Request Evaluation of a Kidney Disease Education and...

    Science.gov (United States)

    2013-07-19

    ... pre-test/post-test surveys to assess: (a) Knowledge gains about kidney disease, (b) awareness of NKDEP resources and importance of kidney health, (c) reported behavior change outcomes and (d) reported health...

  15. New Study Shows 59 Percent of Americans Will Develop Kidney Disease in Their Lifetime

    Science.gov (United States)

    ... pressure or diabetes – by adding a simple urine albumin test for kidney damage to annual physical examinations. “ ... Grams, a nephrologist and lead author of the paper pointed out that while severe kidney disease and ...

  16. Complete staghorn calculus in polycystic kidney disease: infection is still the cause.

    Science.gov (United States)

    Mao, Zhiguo; Xu, Jing; Ye, Chaoyang; Chen, Dongping; Mei, Changlin

    2013-08-01

    Kidney stones in patients with autosomal dominant polycystic kidney disease are common, regarded as the consequence of the combination of anatomic abnormality and metabolic risk factors. However, complete staghorn calculus is rare in polycystic kidney disease and predicts a gloomy prognosis of kidney. For general population, recent data showed metabolic factors were the dominant causes for staghorn calculus, but for polycystic kidney disease patients, the cause for staghorn calculus remained elusive. We report a case of complete staghorm calculus in a polycystic kidney disease patient induced by repeatedly urinary tract infections. This 37-year-old autosomal dominant polycystic kidney disease female with positive family history was admitted in this hospital for repeatedly upper urinary tract infection for 3 years. CT scan revealed the existence of a complete staghorn calculus in her right kidney, while there was no kidney stone 3 years before, and the urinary stone component analysis showed the composition of calculus was magnesium ammonium phosphate. UTI is an important complication for polycystic kidney disease and will facilitate the formation of staghorn calculi. As staghorn calculi are associated with kidney fibrosis and high long-term renal deterioration rate, prompt control of urinary tract infection in polycystic kidney disease patient will be beneficial in preventing staghorn calculus formation.

  17. Caffeine intake by patients with autosomal dominant polycystic kidney disease

    International Nuclear Information System (INIS)

    Vendramini, L.C.; Nishiura, J.L.; Baxmann, A.C.; Heilberg, I.P.

    2012-01-01

    Because caffeine may induce cyst and kidney enlargement in autosomal dominant polycystic kidney disease (ADPKD), we evaluated caffeine intake and renal volume using renal ultrasound in ADPKD patients. Caffeine intake was estimated by the average of 24-h dietary recalls obtained on 3 nonconsecutive days in 102 ADPKD patients (68 females, 34 males; 39 ± 12 years) and compared to that of 102 healthy volunteers (74 females, 28 males; 38 ± 14 years). The awareness of the need for caffeine restriction was assessed. Clinical and laboratory data were obtained from the medical records of the patients. Mean caffeine intake was significantly lower in ADPKD patients versus controls (86 vs 134 mg/day), and 63% of the ADPKD patients had been previously aware of caffeine restriction. Caffeine intake did not correlate with renal volume in ADPKD patients. There were no significant differences between the renal volumes of patients in the highest and lowest tertiles of caffeine consumption. Finally, age-adjusted multiple linear regression revealed that renal volume was associated with hypertension, chronic kidney disease stage 3 and the time since diagnosis, but not with caffeine intake. The present small cross-sectional study indicated a low level of caffeine consumption by ADPKD patients when compared to healthy volunteers, which was most likely due to prior awareness of the need for caffeine restriction. Within the range of caffeine intake observed by ADPKD patients in this study (0-471 mg/day), the renal volume was not directly associated with caffeine intake

  18. Intermittent hemodialysis in dogs with chronic kidney disease stage III

    Directory of Open Access Journals (Sweden)

    Alessandra Melchert

    2017-08-01

    Full Text Available ABSTRACT: Intermittent hemodialysis (IHD is a form of renal replacement that is used in veterinary medicine for cases involving drug removal, electrolyte imbalance, acute kidney injury, and chronic kidney disease (CKD. The aim of the present study was to verify the efficacy of IHD in dogs with CKD staged at grade III and to evaluate the effect of IHD on quality of life. Twelve dogs with CKD at stage III met the inclusion criteria and were divided equally into two groups. The control group (n=6 received only clinical treatment and intravenous fluid therapy, and the hemodialysis group (n=6 received clinical and IHD treatments. Blood samples were collected before and after treatments in both groups. We evaluated complications and clinical parameters of IHD every 30 minutes. Hemodialysis decreased serum urea, creatinine, and phosphorus. Despite the evident removal of nitrogen compounds, dialysis treatment did not increase survival time in these patients. The results of this study do not support the early use of dialysis in dogs with chronic kidney disease stage III.

  19. Caffeine intake by patients with autosomal dominant polycystic kidney disease

    Energy Technology Data Exchange (ETDEWEB)

    Vendramini, L.C.; Nishiura, J.L.; Baxmann, A.C.; Heilberg, I.P. [Disciplina de Nefrologia, Departamento de Medicina, Universidade Federal de São Paulo, São Paulo, SP (Brazil)

    2012-07-20

    Because caffeine may induce cyst and kidney enlargement in autosomal dominant polycystic kidney disease (ADPKD), we evaluated caffeine intake and renal volume using renal ultrasound in ADPKD patients. Caffeine intake was estimated by the average of 24-h dietary recalls obtained on 3 nonconsecutive days in 102 ADPKD patients (68 females, 34 males; 39 ± 12 years) and compared to that of 102 healthy volunteers (74 females, 28 males; 38 ± 14 years). The awareness of the need for caffeine restriction was assessed. Clinical and laboratory data were obtained from the medical records of the patients. Mean caffeine intake was significantly lower in ADPKD patients versus controls (86 vs 134 mg/day), and 63% of the ADPKD patients had been previously aware of caffeine restriction. Caffeine intake did not correlate with renal volume in ADPKD patients. There were no significant differences between the renal volumes of patients in the highest and lowest tertiles of caffeine consumption. Finally, age-adjusted multiple linear regression revealed that renal volume was associated with hypertension, chronic kidney disease stage 3 and the time since diagnosis, but not with caffeine intake. The present small cross-sectional study indicated a low level of caffeine consumption by ADPKD patients when compared to healthy volunteers, which was most likely due to prior awareness of the need for caffeine restriction. Within the range of caffeine intake observed by ADPKD patients in this study (0-471 mg/day), the renal volume was not directly associated with caffeine intake.

  20. Secondary and tertiary hyperparathyroidism in chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Lilit V. Egshatyan

    2017-12-01

    Full Text Available In the treatment of secondary hyperparathyroidism of end-stage chronic kidney disease, vitamin D receptor activation and allosteric modulators of the calcium-sensing receptor – inhibit glandular hyperplasia, reduce parathyroid hormone levels, impact on bone turnover and mineral density. But the use of calcimimetic and vitamin D analogs or mimetics did not reduce the need for parathyroidectomy for refractory hyperparathyroidism. The enlarged parathyroid gland and gland nodular transformation became refractory to medical therapy and patient need for parathyroidectomy. Tertiary hyperparathyroidism is a state of excessive secretion of parathyroid hormone after a long period of secondary hyperparathyroidism and renal transplantation. In this article, we present the case of a Caucasian male with chronic kidney disease (end-stage on chronic hemodialysis and after kidney transplantation and different forms of hyperparathyroidism (secondary and tertiary. Our case study shows that only a multi-interventional strategy is likely to be more effective treatment in cases of severe and refractory to medical therapy hyperparathyroidism.

  1. Renal Tissue Oxygenation in Essential Hypertension and Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Menno Pruijm

    2013-01-01

    Full Text Available Animal studies suggest that renal tissue hypoxia plays an important role in the development of renal damage in hypertension and renal diseases, yet human data were scarce due to the lack of noninvasive methods. Over the last decade, blood oxygenation level-dependent magnetic resonance imaging (BOLD-MRI, detecting deoxyhemoglobin in hypoxic renal tissue, has become a powerful tool to assess kidney oxygenation noninvasively in humans. This paper provides an overview of BOLD-MRI studies performed in patients suffering from essential hypertension or chronic kidney disease (CKD. In line with animal studies, acute changes in cortical and medullary oxygenation have been observed after the administration of medication (furosemide, blockers of the renin-angiotensin system or alterations in sodium intake in these patient groups, underlining the important role of renal sodium handling in kidney oxygenation. In contrast, no BOLD-MRI studies have convincingly demonstrated that renal oxygenation is chronically reduced in essential hypertension or in CKD or chronically altered after long-term medication intake. More studies are required to clarify this discrepancy and to further unravel the role of renal oxygenation in the development and progression of essential hypertension and CKD in humans.

  2. Dietary Treatment of Metabolic Acidosis in Chronic Kidney Disease.

    Science.gov (United States)

    Siener, Roswitha

    2018-04-20

    Chronic kidney disease and reduced glomerular filtration rate are risk factors for the development of chronic metabolic acidosis. The prevention or correction of chronic metabolic acidosis has been found to slow progression of chronic kidney disease. Dietary composition can strongly affect acid⁻base balance. Major determinants of net endogenous acid production are the generation of large amounts of hydrogen ions, mostly by animal-derived protein, which is counterbalanced by the metabolism of base-producing foods like fruits and vegetables. Alkali therapy of chronic metabolic acidosis can be achieved by providing an alkali-rich diet or oral administration of alkali salts. The primary goal of dietary treatment should be to increase the proportion of fruits and vegetables and to reduce the daily protein intake to 0.8⁻1.0 g per kg body weight. Diet modifications should begin early, i.e., even in patients with moderate kidney impairment, because usual dietary habits of many developed societies contribute an increased proportion of acid equivalents due to the high intake of protein from animal sources.

  3. Dietary Treatment of Metabolic Acidosis in Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Roswitha Siener

    2018-04-01

    Full Text Available Chronic kidney disease and reduced glomerular filtration rate are risk factors for the development of chronic metabolic acidosis. The prevention or correction of chronic metabolic acidosis has been found to slow progression of chronic kidney disease. Dietary composition can strongly affect acid–base balance. Major determinants of net endogenous acid production are the generation of large amounts of hydrogen ions, mostly by animal-derived protein, which is counterbalanced by the metabolism of base-producing foods like fruits and vegetables. Alkali therapy of chronic metabolic acidosis can be achieved by providing an alkali-rich diet or oral administration of alkali salts. The primary goal of dietary treatment should be to increase the proportion of fruits and vegetables and to reduce the daily protein intake to 0.8–1.0 g per kg body weight. Diet modifications should begin early, i.e., even in patients with moderate kidney impairment, because usual dietary habits of many developed societies contribute an increased proportion of acid equivalents due to the high intake of protein from animal sources.

  4. Prevalence of chronic kidney disease among patients undergoing transradial percutaneous coronary interventions.

    Science.gov (United States)

    Hossain, Mohammad A; Quinlan, Amy; Heck-Kanellidis, Jennifer; Calderon, Dawn; Patel, Tejas; Gandhi, Bhavika; Patel, Shrinil; Hetavi, Mahida; Costanzo, Eric J; Cosentino, James; Patel, Chirag; Dewan, Asa; Kuo, Yen-Hong; Salman, Loay; Vachharajani, Tushar J

    2018-03-01

    While transradial approach to conduct percutaneous coronary interventions offers multiple advantages, the procedure can cause radial artery damage and occlusion. Because radial artery is the preferred site for the creation of an arteriovenous fistula to provide dialysis, patients with chronic kidney disease are particularly dependent on radial artery for their long-term survival. In this retrospective study, we investigated the prevalence of chronic kidney disease in patients undergoing coronary interventions via radial artery. Stage of chronic kidney disease was based on estimated glomerular filtration rate and National Kidney Foundation - Kidney Disease Outcomes Quality Initiative guidelines. A total of 497 patients undergoing transradial percutaneous coronary interventions were included. Over 70.4% (350/497) of the patients had chronic kidney disease. Stage II chronic kidney disease was observed in 243 (69%) patients (estimated glomerular filtration rate = 76.0 ± 8.4 mL/min). Stage III was observed in 93 (27%) patients (estimated glomerular filtration rate = 49 ± 7.5 mL/min). Stage IV chronic kidney disease was observed in 5 (1%) patients (estimated glomerular filtration rate = 25.6 ± 4.3 mL/min) and Stage V chronic kidney disease was observed in 9 (3%) patients (estimated glomerular filtration rate = 9.3 ± 3.5 mL/min). Overall, 107 of 350 patients (30%) had advanced chronic kidney disease, that is, stage III-V chronic kidney disease. Importantly, 14 of the 107 (13%) patients had either stage IV or V chronic kidney disease. This study finds that nearly one-third of the patients undergoing transradial percutaneous coronary interventions have advanced chronic kidney disease. Because many of these patients may require dialysis, the use of radial artery to conduct percutaneous coronary interventions must be carefully considered in chronic kidney disease population.

  5. Lessons from the Profile of Kidney Diseases Among Afghan Refugees

    Science.gov (United States)

    Otoukesh, Salman; Mojtahedzadeh, Mona; Cooper, Chad J.; Tolouian, Ramin; Said, Sarmad; Ortega, Lauro; Didia, S. Claudia; Behazin, Arash; Sherzai, Dean; Blandon, Pedro

    2014-01-01

    Background Due to a paucity of research on the profile of kidney diseases among refugee populations, specifically Afghan refugees in Iran, this study aimed to illustrate the pattern of kidney disease among Afghan refugees in Iran and create a database for evaluating the performance of future health services. Material/Methods This was a retrospective cross sectional study, in which we collected the demographics and profile of kidney diseases among Afghan refugees between 2005 and 2010 from referrals to the United Nations High Commissioner for Refugees (UNHCR) offices in Iran. Results The total number of referrals in this group of diseases was 3193 out of 23 152 with 41.5% female and 58.5% male. Regarding age distribution, 10.5% were 0–14 years of age, 78% were 15–59, and 11.5% were ≥60. The most common health referral for females and males (0–14) was end-stage renal disease (ESRD), accounting for 34.6%. This was also the main reason of referrals for females and males aged 15–59, accounting for 73.5% and 66.6%, respectively, and in both sexes in the ≥60 age range it was 63.1%. Conclusions The pattern of our renal clinic referrals may gradually change to ESRD, which is associated with a huge economic burden. The need to provide health insurance to everyone or reform the health care system to provide coverage for more of the population can be justified and would improve cost effectiveness. PMID:25208585

  6. Exploring sleep disorders in patients with chronic kidney disease.

    Science.gov (United States)

    Nigam, Gaurav; Camacho, Macario; Chang, Edward T; Riaz, Muhammad

    2018-01-01

    Kidney disorders have been associated with a variety of sleep-related disorders. Therefore, researchers are placing greater emphasis on finding the role of chronic kidney disease (CKD) in the development of obstructive sleep apnea and restless legs syndrome. Unfortunately, the presence of other sleep-related disorders with CKDs and non-CKDs has not been investigated with the same clinical rigor. Recent studies have revealed that myriad of sleep disorders are associated with CKDs. Furthermore, there are a few non-CKD-related disorders that are associated with sleep disorders. In this narrative review, we provide a balanced view of the spectrum of sleep disorders (as identified in International Classification of Sleep disorders-3) related to different types of renal disorders prominently including but not exclusively limited to CKD.

  7. Extracellular microRNA signature in chronic kidney disease.

    Science.gov (United States)

    Muralidharan, Jagdeesan; Ramezani, Ali; Hubal, Monica; Knoblach, Susan; Shrivastav, Shashi; Karandish, Sara; Scott, Richard; Maxwell, Nirmal; Ozturk, Savas; Beddhu, Srinivasan; Kopp, Jeffrey B; Raj, Dominic S

    2017-06-01

    MicroRNAs (miRNAs) are noncoding RNAs that regulate posttranscriptional gene expression. In this study we characterized the circulating and urinary miRNA pattern associated with reduced glomerular filtration rate, using Affymetrix GeneChip miR 4.0 in 28 patients with chronic kidney disease (CKD). Top miRNA discoveries from the human studies were validated in an Alb/TGFβ mouse model of CKD, and in rat renal proximal tubular cells (NRK52E) exposed to TGFβ1. Plasma and urinary levels of procollagen III N-terminal propeptide and collagen IV were elevated in patients with decreased estimated glomerular filtration rate (eGFR). Expression of 384 urinary and 266 circulatory miRNAs were significantly different between CKD patients with eGFR ≥30 vs. kidney fibrosis, and specific urinary and plasma miRNA profile may have diagnostic and prognostic utility in CKD. Copyright © 2017 the American Physiological Society.

  8. Diagnosis of Iron-Deficiency Anemia in Chronic Kidney Disease.

    Science.gov (United States)

    Bahrainwala, Jehan; Berns, Jeffrey S

    2016-03-01

    Anemia is a common and clinically important consequence of chronic kidney disease (CKD). It is most commonly a result of decreased erythropoietin production by the kidneys and/or iron deficiency. Deciding on the appropriate treatment for anemia associated with CKD with iron replacement and erythropoietic-stimulating agents requires an ability to accurately diagnose iron-deficiency anemia. However, the diagnosis of iron-deficiency anemia in CKD patients is complicated by the relatively poor predictive ability of easily obtained routine serum iron indices (eg, ferritin and transferrin saturation) and more invasive gold standard measures of iron deficiency (eg, bone marrow iron stores) or erythropoietic response to supplemental iron. In this review, we discuss the diagnostic utility of currently used serum iron indices and emerging alternative markers of iron stores. Copyright © 2016 Elsevier Inc. All rights reserved.

  9. Screening Fabry's disease in chronic kidney disease patients not on dialysis: a multicenter study.

    Science.gov (United States)

    Yeniçerioğlu, Yavuz; Akdam, Hakan; Dursun, Belda; Alp, Alper; Sağlam Eyiler, Funda; Akın, Davut; Gün, Yelda; Hüddam, Bülent; Batmazoğlu, Mehmet; Gibyeli Genek, Dilek; Pirinççi, Serhat; Ersoy, İsmail Rıfkı; Üzüm, Atilla; Soypaçacı, Zeki; Tanrısev, Mehmet; Çolak, Hülya; Demiral Sezer, Sibel; Bozkurt, Gökay; Akyıldız, Utku Oğan; Akyüz Ünsal, Ayşe İpek; Ünübol, Mustafa; Uslu, Meltem; Eryılmaz, Ufuk; Günel, Ceren; Meteoğlu, İbrahim; Yavaşoğlu, İrfan; Ünsal, Alparslan; Akar, Harun; Okyay, Pınar

    2017-11-01

    Fabry's disease is an X-linked inherited, rare, progressive, lysosomal storage disorder, affecting multiple organs due to the deficient activity of α-galactosidase A (α-Gal A) enzyme. The prevalence has been reported to be 0.15-1% in hemodialysis patients; however, the information on the prevalence in chronic kidney disease not on dialysis is lacking. This study aimed to determine the prevalence of Fabry's disease in chronic kidney disease. The patients older than 18 years, enclosing KDIGO 2012 chronic kidney disease definitions, not on dialysis, were enrolled. Dried blood spots on Guthrie papers were used to analyze α-Gal A enzyme and genetic analysis was performed in individuals with enzyme activity ≤1.2 μmol/L/h. A total of 1453 chronic kidney disease patients not on dialysis from seven clinics in Turkey were screened. The mean age of the study population was 59.3 ± 15.9 years. 45.6% of patients were female. The creatinine clearance of 77.3% of patients was below 60 mL/min/1.73 m 2 , 8.4% had proteinuria, and 2.5% had isolated microscopic hematuria. The mean value of patients' α-Gal A enzyme was detected as 2.93 ± 1.92 μmol/L/h. 152 patients had low levels of α-Gal A enzyme activity (≤1.2 μmol/L/h). In mutation analysis, A143T and D313Y variants were disclosed in three male patients. The prevalence of Fabry's disease in chronic kidney disease not on dialysis was found to be 0.2% (0.4% in male, 0.0% in female). Fabry's disease should be considered in the differential diagnosis of chronic kidney disease with unknown etiology even in the absence of symptoms and signs suggestive of Fabry's disease.

  10. Chronic kidney disease screening methods and its implication for Malaysia: an in depth review.

    Science.gov (United States)

    Almualm, Yasmin; Zaman Huri, Hasniza

    2015-01-01

    Chronic Kidney Disease has become a public health problem, imposing heath, social and human cost on societies worldwide. Chronic Kidney Disease remains asymptomatic till late stage when intervention cannot stop the progression of the disease. Therefore, there is an urgent need to detect the disease early. Despite the high prevalence of Chronic Kidney Disease in Malaysia, screening is still lacking behind. This review discusses the strengths and limitations of current screening methods for Chronic Kidney Disease from a Malaysian point of view. Diabetic Kidney Disease was chosen as focal point as Diabetes is the leading cause of Chronic Kidney Disease in Malaysia. Screening for Chronic Kidney Disease in Malaysia includes a urine test for albuminuria and a blood test for serum creatinine. Recent literature indicates that albuminuria is not always present in Diabetic Kidney Disease patients and serum creatinine is only raised after substantial kidney damage has occurred.  Recently, cystatin C was proposed as a potential marker for kidney disease but this has not been studied thoroughly in Malaysia.  Glomerular Filtration Rate is the best method for measuring kidney function and is widely estimated using the Modification of Diet for Renal Disease equation. Another equation, the Chronic Kidney Disease Epidemiology Collaboration Creatinine equation was introduced in 2009. The new equation retained the precision and accuracy of the Modification of Diet for Renal Disease equation at GFR 60ml/min/1.73m2. In Asian countries, adding an ethnic coefficient to the equation enhanced its performance. In Malaysia, a multi-ethnic Asian population, the Chronic Kidney Disease Epidemiology Collaboration equation should be validated and the Glomerular Filtration Rate should be reported whenever serum creatinine is ordered. Reporting estimated Glomerular Filtration Rate will help diagnose patients who would have been otherwise missed if only albuminuria and serum creatinine are measured.

  11. Mobile Health, a Key Factor Enhancing Disease Prevention Campaigns: Looking for Evidences in Kidney Disease Prevention

    Directory of Open Access Journals (Sweden)

    Nicole Roque Matias

    2017-01-01

    Full Text Available Background: Progressive chronic kidney disease (CKD failure and kidney diseases are increasing at an alarming rate all over the world. However, despite the remarkable advance in health technology, where it has become possible to successfully screen patients and predict kidney progression, a large portion of the world population is still unaware of their disease and risk exposure. Mobile Health (mHealth solutions associated with health campaigns and programs proved to be an effective mean to enhance awareness and behaviour change at individual and social level. Objective: The aim of this survey was to present the results of an environmental scan of what has been happening in the field of kidney disease prevention campaigns in recent years, with a focus on the use of mobile health as a tool to enhance the campaign's effects on targeting people and change their behaviour. Methodology: It was conducted a systematic and comprehensive review, combining experimental studies with theoretical perspectives, to look for evidence regarding the evaluation of kidney disease prevention campaigns. The databases consulted for the present survey were: MEDLINE, PubMed, Google Scholar, PsycINFO, SAGE Journals Online, and Web of Science among other sources, for an analysis period from January 2000 to June 2016. Results: Concerning the 14 analyzed examples with impact on kidney disease prevention campaign evaluation, two main campaigns were referred: The World Kidney Day (WKD campaign, and the Kidney Early Evaluation Program (KEEP. The indicators used in this analisys were in most cases comparable regarding the campaign messages, objectives and interventions tools, although em both cases the use of mHealth or other technologies is residually comparing to other diseases prevention campaigns or programs. Conclusions: This review pointed to the inexistence of behavioural change evidence as a target of the kidney disease prevention campaigns and their evaluation. General

  12. The Impact of Chronic Obstructive Pulmonary Disease and Smoking on Mortality and Kidney Transplantation in End-Stage Kidney Disease.

    LENUS (Irish Health Repository)

    Kent, Brian D

    2012-09-07

    Background: Chronic obstructive pulmonary disease (COPD) and tobacco use are leading causes of morbidity and mortality. The prevalence and clinical impact of COPD on mortality and kidney transplantation among patients who begin dialysis therapy is unclear. Methods: We explored the clinical impact of COPD and continued tobacco use on overall mortality and kidney transplantation in a national cohort study of US dialysis patients. National data on all dialysis patients (n = 769,984), incident between May 1995 and December 2004 and followed until October 31, 2006, were analyzed from the United States Renal Data System. Prevalence and period trends were determined while multivariable Cox regression evaluated relative hazard ratios (RR) for death and kidney transplantation. Results: The prevalence of COPD was 7.5% overall and increased from 6.7 to 8.1% from 1995-2004. COPD correlated significantly with older age, cardiovascular conditions, cancer, malnutrition, poor functional status, and tobacco use. Adjusted mortality risks were significantly higher for patients with COPD (RR = 1.20, 95% CI 1.18-1.21), especially among current smokers (RR = 1.28, 95% CI 1.25-1.32), and varied inversely with advancing age. In contrast, the adjusted risks of kidney transplantation were significantly lower for patients with COPD (RR = 0.47, 95% CI 0.41-0.54, for smokers and RR = 0.54, 95% CI 0.50-0.58, for non-smokers) than without COPD [RR = 0.72, 95% CI 0.70-0.75, for smokers and RR = 1.00 for non-smokers (referent category)]. Conclusions: Patients with COPD who begin dialysis therapy in the US experience higher mortality and lower rates of kidney transplantation, outcomes that are far worse among current smokers.

  13. [DIET CHARACTERISTICS IN PATIENTS WITH CHRONIC KIDNEY DISEASE].

    Science.gov (United States)

    Bašić-Marković, N; Šutić, I; Popović, B; Marković, R; Vučak, J

    2016-12-01

    Because of the increasing number of patients, chronic kidney disease (CKD) has become a significant public health problem. As kidney function decreases, it is necessary to introduce certain dietary modifications. The aim was to investigate what is the appropriate approach to diet of CKD patients, which could contribute to slowing down progression of the disease. Dietary recommendations are individual for each patient, but also vary in the same patient depending on the stage of disease progression because special attention must be paid to appropriate intake of macronutrients (protein, carbohydrates and fats), micronutrients (sodium, potassium, calcium, phosphorus, zinc, selenium, various vitamins), and water. In newly diagnosed patients, it is necessary to assess their nutritional status and energy requirements. It has been shown that protein-energy malnutrition, muscle loss and cachexia are strong predictors of mortality in CKD. Comparing different dietary approaches in everyday life of patients suffering from CKD, it was found that the most effective diet is Mediterranean food style. Studies confirm that Mediterranean diet has a preventive effect on renal function and reduces progression of the disease. Preventive measures, correct identification and early intervention can increase survival of patients and improve their quality of life. Mediterranean diet tailored to individual stages of CKD has been confirmed as the best choice in CKD patients.

  14. 78 FR 59945 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2013-09-30

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Small Grants to Promote Diversity. Date... Diseases Special Emphasis Panel; Mechanisms of Upper Gut and Airway Interaction-Program Project Grant. Date..., Endocrinology and Metabolic Research; 93.848, Digestive Diseases and Nutrition Research; 93.849, Kidney Diseases...

  15. 78 FR 3903 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Meetings

    Science.gov (United States)

    2013-01-17

    ... Diseases Advisory Council, Diabetes, Endocrine and Metabolic Diseases Subcommittee. Date: February 13, 2013... Diabetes and Digestive and Kidney Diseases; Notice of Meetings Pursuant to section 10(d) of the Federal... Diabetes and Digestive and Kidney Diseases Advisory Council. The meetings will be open to the public as...

  16. Adenosine contribution to normal renal physiology and chronic kidney disease.

    Science.gov (United States)

    Oyarzún, Carlos; Garrido, Wallys; Alarcón, Sebastián; Yáñez, Alejandro; Sobrevia, Luis; Quezada, Claudia; San Martín, Rody

    2017-06-01

    Adenosine is a nucleoside that is particularly interesting to many scientific and clinical communities as it has important physiological and pathophysiological roles in the kidney. The distribution of adenosine receptors has only recently been elucidated; therefore it is likely that more biological roles of this nucleoside will be unveiled in the near future. Since the discovery of the involvement of adenosine in renal vasoconstriction and regulation of local renin production, further evidence has shown that adenosine signaling is also involved in the tubuloglomerular feedback mechanism, sodium reabsorption and the adaptive response to acute insults, such as ischemia. However, the most interesting finding was the increased adenosine levels in chronic kidney diseases such as diabetic nephropathy and also in non-diabetic animal models of renal fibrosis. When adenosine is chronically increased its signaling via the adenosine receptors may change, switching to a state that induces renal damage and produces phenotypic changes in resident cells. This review discusses the physiological and pathophysiological roles of adenosine and pays special attention to the mechanisms associated with switching homeostatic nucleoside levels to increased adenosine production in kidneys affected by CKD. Copyright © 2017 Elsevier Ltd. All rights reserved.

  17. Etiology and Outcome of Chronic Kidney Disease in Iranian Children

    Directory of Open Access Journals (Sweden)

    Neamatollah Ataei

    2016-07-01

    Full Text Available Background Considering the significant geographical and ethnical differences in pattern of incidence, etiology and outcome of chronic kidney disease (CKD, the present study aimed to assess the etiology and outcome of CKD in Iranian children. Materials and Methods In a cross-sectional study etiology and outcome of 372 children aged 3 months to 18 years with CKD was studied during the period 1991 –2014. Children (186 boys, 186 girls with Stage 3 to 5 CKDs, defined as a glomerular filtration rate below 60 ml/min per 1.73 m2body surface area, were identified. Results Etiology was congenital anomalies of the kidney and urinary tract in 125 (33.60%, cystic/ hereditary/ congenital diseases in 91 (24.46%, glomerulopathy in 73(19.62%, and cause unknown in 71 (19.09% patients. Forty-eight (13.22% were on conservative treatment, 174(47.93% had end-stage renal disease (ESRD with chronic hemodialysis, 24 (6.61% were on continuous ambulatory peritoneal dialysis. Sixty-eight (18.74% underwent on renal transplant which was successful in 52 (14.33% patients but was associated with abnormal renal function in 16(4.41% children. Finally, 49 (13.50% patients died. Conclusion A large number of children developed CKD secondary to congenital anomalies of the kidney and urinary tract. Planning for screening, early detection and instituting timely treatment of preventable causes could lead to a lower incidence of CKD in this group of children.

  18. Multiparametric Quantitative Ultrasound Imaging in Assessment of Chronic Kidney Disease.

    Science.gov (United States)

    Gao, Jing; Perlman, Alan; Kalache, Safa; Berman, Nathaniel; Seshan, Surya; Salvatore, Steven; Smith, Lindsey; Wehrli, Natasha; Waldron, Levi; Kodali, Hanish; Chevalier, James

    2017-11-01

    To evaluate the value of multiparametric quantitative ultrasound imaging in assessing chronic kidney disease (CKD) using kidney biopsy pathologic findings as reference standards. We prospectively measured multiparametric quantitative ultrasound markers with grayscale, spectral Doppler, and acoustic radiation force impulse imaging in 25 patients with CKD before kidney biopsy and 10 healthy volunteers. Based on all pathologic (glomerulosclerosis, interstitial fibrosis/tubular atrophy, arteriosclerosis, and edema) scores, the patients with CKD were classified into mild (no grade 3 and quantitative ultrasound parameters included kidney length, cortical thickness, pixel intensity, parenchymal shear wave velocity, intrarenal artery peak systolic velocity (PSV), end-diastolic velocity (EDV), and resistive index. We tested the difference in quantitative ultrasound parameters among mild CKD, moderate to severe CKD, and healthy controls using analysis of variance, analyzed correlations of quantitative ultrasound parameters with pathologic scores and the estimated glomerular filtration rate (GFR) using Pearson correlation coefficients, and examined the diagnostic performance of quantitative ultrasound parameters in determining moderate CKD and an estimated GFR of less than 60 mL/min/1.73 m 2 using receiver operating characteristic curve analysis. There were significant differences in cortical thickness, pixel intensity, PSV, and EDV among the 3 groups (all P quantitative ultrasound parameters, the top areas under the receiver operating characteristic curves for PSV and EDV were 0.88 and 0.97, respectively, for determining pathologic moderate to severe CKD, and 0.76 and 0.86 for estimated GFR of less than 60 mL/min/1.73 m 2 . Moderate to good correlations were found for PSV, EDV, and pixel intensity with pathologic scores and estimated GFR. The PSV, EDV, and pixel intensity are valuable in determining moderate to severe CKD. The value of shear wave velocity in

  19. Predictors of advanced chronic kidney disease and end-stage renal disease in HIV-positive persons

    DEFF Research Database (Denmark)

    Nielsen, Lene Ryom; Mocroft, Amanda; Kirk, Ole

    2014-01-01

    Whilst several antiretroviral drugs have been associated with moderate chronic kidney disease (CKD), their contribution to advanced CKD and end-stage renal disease (ESRD) remain unknown.......Whilst several antiretroviral drugs have been associated with moderate chronic kidney disease (CKD), their contribution to advanced CKD and end-stage renal disease (ESRD) remain unknown....

  20. Nutritional management and growth in children with chronic kidney disease.

    Science.gov (United States)

    Rees, Lesley; Jones, Helen

    2013-04-01

    Despite continuing improvements in our understanding of the causes of poor growth in chronic kidney disease, many unanswered questions remain: why do some patients maintain a good appetite whereas others have profound anorexia at a similar level of renal function? Why do some, but not all, patients respond to increased nutritional intake? Is feed delivery by gastrostomy superior to oral and nasogastric routes? Do children who are no longer in the 'infancy' stage of growth benefit from enteral feeding? Do patients with protein energy wasting benefit from increased nutritional input? How do we prevent obesity, which is becoming so prevalent in the developed world? This review will address these issues.

  1. Chronic kidney disease of unknown etiology in Sri Lanka.

    Science.gov (United States)

    Rajapakse, Senaka; Shivanthan, Mitrakrishnan Chrishan; Selvarajah, Mathu

    2016-07-01

    In the last two decades, chronic kidney disease of unknown etiology (CKDu) has emerged as a significant contributor to the burden of chronic kidney disease (CKD) in rural Sri Lanka. It is characterized by the absence of identified causes for CKD. The prevalence of CKDu is 15.1-22.9% in some Sri Lankan districts, and previous research has found an association with farming occupations. A systematic literature review in Pubmed, Embase, Scopus, and Lilacs databases identified 46 eligible peer-reviewed articles and one conference abstract. Geographical mapping indicates a relationship between CKDu and agricultural irrigation water sources. Health mapping studies, human biological studies, and environment-based studies have explored possible causative agents. Most studies focused on likely causative agents related to agricultural practices, geographical distribution based on the prevalence and incidence of CKDu, and contaminants identified in drinking water. Nonetheless, the link between agrochemicals or heavy metals and CKDu remains to be established. No definitive cause for CKDu has been identified. Evidence to date suggests that the disease is related to one or more environmental agents, however pinpointing a definite cause for CKDu is challenging. It is plausible that CKDu is multifactorial. No specific guidelines or recommendations exist for treatment of CKDu, and standard management protocols for CKD apply. Changes in agricultural practices, provision of safe drinking water, and occupational safety precautions are recommended by the World Health Organization.

  2. Disturbed skin barrier in children with chronic kidney disease.

    Science.gov (United States)

    Wojtowicz-Prus, Elzbieta; Kilis-Pstrusinska, Katarzyna; Reich, Adam; Zachwieja, Katarzyna; Miklaszewska, Monika; Szczepanska, Maria; Szepietowski, Jacek C

    2015-02-01

    There are limited data on skin lesions in children with end-stage renal failure. The aim of the study was an evaluation of the skin barrier in children with different stages of chronic kidney disease (CKD). The prevalence of xerosis, its severity, as well as its link selected demographic factors, were examined. The study included 103 children: 72 with CKD stages 3-5 (38 on conservative treatment and 34 on dialysis) and 31 patients with primary monosymptomatic nocturnal enuresis as a control group. Initially, the study subjects described the localisation and severity of dry skin by themselves. Next, clinical evaluation of xerosis, non-invasive corneometric assessment of epidermis moisturising and the measurement of transepidermal water loss were performed. Most CKD children reported dry skin. The problem of xerosis was identified more frequently in patients on dialysis (67.6 %) than on conservative treatment (42.1 %) (p = 0.01). CKD patients divided according to skin dryness did not differ with regards to age, sex, initial kidney disease and CKD duration. Disturbed skin barrier is an important concern of children with CKD, intensifying as the disease progresses. This symptom occurs on early stages of CKD and it should be taken into consideration in the CKD management.

  3. Hydatid Disease of the Kidney: Report of 12 Cases

    Directory of Open Access Journals (Sweden)

    Y. FAZLALIZADEH

    1972-07-01

    Full Text Available The radiology diagnosis of primary hydatid disease of the kidney is possible when a renal mass is noted on the radiograph. part icula rly in the countries where this disease is prevalent. Cha racteristic radiological signs, hydatiduria, eosinophili and specific examination such as Casoni and Weinberg tests are a ll helpful to assist the diagnosis. Twelve cases of primary hydatid disease of the kidney have been seen in our 10 yea rs study. The diagno,sis in the majority of these cases was primarily radiological. In three cases hydatiduria was observed. In one case in which resection of the cyst and partial nephrectomy was done recurrence was observed after nine years. Etude radiologique de J2 cas de kyst hydatique primitive du rein, • La diagnostique radiologique de kyst hydatiquc primitive renale est possible. quand on peut noter une masse rena le en radiographic, particulie rement dans les contrces ou ceue maladie est preva lcnte. Les signes radiologiques cha ractcristiqucs, hyda tidurie, eosinophilie, et exarnen spccifiques, comme teste de Casoni , ct Weimberg assistent au diagnostique. Auteur a prcsentc 12 cas de kyst hydatique primitive renal, diagnostique radiologiquement pendan t ces dix derniers annees. Dans trois cas hydatidurie eta it observe et dans un cas, 9 ans apres la ncphrectomie partiellc et resection de kyst , on a rernarque la rechutte de la maladie.

  4. Use of Readily Accessible Inflammatory Markers to Predict Diabetic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Lauren Winter

    2018-05-01

    Full Text Available Diabetic kidney disease is a common complication of type 1 and type 2 diabetes and is the primary cause of end-stage renal disease in developed countries. Early detection of diabetic kidney disease will facilitate early intervention aimed at reducing the rate of progression to end-stage renal disease. Diabetic kidney disease has been traditionally classified based on the presence of albuminuria. More recently estimated glomerular filtration rate has also been incorporated into the staging of diabetic kidney disease. While albuminuric diabetic kidney disease is well described, the phenotype of non-albuminuric diabetic kidney disease is now widely accepted. An association between markers of inflammation and diabetic kidney disease has previously been demonstrated. Effector molecules of the innate immune system including C-reactive protein, interleukin-6, and tumor necrosis factor-α are increased in patients with diabetic kidney disease. Furthermore, renal infiltration of neutrophils, macrophages, and lymphocytes are observed in renal biopsies of patients with diabetic kidney disease. Similarly high serum neutrophil and low serum lymphocyte counts have been shown to be associated with diabetic kidney disease. The neutrophil–lymphocyte ratio is considered a robust measure of systemic inflammation and is associated with the presence of inflammatory conditions including the metabolic syndrome and insulin resistance. Cross-sectional studies have demonstrated a link between high levels of the above inflammatory biomarkers and diabetic kidney disease. Further longitudinal studies will be required to determine if these readily available inflammatory biomarkers can accurately predict the presence and prognosis of diabetic kidney disease, above and beyond albuminuria, and estimated glomerular filtration rate.

  5. Impact of chronic kidney disease stage on lower-extremity arthroplasty.

    Science.gov (United States)

    Deegan, Brian F; Richard, Raveesh D; Bowen, Thomas R; Perkins, Robert M; Graham, Jove H; Foltzer, Michael A

    2014-07-01

    End-stage renal disease and dialysis is commonly associated with poor outcomes after joint replacement surgery. The goal of this study was to evaluate postoperative complications in patients with less advanced chronic kidney disease undergoing total hip arthroplasty (THA) or total knee arthroplasty (TKA). Patients who underwent THA or TKA between 2004 and 2011 with stage 1, 2, or 3 chronic kidney disease were retrospectively reviewed via an electronic medical record. The authors compared 377 patients who had stage 1 to 2 chronic kidney disease with 402 patients who had stage 3 chronic kidney disease. No significant differences in 90-day readmission or revision rates were found between the stage 1 to 2 and stage 3 patient groups. For patients with stage 3 chronic kidney disease, the overall mortality rate was greater than that in patients with stage 1 to 2 chronic kidney disease. However, when adjusted for comorbid disease, no significant increases were seen in joint infection, readmission, or early revision between patients with stage 1 to 2 chronic kidney disease vs patients with stage 3 chronic kidney disease. The overall incidence of infection was high (3.5%) but far less than reported for patients with end-stage renal disease, dialysis, and kidney transplant. In conclusion, patients with stage 1, 2, or 3 chronic kidney disease may have a higher than expected rate of prosthetic joint infection (3.5%) after total joint arthroplasty. Patients with stage 3 chronic kidney disease are at higher risk for postoperative mortality compared with those with lesser stages of kidney disease. Copyright 2014, SLACK Incorporated.

  6. Gut microbiota–derived short-chain fatty acids and kidney diseases

    Directory of Open Access Journals (Sweden)

    Li L

    2017-12-01

    Full Text Available Lingzhi Li, Liang Ma, Ping Fu Kidney Research Institute, Department of Nephrology, West China Hospital of Sichuan University, Chengdu 610041, China Abstract: Gut microbiota and its metabolites play pivotal roles in host physiology and pathology. Short-chain fatty acids (SCFAs, as a group of metabolites, exert positive regulatory effects on energy metabolism, hormone secretion, immune inflammation, hypertension, and cancer. The functions of SCFAs are related to their activation of transmembrane G protein-coupled receptors and their inhibition of histone acetylation. Though controversial, growing evidence suggests that SCFAs, which regulate inflammation, oxidative stress, and fibrosis, have been involved in kidney disease through the activation of the gut–kidney axis; however, the molecular relationship among gut microbiota–derived metabolites, signaling pathways, and kidney disease remains to be elucidated. This review will provide an overview of the physiology and functions of SCFAs in kidney disease. Keywords: gut microbiome, short-chain fatty acids, kidney diseases, gut–kidney axis

  7. Complementary and Alternative Medicine Use Among Patients With Chronic Kidney Disease and Kidney Transplant Recipients.

    Science.gov (United States)

    Osman, Noha A; Hassanein, Safaa M; Leil, Marwa M; NasrAllah, Mohamed M

    2015-11-01

    To explore and compare complementary and alternative medicine (CAM) practice among subsets of patients with chronic kidney disease (CKD) and renal allograft recipients. Cross-sectional survey questionnaire. Three outpatient nephrology clinics and dialysis centers in Egypt. A total of 1005 subjects were included in the study (560 predialyis patients with CKD 3-4, 245 patients on hemodialysis, and 200 transplant recipients). Face to face interview with CKD patients. The survey inquired about epidemiological data, types, sources, and patterns of CAM used as well as the effect of CAM use on the patients' interaction with modern medicine and clinical caregivers. (1) Prevalence and types of CAM used by CKD patients; (2) Associations and correlates of CAM use including epidemiological features, impact of CAM use on adherence to conventional treatment and interaction of the users with modern medical systems; (3) Differences in CAM practice between subsets of CKD patients viz. hemodialysis patients, CKD 3-4, and transplant recipients. Overall, 522 patients (52%) were using CAM (64% of predialyis patients, 33% of dialysis patients, and 40.5% of transplant recipients, P transplant recipients were more likely to report P Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

  8. Kidney Disease in Oman: a View of the Current and Future Landscapes.

    Science.gov (United States)

    Al Alawi, Intisar Hamed; Al Salmi, Issa; Al Mawali, Adhra; Sayer, John A

    2017-07-01

    Oman is located in the southeast of Arabian Peninsula with a relatively young population of about 3 831 553 people. The Ministry of Health, which is the healthcare provider, is facing a challenge with the increased levels of noncommunicable diseases including chronic kidney disease. A growing number of patients progress to end-stage kidney disease (ESKD), demanding renal replacement therapy. In 2014, there were 1339 of ESKD patients receiving dialysis and almost 1400 patients received kidney transplants. The estimated annual incidence of ESKD is 120 patients per million population. Diabetes mellitus and hypertensive nephropathy are the commonly identified causes of ESKD. Many patients with glomerulonephritis, systemic lupus erythematosus, nephrolithiasis, and inherited kidney disease present with advanced chronic kidney disease. This article reviews the current status of kidney disease in Oman and addresses the present and future needs, through a systematic-review of all related papers.

  9. Hypoxia: The Force that Drives Chronic Kidney Disease

    Science.gov (United States)

    Fu, Qiangwei; Colgan, Sean P; Shelley, Carl Simon

    2016-01-01

    In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy. PMID:26847481

  10. Kidney Versus Combined Kidney and Liver Transplantation in Young People With Autosomal Recessive Polycystic Kidney Disease: Data From the European Society for Pediatric Nephrology/European Renal Association-European Dialysis and Transplant (ESPN/ERA-EDTA) Registry

    NARCIS (Netherlands)

    Mekahli, Djalila; van Stralen, Karlijn J.; Bonthuis, Marjolein; Jager, Kitty J.; Balat, Ayşe; Benetti, Elisa; Godefroid, Nathalie; Edvardsson, Vidar O.; Heaf, James G.; Jankauskiene, Augustina; Kerecuk, Larissa; Marinova, Svetlana; Puteo, Flora; Seeman, Tomas; Zurowska, Aleksandra; Pirenne, Jacques; Schaefer, Franz; Groothoff, Jaap W.; Levtchenko, E.; Haffner, D.; Bjerre, A.; Massy, Z.; Shtiza, D.; Kramar, R.; Oberbauer, R.; Baiko, S.; Sukalo, A.; van Hoeck, K.; Collart, F.; des Grottes, J. M.; Pokrajac, D.; Roussinov, D.; Batinić , D.; Lemac, M.; Slavicek, J.; Seeman, T.; Vondrak, K.; Heaf, J. G.; Toots, U.; Finne, P.; Grö nhagen-Riska, C.; Couchoud, C.; Lasalle, M.; Sahpazova, E.; Abazi, N.; Ristoka Bojkovska, N.; von Gersdorff, G.; Scholz, C.; Tö nshoff, B.; Krupka, K.

    2016-01-01

    The choice for either kidney or combined liver-kidney transplantation in young people with kidney failure and liver fibrosis due to autosomal recessive polycystic kidney disease (ARPKD) can be challenging. We aimed to analyze the characteristics and outcomes of transplantation type in these

  11. Kidney Versus Combined Kidney and Liver Transplantation in Young People With Autosomal Recessive Polycystic Kidney Disease: Data From the European Society for Pediatric Nephrology/European Renal Association-European Dialysis and Transplant (ESPN/ERA-EDTA) Registry

    NARCIS (Netherlands)

    Mekahli, D.; Stralen, K.J. van; Bonthuis, M.; Jager, K.J.; Balat, A.; Benetti, E.; Godefroid, N.; Edvardsson, V.O.; Heaf, J.G.; Jankauskiene, A.; Kerecuk, L.; Marinova, S.; Puteo, F.; Seeman, T.; Zurowska, A.; Pirenne, J.; Schaefer, F.; Groothoff, J.W.; Hoitsma, A.J.; et al.,

    2016-01-01

    BACKGROUND: The choice for either kidney or combined liver-kidney transplantation in young people with kidney failure and liver fibrosis due to autosomal recessive polycystic kidney disease (ARPKD) can be challenging. We aimed to analyze the characteristics and outcomes of transplantation type in

  12. Uric acid and chronic kidney disease: which is chasing which?

    Science.gov (United States)

    Johnson, Richard J.; Nakagawa, Takahiko; Jalal, Diana; Sánchez-Lozada, Laura Gabriela; Kang, Duk-Hee; Ritz, Eberhard

    2013-01-01

    Serum uric acid is commonly elevated in subjects with chronic kidney disease (CKD), but was historically viewed as an issue of limited interest. Recently, uric acid has been resurrected as a potential contributory risk factor in the development and progression of CKD. Most studies documented that an elevated serum uric acid level independently predicts the development of CKD. Raising the uric acid level in rats can induce glomerular hypertension and renal disease as noted by the development of arteriolosclerosis, glomerular injury and tubulointerstitial fibrosis. Pilot studies suggest that lowering plasma uric acid concentrations may slow the progression of renal disease in subjects with CKD. While further clinical trials are necessary, uric acid is emerging as a potentially modifiable risk factor for CKD. Gout was considered a cause of CKD in the mid-nineteenth century [1], and, prior to the availability of therapies to lower the uric acid level, the development of end-stage renal disease was common in gouty patients. In their large series of gouty subjects Talbott and Terplan found that nearly 100% had variable degrees of CKD at autopsy (arteriolosclerosis, glomerulosclerosis and interstitial fibrosis) [2]. Additional studies showed that during life impaired renal function occurred in half of these subjects [3]. As many of these subjects had urate crystals in their tubules and interstitium, especially in the outer renal medulla, the disease became known as gouty nephropathy. The identity of this condition fell in question as the presence of these crystals may occur in subjects without renal disease; furthermore, the focal location of the crystals could not explain the diffuse renal scarring present. In addition, many subjects with gout also had coexistent conditions such as hypertension and vascular disease, leading some experts to suggest that the renal injury in gout was secondary to these latter conditions rather than to uric acid per se [4]. Indeed, gout was

  13. Prevalence and variation of Chronic Kidney Disease in the Irish health system: initial findings from the National Kidney Disease Surveillance Programme.

    LENUS (Irish Health Repository)

    Stack, Austin G

    2014-01-01

    Chronic Kidney Disease (CKD) is a major non-communicable chronic disease that is associated with adverse clinical and economic outcomes. Passive surveillance systems are likely to improve efforts for prevention of chronic kidney disease (CKD) and inform national service planning. This study was conducted to determine the overall prevalence of CKD in the Irish health system, assess period trends and explore patterns of variation as part of a novel surveillance initiative.

  14. Hypoxia Induced Factor in Chronic Kidney Disease: Friend or Foe?

    Science.gov (United States)

    Li, Weiying; Zhao, Yuliang; Fu, Ping

    2017-01-01

    Many studies have shown evidence that erythropoiesis-stimulating agents (ESAs), as a classic treatment for chronic kidney disease (CKD)-related anemia, have several disadvantages and may trigger various adverse events with long-term use. The hypoxia-induced factor (HIF) pathway has been intensively investigated in kidney disease, especially in CKD, as research has shown that HIF-mediated erythropoiesis might work as a potential therapeutic strategy for managing CKD-related anemia. Development of prolyl hydroxylase domain inhibitors (PHIs), as an effective HIF activator, is a valuable step toward finding a replacement for ESAs, which showed an effective erythropoiesis through a comprehensive and physiological approach by promoting erythropoietin production, increasing iron bioavailability and improving chronic inflammatory status. Heretofore no adverse events or obvious off-target effects have been reported in clinical trials of PHIs. Nevertheless, a cautious inspection with extended follow-up period is warranted to validate the safety of prolonged HIF elevation, especially considering its ambiguous role in fibrogenesis and inflammation responses and possible risks in accelerating vascular calcification and tumorigenesis. A weighed dosing strategy might be the key to circumvent the unexpected side-effect brought by pleotropic effects of HIF elevation and achieve a selective augmentation of HIF-mediated signaling pathway. New studies with longer follow-up period and adequate analysis about the risks for proinflammation, vascular calcification and tumorigenesis are needed to ensure the drugs are safe for long-term use before being widely accepted in daily clinical practice.

  15. New Targets for End-Stage Chronic Kidney Disease Therapy

    Directory of Open Access Journals (Sweden)

    Prakoura Niki

    2015-05-01

    Full Text Available Severe forms of chronic kidney disease can lead to a critical, end-stage condition, requiring renal replacement therapy, which may involve a form of dialysis or renal transplantation. Identification and characterization of novel markers and/or targets of therapy that could be applied in these critically ill patients remains the focus of the current research in the field of critical care medicine and has been the objective of our studies for some years past. To this end, we used models of renal vascular disease, Ang II, L-NAME or mice overexpressing renin, treated with AT1 antagonists at different stages of progression, to create cohorts of animals during progression, reversal or escape from therapy. Transcriptomic analysis and comparisons were performed and genes were selected according to the following criteria: a not previously described in the kidney, b highly upregulated during progression and returning to the normal levels during reversal, and c producing proteins that are either circulating or membrane receptors.

  16. Protein-Energy Wasting and Mortality in Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Ezio Gianetta

    2011-05-01

    Full Text Available Protein-energy wasting (PEW is common in patients with chronic kidney disease (CKD and is associated with an increased death risk from cardiovascular diseases. However, while even minor renal dysfunction is an independent predictor of adverse cardiovascular prognosis, PEW becomes clinically manifest at an advanced stage, early before or during the dialytic stage. Mechanisms causing loss of muscle protein and fat are complex and not always associated with anorexia, but are linked to several abnormalities that stimulate protein degradation and/or decrease protein synthesis. In addition, data from experimental CKD indicate that uremia specifically blunts the regenerative potential in skeletal muscle, by acting on muscle stem cells. In this discussion recent findings regarding the mechanisms responsible for malnutrition and the increase in cardiovascular risk in CKD patients are discussed. During the course of CKD, the loss of kidney excretory and metabolic functions proceed together with the activation of pathways of endothelial damage, inflammation, acidosis, alterations in insulin signaling and anorexia which are likely to orchestrate net protein catabolism and the PEW syndrome.

  17. Systemic Redox Imbalance in Chronic Kidney Disease: A Systematic Review

    Science.gov (United States)

    Kaltsatou, Antonia; Jamurtas, Athanasios Z.; Koutedakis, Yiannis; Stefanidis, Ioannis; Sakkas, Giorgos K.

    2016-01-01

    Patients with chronic kidney disease (CKD) experience imbalance between oxygen reactive species (ROS) production and antioxidant defenses leading to cell and tissue damage. However, it remains unclear at which stage of renal insufficiency the redox imbalance becomes more profound. The aim of this systematic review was to provide an update on recent advances in our understanding of how the redox status changes in the progression of renal disease from predialysis stages 1 to 4 to end stage 5 and whether the various treatments and dialysis modalities influence the redox balance. A systematic review was conducted searching PubMed and Scopus by using the Cochrane and PRISMA guidelines. In total, thirty-nine studies met the inclusion criteria and were reviewed. Even from an early stage, imbalance in redox status is evident and as the kidney function worsens it becomes more profound. Hemodialysis therapy per se seems to negatively influence the redox status by the elevation of lipid peroxidation markers, protein carbonylation, and impairing erythrocyte antioxidant defense. However, other dialysis modalities do not so far appear to confer advantages. Supplementation with antioxidants might assist and should be considered as an early intervention to halt premature atherogenesis development at an early stage of CKD. PMID:27563376

  18. Systemic Redox Imbalance in Chronic Kidney Disease: A Systematic Review

    Directory of Open Access Journals (Sweden)

    Konstantina P. Poulianiti

    2016-01-01

    Full Text Available Patients with chronic kidney disease (CKD experience imbalance between oxygen reactive species (ROS production and antioxidant defenses leading to cell and tissue damage. However, it remains unclear at which stage of renal insufficiency the redox imbalance becomes more profound. The aim of this systematic review was to provide an update on recent advances in our understanding of how the redox status changes in the progression of renal disease from predialysis stages 1 to 4 to end stage 5 and whether the various treatments and dialysis modalities influence the redox balance. A systematic review was conducted searching PubMed and Scopus by using the Cochrane and PRISMA guidelines. In total, thirty-nine studies met the inclusion criteria and were reviewed. Even from an early stage, imbalance in redox status is evident and as the kidney function worsens it becomes more profound. Hemodialysis therapy per se seems to negatively influence the redox status by the elevation of lipid peroxidation markers, protein carbonylation, and impairing erythrocyte antioxidant defense. However, other dialysis modalities do not so far appear to confer advantages. Supplementation with antioxidants might assist and should be considered as an early intervention to halt premature atherogenesis development at an early stage of CKD.

  19. Chronic Kidney Disease, Fluid Overload and Diuretics: A Complicated Triangle.

    Science.gov (United States)

    Khan, Yusra Habib; Sarriff, Azmi; Adnan, Azreen Syazril; Khan, Amer Hayat; Mallhi, Tauqeer Hussain

    2016-01-01

    Despite promising role of diuretics to manage fluid overload among chronic kidney disease (CKD) patients, their use is associated with adverse renal outcomes. Current study aimed to determine the extent of renal deterioration with diuretic therapy. A total 312 non-dialysis dependent CKD (NDD-CKD) patients were prospectively followed-up for one year. Fluid overload was assessed via bioimpedance spectroscopy. Estimated GFR (eGFR) was calculated from serum creatinine values by using Chronic Kidney Disease- Epidemiology Collaboration (CKD-EPI) equation. Out of 312 patients, 64 (20.5%) were hypovolemic while euvolemia and hypervolemia were observed in 113 (36.1%) and 135 (43.4%) patients. Overall 144 patients were using diuretics among which 98 (72.6%) were hypervolemic, 35 (30.9%) euvolemic and 11 (17.2%) were hypovolemic. The mean decline in estimated GFR of entire cohort was -2.5 ± 1.4 ml/min/1.73m2 at the end of follow up. The use of diuretics was significantly associated with decline in eGFR. A total of 36 (11.5%) patients initiated renal replacement therapy (RRT) and need of RRT was more profound among diuretic users. The use of diuretics was associated with adverse renal outcomes indicated by decline in eGFR and increasing risk of RRT initiation in our cohort of NDD-CKD patients. Therefore, it is cautiously suggested to carefully prescribe diuretics by keeping in view benefit versus harm for each patient.

  20. Assessment of diet in chronic kidney disease female predialysis patients.

    Science.gov (United States)

    Włodarek, Dariusz; Głąbska, Dominika; Rojek-Trębicka, Jadwiga

    2014-01-01

    Nutrition is important in the therapy of predialysis patients. The aim of the presented single-centre descriptive study was to assess the diet in chronic kidney disease female predialysis patients with no previous dietary intervention, in comparison with recommendations, as well as the analysis of the energy, protein and phosphate intake in correlation with chosen laboratory measurements. The research was carried out in 31 female predialysis patients with CKD of different etiology, aged 29-79 years (GFR: 19.4±9.7 ml/min/1.73 m2). Main outcome measures were self-reported data from three-day dietary recall. Nutrients content and energy value of diet were compared with guidelines for chronic kidney disease patients or, in case of nutrients when they are not settled, with the recommendations for healthy women. All patients had a lower energy intake than the recommended level. At the same time, 35.8% of patients were characterised by improper protein intake--too low or too high. The majority of patients had low intake of most of vitamins and minerals. The total, animal and plant protein were positively correlated with the energy value of diet and with amount of most of the nutrients. Values of GFR were positively correlated with animal protein intake, while phosphate and creatinine in blood were negatively correlated with total and animal protein intake. The study highlights that diet of CKD predialysis patients with no previous dietary intervention is not properly balanced.

  1. IgG4-related kidney disease – an update

    Science.gov (United States)

    Kawano, Mitsuhiro; Saeki, Takako

    2015-01-01

    Purpose of review IgG4-related disease (IgG4-RD) is a recently recognized systemic inflammatory disorder that can affect most organs/tissues such as sarcoidosis. The kidney is a frequently affected organ with tubulointerstitial nephritis (TIN), the representative lesion of IgG4-RD. This review focuses on the latest knowledge of IgG4-related kidney disease (IgG4-RKD). Recent findings A wide range of renal manifestations of IgG4-RD, that is TIN, membranous glomerulonephritis (MGN) and other glomerular lesions, and pyelitis, are collectively referred to as IgG4-RKD. Clinically, decreased renal function, or characteristic imaging findings such as multiple low-density lesions on contrast-enhanced computed tomography or diffuse thickening of the renal pelvic wall, are typical presenting features. Although a rapid response to corticosteroid therapy is a very important feature of IgG4-TIN, in cases in which renal function is moderately to severely decreased before therapy, only partial recovery of renal function is obtained. Summary TIN with characteristic imaging findings is a typical manifestation of IgG4-RKD in the interstitium, while MGN is a representative manifestation of the glomerular lesions. Although IgG4 is a central feature of IgG4-RD, the recent discovery of IgG4-negative IgG4-RD raises questions about the causative role of the IgG4 molecule in this context. PMID:25594543

  2. Biomarkers of cardiovascular stress and incident chronic kidney disease.

    Science.gov (United States)

    Ho, Jennifer E; Hwang, Shih-Jen; Wollert, Kai C; Larson, Martin G; Cheng, Susan; Kempf, Tibor; Vasan, Ramachandran S; Januzzi, James L; Wang, Thomas J; Fox, Caroline S

    2013-11-01

    Growth differentiation factor-15 (GDF-15), soluble ST2 (sST2), and high-sensitivity troponin I (hsTnI) are emerging predictors of adverse clinical outcomes. We examined whether circulating concentrations are related to the development of kidney disease in the community. Plasma GDF-15, sST2, and hsTnI concentrations were measured in 2614 Framingham Offspring cohort participants (mean age 57 years, 54% women) at the sixth examination cycle (1995-1998). Associations of biomarkers with incident chronic kidney disease [CKD, eGFR statistically significant in primary analyses. Participants were followed over a mean of 9.5 years. Higher plasma GDF-15 was associated with incident CKD [multivariable-adjusted odds ratio (OR) 1.9 per 1-U increase in log-GDF-15, 95% CI 1.6-2.3, P statistic increased from 0.826 to 0.845 (P = 0.0007), and categorical net reclassification was 6.3% (95% CI, 2.7-9.9%). Higher circulating GDF-15 is associated with incident renal outcomes and improves risk prediction of incident CKD. These findings may provide insights into the mechanisms of renal injury.

  3. Chronic kidney disease: information on southern brazilian patients with kidney disease - 10.4025/actascihealthsci.v34ispec.16048 Chronic kidney disease: information on southern brazilian patients with kidney disease - 10.4025/actascihealthsci.v34ispec.16048

    Directory of Open Access Journals (Sweden)

    Maria Dalva de Barros Carvalho

    2012-12-01

    Full Text Available The profile of patients undergoing haemodialysis in the dialysis unit of Hospital Santa Casa de Maringá, Maringá PR Brazil, is provided. A questionnaire on social and economic data and underlying diseases prior to the Chronic Kidney Disease (CKD identified the patients’ profile. The project was approved by the Ethics Committee of the institution. Eighty-three patients, with 54.21% males, were interviewed. Age bracket ranged between 20 and 59 years in 65.06% of patients. Only 27.71% maintained jobs after the diagnosis and the start of treatment; 63.86% had an average personal income between 1 and 3 minimum wages; 63.85% did not practice any physical activity. Moreover, 53.01% belonged to the European-Brazilian white group; 20.48% to the Afro-Brazilian brown group; 19.28% to the Afro-Brazilian Negro group; 6.02% to other ethnic groups. Further, 85.54% patients reported having an underlying disease prior to the CKD, namely, 61.45% were hypertensive; 31.33% were diabetics and 20.48% had other diseases. Results show the need of a greater attention to these patients’ health care to reduce the negative impacts related to the chronic disease focused.The profile of patients undergoing haemodialysis in the dialysis unit of Hospital Santa Casa de Maringá, Maringá PR Brazil, is provided. A questionnaire on social and economic data and underlying diseases prior to the Chronic Kidney Disease (CKD identified the patients’ profile. The project was approved by the Ethics Committee of the institution. Eighty-three patients, with 54.21% males, were interviewed. Age bracket ranged between 20 and 59 years in 65.06% of patients. Only 27.71% maintained jobs after the diagnosis and the start of treatment; 63.86% had an average personal income between 1 and 3 minimum wages; 63.85% did not practice any physical activity. Moreover, 53.01% belonged to the European-Brazilian white group; 20.48% to the Afro-Brazilian brown group; 19.28% to the Afro-Brazilian Negro

  4. Exploratory Cluster Analysis to Identify Patterns of Chronic Kidney Disease in the 500 Cities Project.

    Science.gov (United States)

    Liu, Shelley H; Li, Yan; Liu, Bian

    2018-05-17

    Chronic kidney disease is a leading cause of death in the United States. We used cluster analysis to explore patterns of chronic kidney disease in 500 of the largest US cities. After adjusting for socio-demographic characteristics, we found that unhealthy behaviors, prevention measures, and health outcomes related to chronic kidney disease differ between cities in Utah and those in the rest of the United States. Cluster analysis can be useful for identifying geographic regions that may have important policy implications for preventing chronic kidney disease.

  5. 75 FR 11188 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2010-03-10

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, Liver Disease Ancillary Studies. Date... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the.... (301) 594-8895. [email protected] . Name of Committee: National Institute of Diabetes and...

  6. 76 FR 63313 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting

    Science.gov (United States)

    2011-10-12

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, Liver Cell Membrane Proteins. Date... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting Pursuant to section 10(d) of the..., Diabetes, Endocrinology and Metabolic Research; 93.848, Digestive Diseases and Nutrition Research; 93.849...

  7. 77 FR 9671 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting

    Science.gov (United States)

    2012-02-17

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Liver Tissue and Cell Distribution... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting Pursuant to section 10(d) of the... Assistance Program Nos. 93.847, Diabetes, Endocrinology and Metabolic Research; 93.848, Digestive Diseases...

  8. Dyslipidemia in patients with chronic kidney disease: etiology and management

    Directory of Open Access Journals (Sweden)

    Mikolasevic I

    2017-02-01

    Full Text Available Ivana Mikolasevic,1,2 Marta Žutelija,3 Vojko Mavrinac,1 Lidija Orlic 2 1Department of Gastroenterology, 2Department of Nephrology, Dialysis and Kidney Transplantation, UHC Rijeka, 3School of Medicine, Rijeka, Croatia Abstract: Patients with chronic kidney disease (CKD, including those with end-stage renal disease, treated with dialysis, or renal transplant recipients have an increased risk for cardiovascular disease (CVD morbidity and mortality. Dyslipidemia, often present in this patient population, is an important risk factor for CVD development. Specific quantitative and qualitative changes are seen at different stages of renal impairment and are associated with the degree of glomerular filtration rate declining. Patients with non-dialysis-dependent CKD have low high-density lipoproteins (HDL, normal or low total cholesterol (TC and low-density lipoprotein (LDL cholesterol, increased triglycerides as well as increased apolipoprotein B (apoB, lipoprotein(a (Lp (a, intermediate- and very-low-density lipoprotein (IDL, VLDL; “remnant particles”, and small dense LDL particles. In patients with nephrotic syndrome lipid profile is more atherogenic with increased TC, LDL, and triglycerides. Lipid profile in hemodialysis (HD patients is usually similar to that in non-dialysis-dependent CKD patients. Patients on peritoneal dialysis (PD have more altered dyslipidemia compared to HD patients, which is more atherogenic in nature. These differences may be attributed to PD per se but may also be associated with the selection of dialytic modality. In renal transplant recipients, TC, LDL, VLDL, and triglycerides are elevated, whereas HDL is significantly reduced. Many factors can influence post-transplant dyslipidemia including immunosuppressive agents. This patient population is obviously at high risk; hence, prompt diagnosis and management are required to improve their clinical outcomes. Various studies have shown statins to be effective in the

  9. Optimal management of bone mineral disorders in chronic kidney disease and end stage renal disease.

    Science.gov (United States)

    Lundquist, Andrew L; Nigwekar, Sagar U

    2016-03-01

    The review summarizes recent studies on chronic kidney disease-mineral bone disorders, with a focus on new developments in disease management. The term chronic kidney disease-mineral bone disorder has come to describe an increasingly complex network of alterations in minerals and skeletal disorders that contribute to the significant cardiovascular morbidity and mortality seen in patients with chronic kidney disease and end stage renal disease. Clinical studies continue to suggest associations with clinical outcomes, yet current clinical trials have failed to support causality. Variability in practice exists as current guidelines for management of mineral bone disorders are often based on weak evidence. Recent studies implicate novel pathways for therapeutic intervention in clinical trials. Mineral bone disorders in chronic kidney disease arise from alterations in a number of molecules in an increasingly complex physiological network interconnecting bone and the cardiovascular system. Despite extensive associations with improved outcomes in a number of molecules, clinical trials have yet to prove causality and there is an absence of new therapies available to improve patient outcomes. Additional clinical trials that can incorporate the complexity of mineral bone disorders, and with the ability to intervene on more than one pathway, are needed to advance patient care.

  10. Spectrum of kidney diseases in Africa: malaria, schistosomiasis, sickle cell disease, and toxins.

    Science.gov (United States)

    Arogundade, Fatiu A; Hassan, Muzamil O; Omotoso, Bolanle A; Oguntola, Stephen O; Okunola, Oluyomi O; Sanusi, Abubakr A; Akinsola, Adewale

    Kidney diseases have assumed epidemic proportions in both developed and developing countries, particularly chronic kidney disease (CKD). While treatment modalities are available and accessible in developed economies with improvement in outcomes, survival, and quality of life, they are either unavailable or inaccessible in nations with emerging economies, particularly in sub-Saharan Africa (SSA), with an attendant worsening outcome and survival for CKD patients. The epidemiology of CKD in SSA has revealed that it preferentially affects adults in their economically productive years, usually below the age of 50 years, with consequent drain on the economy. This derives mainly from the major etiologies in the region, which are infection-induced chronic glomerulonephritis and hypertension, compounded by poverty as well as societal and health underdevelopment, poor resource allocation to health, and underdeveloped health infrastructures. This has made preventive nephrology a major goal in the sub-region, although those who have already developed CKD must be managed up to tertiary levels. In this review, we assessed the contributions of parasitic diseases (i.e., malaria and schistosomiasis), sickle cell disease and nephrotoxins with the aim of espousing their contributions to the burden of kidney disease, and proposing management options with the goal of ultimately reducing the burden of kidney disease in these disadvantaged populations.

  11. The Evolving World of Chronic Kidney Disease Mineral Bone Disorder

    Directory of Open Access Journals (Sweden)

    Antonio Bellasi

    2013-07-01

    Full Text Available Chronic kidney disease – mineral and bone disorder (CKD-MBD is associated with a significant morbidity and mortality. In vitro and animal models suggest that phosphorous, calcium, parathyroid hormone, and vitamin D abnormalities, mediate the cardiovascular and bone diseases that characterise CKD-MBD and increase the risk of death. Currently, mineral abnormalities are corrected through phosphorous restriction, phosphate binders, calcimimetics and vitamin D administration. Nonetheless, data in humans that support the use of these compounds are still scarce, mainly based on observational studies. Thus, a considerable number of doubts and questions still challenge clinicians dealing with CKD patients and mineral metabolism imbalances. We herein critically review clinical evidence that support the use of different drugs in CKD-MBD.

  12. Is Autosomal Dominant Polycystic Kidney Disease Becoming a Pediatric Disorder?

    Directory of Open Access Journals (Sweden)

    Stéphanie De Rechter

    2017-12-01

    Full Text Available Autosomal dominant polycystic kidney disease (ADPKD affects 1 in 400 to 1,000 live births, making it the most common monogenic cause of renal failure. Although no definite cure is available yet, it is important to affect disease progression by influencing modifiable factors such as hypertension and proteinuria. Besides this symptomatic management, the only drug currently recommended in Europe for selected adult patients with rapid disease progression, is the vasopressin receptor antagonist tolvaptan. However, the question remains whether these preventive interventions should be initiated before extensive renal damage has occurred. As renal cyst formation and expansion begins early in life, frequently in utero, ADPKD should no longer be considered an adult-onset disease. Moreover, the presence of hypertension and proteinuria in affected children has been reported to correlate well with disease severity. Until now, it is controversial whether children at-risk for ADPKD should be tested for the presence of the disease, and if so, how this should be done. Herein, we review the spectrum of pediatric ADPKD and discuss the pro and contra of testing at-risk children and the challenges and unmet needs in pediatric ADPKD care.

  13. Gender hormones and the progression of experimental polycystic kidney disease.

    Science.gov (United States)

    Stringer, Kenneth D; Komers, Radko; Osman, Shukri A; Oyama, Terry T; Lindsley, Jessie N; Anderson, Sharon

    2005-10-01

    Male gender is a risk factor for progression of autosomal-dominant polycystic kidney disease (ADPKD), clinically and in the Han:SPRD rat model. Orchiectomy limits progression, but mechanisms of the detrimental effect of androgen, and/or beneficial effects of estrogen, are not known. This protocol tested the hypothesis that male gender (intact androgen status) promotes progression, while female gender (intact estrogen status) is protective; and that these disease-modifying effects are due to changes in expression of known fibrotic mediators. Studies were performed in male and female noncystic control (+/+) and cystic (+/-) rats subjected to orchiectomy, ovariectomy, or sham operation. At 12 weeks of age, renal function was measured. Blood and kidneys were taken for measurement of plasma and renal renin, endothelin (ET-1), endothelial nitric oxide synthase (eNOS), and vascular endothelial growth factor (VEGF), using biochemical, protein expression, and immunohistochemical methods. Cystic male rats exhibited significantly reduced glomerular filtration (GFR) and effective renal plasma flow (ERPF) rates, with suppression of plasma and renal renin, up-regulation of renal ET-1 and eNOS, and down-regulation of renal VEGF expression. Orchiectomy attenuated the fall in GFR and ERPF, while numerically limiting changes in eNOS and VEGF. Female rats exhibited less cystic growth, with normal renin status, lesser elevation of renal ET-1, and proportionately lesser changes in VEGF and eNOS. Ovariectomy led to higher blood pressure and reduced GFR and ERPF, with a trend toward upregulation of ET-1, and significant down-regulation of VEGF and eNOS. Female gender is protective, but ovariectomy attenuates the protective effect of female gender, in association with changes in renal expression of ET-1, VEGF, and eNOS. The accelerated disease in male rats can be attenuated by orchiectomy and consequent changes in expression of disease mediators.

  14. ISCHEMIC HEART DISEASE IN PATIENTS OF CHRONIC KIDNEY DISEASE ON MAINTENANCE HEMODIALYSIS

    OpenAIRE

    Dr. Aijaz Ahmed, Dr. Muhammad Nadeem Ahsan, Dr. Pooran Mal*, Dr. Hamid Nawaz Ali Memon, Dr. Samreen and Dr. Sajjad Ali

    2017-01-01

    Objective: To determine the frequency of ischemic heart disease in patients of chronic kidney disease on maintenance hemodialysis Patients and Methods: A total of 160 patients with diagnosis of CKD in department of Nephrology, Liaquat National Hospital Karachi were recruited in this six months cross sectional study. Demographic information was recorded. Then patients were underwent ECG. Reports were assessed and ischemic heart disease was labeled while all the data was collected using the pro...

  15. Prevalence estimates of chronic kidney disease in Canada: results of a nationally representative survey

    Science.gov (United States)

    Arora, Paul; Vasa, Priya; Brenner, Darren; Iglar, Karl; McFarlane, Phil; Morrison, Howard; Badawi, Alaa

    2013-01-01

    Background: Chronic kidney disease is an important risk factor for death and cardiovascular-related morbidity, but estimates to date of its prevalence in Canada have generally been extrapolated from the prevalence of end-stage renal disease. We used direct measures of kidney function collected from a nationally representative survey population to estimate the prevalence of chronic kidney disease among Canadian adults. Methods: We examined data for 3689 adult participants of cycle 1 of the Canadian Health Measures Survey (2007–2009) for the presence of chronic kidney disease. We also calculated the age-standardized prevalence of cardiovascular risk factors by chronic kidney disease group. We cross-tabulated the estimated glomerular filtration rate (eGFR) with albuminuria status. Results: The prevalence of chronic kidney disease during the period 2007–2009 was 12.5%, representing about 3 million Canadian adults. The estimated prevalence of stage 3–5 disease was 3.1% (0.73 million adults) and albuminuria 10.3% (2.4 million adults). The prevalence of diabetes, hypertension and hypertriglyceridemia were all significantly higher among adults with chronic kidney disease than among those without it. The prevalence of albuminuria was high, even among those whose eGFR was 90 mL/min per 1.73 m2 or greater (10.1%) and those without diabetes or hypertension (9.3%). Awareness of kidney dysfunction among adults with stage 3–5 chronic kidney disease was low (12.0%). Interpretation: The prevalence of kidney dysfunction was substantial in the survey population, including individuals without hypertension or diabetes, conditions most likely to prompt screening for kidney dysfunction. These findings highlight the potential for missed opportunities for early intervention and secondary prevention of chronic kidney disease. PMID:23649413

  16. [Wasting in chronic kidney disease: Refeeding techniques and artificial nutrition practices].

    Science.gov (United States)

    Pasian, Céline; Azar, Raymond; Fouque, Denis

    2016-12-01

    Protein energy wasting (PEW) is an independent factor associated with morbi-mortality in chronic kidney disease. Wasting is particularly common in chronic diseases of organs such as kidney disease with a major impact at the stage of dialysis. It covers 20 to 70% of patients diagnosed with chronic kidney disease according to the degree of evolution of the disease and the diagnostic method used patients. Mechanisms of PEW are based mainly on anorexia and metabolic abnormalities caused by kidney disease. Nutritional treatment differs depending on the stage of the kidney disease acute or chronic treated whether or not by dialysis. Nutritional monitoring should be regular, individualized and collaborative to detect a risk of PEW or treat installed PEW. Refeeding techniques should allow all the nutritional needs. Their indications depend on the clinic, biochemical assessment and nutrient intake. Copyright © 2016 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.

  17. Cognitive remediation in pediatric chronic kidney disease and end-stage kidney disease: rationale, candidate interventions, and applicability.

    Science.gov (United States)

    Javalkar, Karina; Ferris, Maria E; Cuttance, Jessica; Hooper, Stephen R

    2017-11-01

    The purpose of this paper is to address the potential use of cognitive remediation interventions for children and adolescents with chronic kidney disease (CKD) and end-stage kidney disease (ESKD). The prevalence and risk for neurocognitive dysfunction in children with this condition remains high, but, to date, interventions targeting these challenges have not been attempted either individually or as part of a larger treatment program. This is the next logical step in addressing the neurocognitive dysfunction that can be present in pediatric CKD/ESKD, with the field needing to determine the efficacy of cognitive remediation approaches for this population. To our knowledge, this paper is the first to raise this possibility by identifying candidate treatments addressing the neurocognitive challenges observed in children and adolescents with CKD/ESKD. Initially, we present the rationale for the importance of addressing the cognitive difficulties in this population, including an overview of the literature documenting the neurocognitive deficits associated with pediatric-onset CKD/ESKD. This is followed by a review of five candidate cognitive remediation programs that may be applicable to patients with this condition, and associated factors that could affect such treatment. The paper concludes with suggestions for both clinical and research initiatives that could be implemented to examine cognitive remediation as potential components of a larger treatment program for children and adolescents with CKD/ESKD.

  18. Genetic basis of kidney cancer: Role of genomics for the development of disease-based therapeutics

    Science.gov (United States)

    Linehan, W. Marston

    2012-01-01

    Kidney cancer is not a single disease; it is made up of a number of different types of cancer, including clear cell, type 1 papillary, type 2 papillary, chromophobe, TFE3, TFEB, and oncocytoma. Sporadic, nonfamilial kidney cancer includes clear cell kidney cancer (75%), type 1 papillary kidney cancer (10%), papillary type 2 kidney cancer (including collecting duct and medullary RCC) (5%), the microphalmia-associated transcription (MiT) family translocation kidney cancers (TFE3, TFEB, and MITF), chromophobe kidney cancer (5%), and oncocytoma (5%). Each has a distinct histology, a different clinical course, responds differently to therapy, and is caused by mutation in a different gene. Genomic studies identifying the genes for kidney cancer, including the VHL, MET, FLCN, fumarate hydratase, succinate dehydrogenase, TSC1, TSC2, and TFE3 genes, have significantly altered the ways in which patients with kidney cancer are managed. While seven FDA-approved agents that target the VHL pathway have been approved for the treatment of patients with advanced kidney cancer, further genomic studies, such as whole genome sequencing, gene expression patterns, and gene copy number, will be required to gain a complete understanding of the genetic basis of kidney cancer and of the kidney cancer gene pathways and, most importantly, to provide the foundation for the development of effective forms of therapy for patients with this disease. PMID:23038766

  19. End Stage and Chronic Kidney Disease:Associations with Renal Cancer

    Directory of Open Access Journals (Sweden)

    Paul eRusso

    2012-04-01

    Full Text Available There is a well known association between end stage renal disease and the development of kidney cancer in the native kidney of patients requiring renal replacement therapy. There is now emerging evidence that lesser degrees of renal insufficiency (chronic kidney disease, CKD are also associated with an increased likelihood of cancer in general and kidney cancer in particular. Nephro pathological changes are commonly observed in the non tumor bearing portions of kidney resected at the time of partial and radical nephrectomy. In addition, patients with renal cancer are more likely to have CKD at the time of diagnosis and treatment than the general population. The exact mechanism by which renal insufficiency transforms normal kidney cells into tumor cells is not known. Possible mechanisms include uremic immune inhibition or increased exposure to circulating toxins not adequately cleared by the kidneys. Surgeons managing kidney tumors must have an increased awareness of their patient’s renal functional status as they plan their resection. Kidney sparing approaches, including partial nephrectomy or active surveillance in older and morbidly ill patients, can prevent CKD or delay the further decline in renal function which is well documented with radical nephrectomy. Despite emerging evidence that partial nephrectomy provides equivalent local tumor control to radical nephrectomy while at the same time preventing CKD, this operation remains under utilized in the United States and abroad. Increased awareness of the bi directional relationship between kidney function and kidney cancer is essential in the contemporary management of kidney cancer.

  20. AMBULATORY BLOOD PRESSURE PATTERNS IN CHILDREN WITH CHRONIC KIDNEY DISEASE

    Science.gov (United States)

    Samuels, Joshua; Ng, Derek; Flynn, Joseph T.; Mitsnefes, Mark; Poffenbarger, Tim; Warady, Bradley A.; Furth, Susan

    2012-01-01

    Ambulatory blood pressure monitoring (ABPM) is the best method of detecting abnormal blood pressure (BP) in patients with chronic kidney disease (CKD), whose hypertension may be missed with office BP measurements. We report ABPM findings in 332 children 1 year after entry in the Chronic Kidney Disease in Children (CKiD) cohort study. All subjects underwent casual and ambulatory BP measurement. BP was categorized based on casual and ABPM results into normal, white coat, masked, and ambulatory hypertension. Only half of the subjects had a normal ABPM. BP load was elevated (>25%) in 52% (n= 172) while mean BP was elevated in 32% (n= 105). In multivariate analysis, those using an ACE inhibitor (ACEi) were 89% more likely to have a normal ABPM than those who did not report using an ACEi (OR: 1.89, 95%CI: 1.17, 3.04). For every 20% faster decline in annualized GFR change, the odds of an abnormal ABPM increased 26% (OR: 1.26, 95%CI: 0.97, 1.64; p= 0.081). A 2.25 fold increase in urine protein:creatinine ratio annualized change was associated with a 39% higher odds of an abnormal ABPM (OR: 1.39, 95%CI: 1.06, 1.82; p= 0.019). Abnormalities on ABPM are common in children with CKD, and are strongly associated with known risk factors for end stage renal disease. Individuals on ACEi were less likely to have abnormal ABPM, suggesting a possible therapeutic intervention. ABPM should be used to monitor risk and guide therapy in children with CKD. PMID:22585950

  1. Glucose Transporters in Diabetic Kidney Disease-Friends or Foes?

    Science.gov (United States)

    Wasik, Anita A; Lehtonen, Sanna

    2018-01-01

    Diabetic kidney disease (DKD) is a major microvascular complication of diabetes and a common cause of end-stage renal disease worldwide. DKD manifests as an increased urinary protein excretion (albuminuria). Multiple studies have shown that insulin resistance correlates with the development of albuminuria in non-diabetic and diabetic patients. There is also accumulating evidence that glomerular epithelial cells or podocytes are insulin sensitive and that insulin signaling in podocytes is essential for maintaining normal kidney function. At the cellular level, the mechanisms leading to the development of insulin resistance include mutations in the insulin receptor gene, impairments in the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway, or perturbations in the trafficking of glucose transporters (GLUTs), which mediate the uptake of glucose into cells. Podocytes express several GLUTs, including GLUT1, GLUT2, GLUT3, GLUT4, and GLUT8. Of these, the most studied ones are GLUT1 and GLUT4, both shown to be insulin responsive in podocytes. In the basal state, GLUT4 is preferentially located in perinuclear and cytosolic vesicular structures and to a lesser extent at the plasma membrane. After insulin stimulation, GLUT4 is sorted into GLUT4-containing vesicles (GCVs) that translocate to the plasma membrane. GCV trafficking consists of several steps, including approaching of the GCVs to the plasma membrane, tethering, and docking, after which the lipid bilayers of the GCVs and the plasma membrane fuse, delivering GLUT4 to the cell surface for glucose uptake into the cell. Studies have revealed novel molecular regulators of the GLUT trafficking in podocytes and unraveled unexpected roles for GLUT1 and GLUT4 in the development of DKD, summarized in this review. These findings pave the way for better understanding of the mechanistic pathways associated with the development and progression of DKD and aid in the development of new treatments for this devastating disease.

  2. Cosmic Transmission of Periodontal, Cardiovascular and Kidney Disease via Nanobacteria

    Directory of Open Access Journals (Sweden)

    Jafar Kolahi

    2011-04-01

    Full Text Available Introduction: Nanobacteria (NB are mysterious particles that have spurred one of the biggest controversies in modern micro-biology. NB has been reported to be present in animal and human blood, tissue culture cell lines, wastewater and etc. NB appear to cause or contribute to common diseases of the mankind e.g. periodontitis, formation of kidney stone, heart calcifications, coronary artery calcification, atherosclerotic plaque. Recent data on the far-ultraviolet extinction of starlight in our galaxy and in external galaxies is interpreted in terms of the widespread occurrence of organic particles of optical refractive index 1.4 and radii less than or equal to 20 nm. Such particles are candidates for NB such as recently been found in abundance on the Earth. Unbelievably nanobacteria-like rods observed at the surface of the Tataouine meteorite and Martian rock.The hypothesis: It seems logic to hypothesize that aliens from inner space, nanobacteria, can bring us new disease such as periodontal, cardiovascular and kidney diseases via space travels or meteorites or interstellar dusts.Evaluation of the hypothesis: The main criticism with this idea is how NB can keep alive during transfer among seriously life threatening condition in interstellar space. NB are generally thought to be very difficult to deactivation, exceptionally resistant to heat, are not deactivated by physical or chemical treatments including autoclaving, UV treatment, and various biocides. Health care providers, health policy makers and space agencies e.g. NASA and European Space Agency should make a concentrated effort to prevent transmission of NB especially following space travels.

  3. Chronic kidney disease in Asia: Protocol for a collaborative overview.

    Science.gov (United States)

    Liyanage, Thaminda; Ninomiya, Toshiharu; Perkovic, Vlado; Woodward, Mark; Stirnadel-Farrant, Heide; Matsushita, Kunihiro; Iseki, Kunitoshi; Seong, Hooi Lai; Monaghan, Helen; Jha, Vivekanand

    2017-06-01

    The burden of chronic kidney disease (CKD) is growing rapidly around the world. However, there is limited information on the overall regional prevalence of CKD, as well as the prognostic implications and treatment patterns in Asian region. We have established the Asian Renal Collaboration (ARC) with the goal of consolidating region-wide data regarding CKD. This collaborative project will synthesize data and perform meta-analyses of observational studies conducted in Asia. Studies will be identified through a systematic literature search including abstracts, proceedings of meetings, electronic databases such as MEDLINE and EMBASE. Personal enquiry among collaborators and experts in the region will identify additional studies, or other data sources such as registries. Both cross-sectional and longitudinal studies that describe the prevalence of CKD and its complications will be included, as will longitudinal studies that describe important clinical outcomes for people with CKD. Individual participant data will be sought, where possible, from each of the studies included in the collaboration for baseline parameters and subsequent outcomes, in order to maximize flexibility and consistency of data analyses. This study is an initiative offering a unique opportunity to obtain information about the prevalence and manifestations of CKD in Asia, as well as its risk factors. The ARC will also provide insights into important outcomes including progression of CKD, CKD complications, cardiovascular disease and death. These findings will improve our understanding of kidney disease in Asia, and thus help inform service provision, preventive care and further research across the region. © 2016 Asian Pacific Society of Nephrology.

  4. The definition, classification, and prognosis of chronic kidney disease: a KDIGO Controversies Conference report.

    Science.gov (United States)

    Levey, Andrew S; de Jong, Paul E; Coresh, Josef; El Nahas, Meguid; Astor, Brad C; Matsushita, Kunihiro; Gansevoort, Ron T; Kasiske, Bertram L; Eckardt, Kai-Uwe

    2011-07-01

    The definition and classification for chronic kidney disease was proposed by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF-KDOQI) in 2002 and endorsed by the Kidney Disease: Improving Global Outcomes (KDIGO) in 2004. This framework promoted increased attention to chronic kidney disease in clinical practice, research and public health, but has also generated debate. It was the position of KDIGO and KDOQI that the definition and classification should reflect patient prognosis and that an analysis of outcomes would answer key questions underlying the debate. KDIGO initiated a collaborative meta-analysis and sponsored a Controversies Conference in October 2009 to examine the relationship of estimated glomerular filtration rate (GFR) and albuminuria to mortality and kidney outcomes. On the basis of analyses in 45 cohorts that included 1,555,332 participants from general, high-risk, and kidney disease populations, conference attendees agreed to retain the current definition for chronic kidney disease of a GFR 30 mg/g, and to modify the classification by adding albuminuria stage, subdivision of stage 3, and emphasizing clinical diagnosis. Prognosis could then be assigned based on the clinical diagnosis, stage, and other key factors relevant to specific outcomes. KDIGO has now convened a workgroup to develop a global clinical practice guideline for the definition, classification, and prognosis of chronic kidney disease.

  5. Chronic kidney disease and bleeding risk in patients at high cardiovascular risk: a cohort study.

    Science.gov (United States)

    Ocak, G; Rookmaaker, M B; Algra, A; de Borst, G J; Doevendans, P A; Kappelle, L J; Verhaar, M C; Visseren, F L

    2018-01-01

    Essentials The association between chronic kidney disease and bleeding is unknown. We followed 10 347 subjects at high cardiovascular risk for bleeding events. Chronic kidney disease was associated with a 1.5-fold increased bleeding risk. Especially albuminuria rather than decreased kidney function was associated with bleeding events. Background There are indications that patients with chronic kidney disease have an increased bleeding risk. Objectives To investigate the association between chronic kidney disease and bleeding in patients at high cardiovascular risk. Methods We included 10 347 subjects referred to the University Medical Center Utrecht (the Netherlands) from September 1996 to February 2015 for an outpatient visit with classic risk factors for arterial disease or with symptomatic arterial disease (Second Manifestation of Arterial disease [SMART] cohort). Patients were staged according to the KDIGO guidelines, on the basis of estimated glomerular filtration rate (eGFR) and albuminuria, and were followed for the occurrence of major hemorrhagic events until March 2015. Hazard ratios (HRs) with 95% confidence intervals (CIs) for bleeding were calculated with Cox proportional hazards analyses. Results The incidence rate for bleeding in subjects with chronic kidney disease was 8.0 per 1000 person-years and that for subjects without chronic kidney disease was 3.5 per 1000 person-years. Patients with chronic kidney disease (n = 2443) had a 1.5-fold (95% CI 1.2-1.9) increased risk of bleeding as compared with subjects without chronic kidney disease (n = 7904) after adjustment. Subjects with an eGFR of Chronic kidney disease is a risk factor for bleeding in patients with classic risk factors for arterial disease or with symptomatic arterial disease, especially in the presence of albuminuria. © 2017 University Medical Center Utrecht. Journal of Thrombosis and Haemostasis © 2017 International Society on Thrombosis and Haemostasis.

  6. Association between Nephrolithiasis, Hypertension and Obesity in Polycystic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Valbona Bajrami

    2015-12-01

    Full Text Available AIM: We aim to define the correlations between nephrolithiasis, hypertension, age and obesity in patients with autosomal dominant polycystic kidney disease (ADPKD in Albania. MATERIAL AND METHODS: We included 100 patients with autosomal dominant polycystic kidney from 2011 to 2014. The patients underwent X-ray and renal ultrasonography. We performed the metabolic evaluation of blood and urine. RESULTS: The patients with renal stones had a higher level of mean systolic and diastolic blood pressure compared with patients without stones (155 ± 12 mmHg vs. 145 ± 8 mmHg, and 105 ± 0.9 mmHg vs. 92 ± 1.28 mmHg, respectively. Patients with renal stones were older (47 ± 15 vs. 38 ± 5 years, had a higher prevalence of obesity [body mass index (BMI: 28 ± 2.4 vs. 25.7 ± 0.6], had higher levels of total cholesterol level (220 ± 5 mg/dl vs. 203 ± 4 mg/dl as well as triglyceride levels (160 ± 9 mg/dl vs. 126 ± 4 mg/dl, compared with no renal stone individuals. CONCLUSION: ADPKD patients with renal stones in our study had a higher mean level of systolic and diastolic blood pressure, BMI and cholesterol and triglycerides levels compared with individuals without renal stones.

  7. Ramadan fasting and chronic kidney disease: A systematic review.

    Science.gov (United States)

    Bragazzi, Nicola Luigi

    2014-07-01

    Ramadan fasting represents one of the five pillars of the Islam creed according to the Sunnah and the second practice of faith for the Shiaa. Even though patients are exempted from observing this religious duty, they may be eager to share this particular moment of the year with their family and peers. However, there are no guidelines or standardized protocols that can help physicians to properly address the issue of patients with chronic kidney disease (CKD) fasting in Ramadan and to correctly advise them. Moreover, in a more interconnected and globalized society, in which more and more Muslim patients live in the Western countries, this topic is of high interest also for the general practitioner. For this purpose, we carried out a systematic review, including also articles written in Arabic, Turkish, and Persian languages. Our main findings are that: recipients of kidney allograft can safely fast during Ramadan;evidences for safety in patients with nephrolithiasis and CKD are instead mixed and controversial. On the other hand,most studies have been carried out during Ramadan falling in cold seasons, and there is scarce information about Ramadan fasting in hot seasons. For these reasons, the findings may be not generalizable and therefore cautions should be taken and applied; the physicians should carefully monitor their patients during the fasting period with an adequate follow-up, in order to avoid any injurious effect.

  8. Recent Advances in Traditional Chinese Medicine for Kidney Disease.

    Science.gov (United States)

    Zhong, Yifei; Menon, Madhav C; Deng, Yueyi; Chen, Yiping; He, John Cijiang

    2015-09-01

    Because current treatment options for chronic kidney disease (CKD) are limited, many patients seek out alternative therapies such as traditional Chinese medicine. However, there is a lack of evidence from large clinical trials to support the use of traditional medicines in patients with CKD. Many active components of traditional medicine formulas are undetermined and their toxicities are unknown. Therefore, there is a need for research to identify active compounds from traditional medicines and understand the mechanisms of action of these compounds, as well as their potential toxicity, and subsequently perform well-designed, randomized, controlled, clinical trials to study the efficacy and safety of their use in patients with CKD. Significant progress has been made in this field within the last several years. Many active compounds have been identified by applying sophisticated techniques such as mass spectrometry, and more mechanistic studies of these compounds have been performed using both in vitro and in vivo models. In addition, several well-designed, large, randomized, clinical trials have recently been published. We summarize these recent advances in the field of traditional medicines as they apply to CKD. In addition, current barriers for further research are also discussed. Due to the ongoing research in this field, we believe that stronger evidence to support the use of traditional medicines for CKD will emerge in the near future. Copyright © 2015 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

  9. Oxidative Stress in Diabetic Nephropathy with Early Chronic Kidney Disease

    Directory of Open Access Journals (Sweden)

    Alejandra Guillermina Miranda-Díaz

    2016-01-01

    Full Text Available The increase in the prevalence of diabetes mellitus (DM and the secondary kidney damage produces diabetic nephropathy (DN. Early nephropathy is defined as the presence of microalbuminuria (30–300 mg/day, including normal glomerular filtration rate (GFR or a mildly decreased GFR (60–89 mL/min/1.73 m2, with or without overt nephropathy. The earliest change caused by DN is hyperfiltration with proteinuria. The acceptable excretion rate of albumin in urine is 300 mg/day. Chronic kidney disease (CKD is characterized by abnormalities in renal function that persist for >3 months with health implications. Alterations in the redox state in DN are caused by the persistent state of hyperglycemia and the increase in advanced glycation end products (AGEs with ability to affect the renin-angiotensin system and the transforming growth factor-beta (TGF-β, producing chronic inflammation and glomerular and tubular hypertrophy and favoring the appearance of oxidative stress. In DN imbalance between prooxidant/antioxidant processes exists with an increase in reactive oxygen species (ROS. The overproduction of ROS diminishes expression of the antioxidant enzymes (manganese superoxide dismutase, glutathione peroxidase, and catalase. The early detection of CKD secondary to DN and the timely identification of patients would permit decreasing its impact on health.

  10. Screening for Chronic Kidney Disease: Preventing Harm or Harming the Healthy?

    OpenAIRE

    Echouffo-Tcheugui, Justin B.; Kengne, Andre P.

    2012-01-01

    Editors' Summary Background Chronic kidney disease (CKD)—the gradual loss of kidney function—is increasingly common worldwide. In the US, for example, about 26 million adults have CKD, and millions more are at risk of developing the condition. Throughout life, small structures called nephrons inside the kidneys filter waste products and excess water from the blood to make urine. If the nephrons stop working because of injury or disease, the rate of blood filtration decreases, and dangerous am...

  11. Patient-Reported Outcomes in Patients with Chronic Kidney Disease and Kidney Transplant—Part 1

    Directory of Open Access Journals (Sweden)

    Evan Tang

    2018-01-01

    Full Text Available Chronic kidney disease (CKD is a complex medical condition that is associated with several comorbidities and requires comprehensive medical management. Given the chronic nature of the condition, its frequent association with psychosocial distress, and its very significant symptom burden, the subjective patient experience is key toward understanding the true impact of CKD on the patients’ life. Patient-reported outcome measures are important tools that can be used to support patient-centered care and patient engagement during the complex management of patients with CKD. The routine collection and use of patient-reported outcomes (PROs in clinical practice may improve quality of care and outcomes, and may provide useful data to understand the disease from both an individual and a population perspective. Many tools used to measure PROs focus on assessing health-related quality of life, which is significantly impaired among patients with CKD. Health-related quality of life, in addition to being an important outcome itself, is associated with clinical outcomes such as health care use and mortality. In Part 1 of this review, we provide an overview of PROs and implications of their use in the context of CKD. In Part 2, we will review the selection of appropriate measures and the relevant domains of interest for patients with CKD.

  12. ECG abnormalities in patients with chronic kidney disease

    International Nuclear Information System (INIS)

    Shafi, S.; Saleem, M.; Anjum, R.; Abdullah, W.; Shafi, T.

    2017-01-01

    Chronic kidney disease (CKD) is associated with increased risk of cardiovascular disease. Electrocardiographic (ECG) abnormalities are common in CKD patients. However, there is variation in literature regarding frequency of ECG abnormalities in CKD patients and limited information in local population. Methods: The study design was cross-sectional in nature. All patients between ages of 20-80 years with CKD not previously on renal replacement therapy who were admitted to nephrology ward at a tertiary care facility over a 6-month period were included. All patients underwent 12 lead electrocardiograms (ECG). ECG abnormalities were defined based on accepted standard criteria. Results: Total number of patients included in the study was 124. Mean age of all patients was 49.9+-13.8 years, 106 (84.8%) had hypertension, 84 (70%) had diabetes mellitus, and 35 (29.9%) had known cardiovascular disease. Mean serum creatinine was 7.2+-3.4 mg/dl, mean eGFR was 10.6+-9.2 ml/min/1.73 m/sup 2/. Overall 78.4% of all CKD patients have one or more ECG abnormality. Left ventricular hypertrophy (40%), Q waves (27.2%), ST segment elevation or depression (23.4%), prolonged QRS duration (19.2%), tachycardia (17.6%) and left and right atrial enlargement (17.6%) were the most common abnormalities. Conclusion: ECG abnormalities are common in hospitalized CKD patients in local population. All hospitalized CKD patients should undergo ECG to screen for cardiovascular disease. (author)

  13. Complementary bodybuilding: A potential risk for permanent kidney disease

    Directory of Open Access Journals (Sweden)

    Wael El-Reshaid

    2018-01-01

    Full Text Available We report our experience of renal disease associated with bodybuilders who had been on high-protein diet, anabolic androgenic steroids (AASs, and growth hormone (GH for years. A total of 22 adult males who volunteered information about use of high protein diet and AAS or GH were seen over a six-year period with renal disease. Kidney biopsy revealed focal segmental glomerulosclerosis (FSGS in eight, nephroangiosclerosis in four, chronic interstitial nephritis in three, acute interstitial nephritis in two, nephrocalcinosis with chronic interstitial nephritis in two, and single patients with membranous glomerulopathy, crescentic glomerulopathy, and sclerosing glomerulonephritis. Patients with FSGS had a longer duration of exposure, late presentation, and worse prognosis. Those with interstitial disease had shorter exposure time and earlier presentation and had improved or stabilized after discontinuation of their practice. There is a need for health education for athletes and bodybuilders to inform them about the risks of renal disease involved with the use of high-protein diet, AAS, and GH.

  14. Complementary bodybuilding: A potential risk for permanent kidney disease.

    Science.gov (United States)

    El-Reshaid, Wael; El-Reshaid, Kamel; Al-Bader, Shaikha; Ramadan, Ahmad; Madda, John Patrick

    2018-01-01

    We report our experience of renal disease associated with bodybuilders who had been on high-protein diet, anabolic androgenic steroids (AASs), and growth hormone (GH) for years. A total of 22 adult males who volunteered information about use of high protein diet and AAS or GH were seen over a six-year period with renal disease. Kidney biopsy revealed focal segmental glomerulosclerosis (FSGS) in eight, nephroangiosclerosis in four, chronic interstitial nephritis in three, acute interstitial nephritis in two, nephrocalcinosis with chronic interstitial nephritis in two, and single patients with membranous glomerulopathy, crescentic glomerulopathy, and sclerosing glomerulonephritis. Patients with FSGS had a longer duration of exposure, late presentation, and worse prognosis. Those with interstitial disease had shorter exposure time and earlier presentation and had improved or stabilized after discontinuation of their practice. There is a need for health education for athletes and bodybuilders to inform them about the risks of renal disease involved with the use of high-protein diet, AAS, and GH.

  15. [The French Chronic Kidney Disease-Renal Epidemiology and Information Network (CKD-REIN) cohort study: To better understand chronic kidney disease].

    Science.gov (United States)

    Stengel, Bénédicte; Combe, Christian; Jacquelinet, Christian; Briançon, Serge; Fouque, Denis; Laville, Maurice; Frimat, Luc; Pascal, Christophe; Herpe, Yves-Édouard; Morel, Pascal; Deleuze, Jean-François; Schanstra, Joost P; Pisoni, Ron L; Robinson, Bruce M; Massy, Ziad A

    2016-04-01

    Preserving kidney function and improving the transition from chronic kidney disease to end stage is a research and healthcare challenge. The national Chronic Kidney Disease-Renal Epidemiology and Information Network (CKD-REIN) cohort was established to identify the determinants, biomarkers and practice patterns associated with chronic kidney disease outcomes. The study will include more than 3000 adult patients with moderate to advanced chronic kidney disease from a representative sample of 40 nephrology clinics with respect to regions and legal status, public or private. Patients are recruited during a routine visit and followed for 5 years, before and after starting renal replacement therapy. Patient-level clinical, biological, and lifestyle data are collected annually, as well as provider-level data on clinical practices, coordinated with the International Chronic Kidney Disease Outcomes and Practice Pattern Study. Blood and urine samples are stored in a biobank. Major studied outcomes include survival, patient-reported outcomes, disease progression and hospitalizations. More than 13,000 eligible patients with chronic kidney disease were identified, 60% with stage 3 and 40% with stage 4. Their median age is 72 years [interquartile range, 62-80 years], 60% are men and 38% have diabetes. By the end of December 2015, 2885 patients were included. The CKD-REIN cohort will serve to improve our understanding of chronic kidney disease and provide evidence to improve patient survival and quality of life as well as health care system performances. Copyright © 2016 Association Société de néphrologie. All rights reserved.

  16. The association between individual counselling and health behaviour change: the See Kidney Disease (SeeKD) targeted screening programme for chronic kidney disease

    OpenAIRE

    Galbraith, Lauren; Hemmelgarn, Brenda; Manns, Braden; Samuel, Susan; Kappel, Joanne; Valk, Nadine; Ronksley, Paul

    2016-01-01

    Background Health behaviour change is an important component of management for patients with chronic kidney disease (CKD); however, the optimal method to promote health behaviour change for self-management of CKD is unknown. The See Kidney Disease (SeeKD) targeted screening programme screened Canadians at risk for CKD and promoted health behaviour change through individual counselling and goal setting. Objectives The objectives of this study are to determine the effectiveness of individual co...

  17. Oral health in patients with chronic kidney disease - emphasis on periodontitis

    OpenAIRE

    Nylund, Karita

    2017-01-01

    ORAL HEALTH IN PATIENTS WITH CHRONIC KIDNEY DISEASE - EMPHASIS ON PERIODONTITIS Background: Periodontitis is a common bacteria-induced chronic inflammatory disease with mild symptoms. It leads to destruction of the periodontium and finally to tooth loss in a susceptible patient. Periodontitis is associated with many systemic diseases such as diabetes, atherosclerosis, cardiovascular diseases, and chronic kidney disease (CKD) through low-grade systemic inflammation. However, no causality c...

  18. Hepcidin: an important iron metabolism regulator in chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Sandra Azevedo Antunes

    Full Text Available Abstract Anemia is a common complication and its impact on morbimortality in patients with chronic kidney disease (CKD is well known. The discovery of hepcidin and its functions has contributed to a better understanding of iron metabolism disorders in CKD anemia. Hepcidin is a peptide mainly produced by hepatocytes and, through a connection with ferroportin, it regulates iron absorption in the duodenum and its release of stock cells. High hepcidin concentrations described in patients with CKD, especially in more advanced stages are attributed to decreased renal excretion and increased production. The elevation of hepcidin has been associated with infection, inflammation, atherosclerosis, insulin resistance and oxidative stress. Some strategies were tested to reduce the effects of hepcidin in patients with CKD, however more studies are necessary to assess the impact of its modulation in the management of anemia in this population.

  19. Assessment of diet in chronic kidney disease female predialysis patients

    Directory of Open Access Journals (Sweden)

    Dariusz Włodarek

    2014-11-01

    Full Text Available [b]introduction and objective[/b]. Nutrition is important in the therapy of predialysis patients. The aim of the presented single-centre descriptive study was to assess the diet in chronic kidney disease female predialysis patients with no previous dietary intervention, in comparison with recommendations, as well as the analysis of the energy, protein and phosphate intake in correlation with chosen laboratory measurements. [b]materials and methods.[/b] The research was carried out in 31 female predialysis patients with CKD of different etiology, aged 29–79 years (GFR: 19.4±9.7ml/min/1.73m [sup]2[/sup] . Main outcome measures were self-reported data from three-day dietary recall. Nutrients content and energy value of diet were compared with guidelines for chronic kidney disease patients or, in case of nutrients when they are not settled, with the recommendations for healthy women. [b]results[/b]. All patients had a lower energy intake than the recommended level. At the same time, 35.8% of patients were characterised by improper protein intake – too low or too high. The majority of patients had low intake of most of vitamins and minerals. The total, animal and plant protein were positively correlated with the energy value of diet and with amount of most of the nutrients. Values of GFR were positively correlated with animal protein intake, while phosphate and creatinine in blood were negatively correlated with total and animal protein intake. [b]conclusions[/b]. The study highlights that diet of CKD predialysis patients with no previous dietary intervention is not properly balanced.

  20. Epidemiological Transition of End-Stage Kidney Disease in Oman.

    Science.gov (United States)

    Al Ismaili, Faisal; Al Salmi, Issa; Al Maimani, Yaqoub; Metry, Abdul Massiah; Al Marhoobi, Humood; Hola, Alan; Pisoni, Ronald L

    2017-01-01

    The number of persons receiving renal replacement therapy (RRT) is estimated at more than 2.5 million worldwide, and is growing by 8% annually. Registries in the developing world are not up to standards compared to the United States Renal Data System (USRDS). Herein we examine the causes, progression, and magnitude of end-stage kidney disease (ESKD) over 3 decades in Oman. We examined ESKD data from 1983 to 2013. Data from 1998 to 2013 were obtained through an Information Management System. Data before 2008 were collected from patients' files. A questionnaire based on USRDS form 2728 was completed by nephrologists once a citizen reached ESKD. A total of 4066 forms were completed, with a response rate of 90% (52% male). The mean (SD) age was 50.1 (14.0) years. By 31 December 2013, there were 2386 patients alive on RRT, of whom 1206 were on hemodialysis (50.5%), 1080 were living with a functioning kidney transplant (45.3%), and 100 were receiving peritoneal dialysis (4.2%). The incidence of ESKD on RRT was 21, 75, and 120 per million population in 1983, 2001, and 2013, respectively. Similarly, the prevalence of ESKD was 49, 916, and 2386 in 1983, 2001, and 2013 respectively. Among patients with ESKD on RRT, a progressive rise was seen in diabetic nephropathy, with 5.8%, 32.1%, and 46% in 1983, 2001, and 2013 respectively. The incidence and prevalence of ESKD has increased progressively over last 30 years. This is anticipated to continue at an even higher rate in view of the progressive rise in noncommunicable diseases. Continuous improvement in registries is required to improve capturing of ESKD patients for providing accurate data to health authorities, and enhancing public awareness of the magnitude, future trends, treatments, and outcomes regarding ESKD.

  1. Prevalence of chronic kidney disease in Peruvian primary care setting.

    Science.gov (United States)

    Herrera-Añazco, Percy; Taype-Rondan, Alvaro; Lazo-Porras, María; Alberto Quintanilla, E; Ortiz-Soriano, Victor Manuel; Hernandez, Adrian V

    2017-07-19

    Chronic Kidney Disease (CKD) is a worldwide public health problem. There are few studies in Latin America, especially in primary care settings. Our objective was to determine the prevalence, stages, and associated factors of CKD in primary care setting. We did a retrospective secondary analysis of a database from the Diabetes and Hypertension Primary Care Center of the Peruvian Social Security System (EsSalud) in Lima, Peru. We defined CKD as the presence of eGFR 30 mg/day in 24 h, according to Kidney Disease: Improving Global Outcomes (KDIGO). Factors associated with CKD were evaluated with Poisson Regression models; these factors included age, gender, type 2 diabetes mellitus (DM2), hypertension (HTN), body mass index (BMI), and uric acid. Associations were described as crude and adjusted prevalence ratios (PR) and their 95% confidence intervals (95% CI). We evaluated 1211 patients (women [59%], mean age 65.8 years [SD: 12.7]). Prevalence of CKD was 18%. Using the estimated glomerular filtration rate (eGFR), the prevalence was 9.3% (95% CI 5.3 - 13.3) in patients without HTN or DM2; 20.2% (95% CI 17.6 - 22.8) in patients with HTN, and 23.9% (95% CI 19.4 - 28.4) in patients with DM2. The most common stages were 1 and 2 with 41.5% and 48%, respectively. Factors associated with CKD in the adjusted analysis were: age in years (PR = 1.03, 95% CI 1.01 - 1.04), DM2 (PR = 3.37, 95% CI 1.09 - 10.39), HTN plus DM2 (PR = 3.90, 95% CI 1.54 - 9.88), and uric acid from 5 to DM2, older age and hyperuricemia have higher prevalence of CKD.

  2. Patient education for phosphorus management in chronic kidney disease

    Directory of Open Access Journals (Sweden)

    Kalantar-Zadeh K

    2013-05-01

    Full Text Available Kamyar Kalantar-ZadehHarold Simmons Center for Kidney Disease Research and Epidemiology, Division of Nephrology and Hypertension, University of California Irvine’s School of Medicine, Irvine, CA, USAObjectives: This review explores the challenges and solutions in educating patients with chronic kidney disease (CKD to lower serum phosphorus while avoiding protein insufficiency and hypercalcemia.Methods: A literature search including terms “hyperphosphatemia,” “patient education,” “food fatigue,” “hypercalcemia,” and “phosphorus–protein ratio” was undertaken using PubMed.Results: Hyperphosphatemia is a strong predictor of mortality in advanced CKD and is remediated via diet, phosphorus binders, and dialysis. Dietary counseling should encourage the consumption of foods with the least amount of inorganic or absorbable phosphorus, low phosphorus-to-protein ratios, and adequate protein content, and discourage excessive calcium intake in high-risk patients. Emerging educational initiatives include food labeling using a “traffic light” scheme, motivational interviewing techniques, and the Phosphate Education Program – whereby patients no longer have to memorize the phosphorus content of each individual food component, but only a “phosphorus unit” value for a limited number of food groups. Phosphorus binders are associated with a clear survival advantage in CKD patients, overcome the limitations associated with dietary phosphorus restriction, and permit a more flexible approach to achieving normalization of phosphorus levels.Conclusion: Patient education on phosphorus and calcium management can improve concordance and adherence and empower patients to collaborate actively for optimal control of mineral metabolism.Keywords: hyperphosphatemia, renal diet, phosphorus binders, educational programs, food fatigue, concordance

  3. Prevalence of anemia in predialysis chronic kidney disease patients

    Directory of Open Access Journals (Sweden)

    FAM Shaheen

    2011-01-01

    Full Text Available To evaluate the prevalence of anemia in a large cohort that comprises patients in different stages of chronic kidney disease (CKD in the kingdom of Saudi Arabia (KSA, we conducted a multi-center cross-sectional study of a cohort of CKD patients who have not started dialysis. The study patients were recruited from the nephrology clinics in 11 different medical centers distributed all over the regions of the KSA. For the estimated glomerular filtration rate (GFR, we used the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI equation. There were 250 study patients who fulfilled the criteria for the study. The patients were stratified according to their GFR as follows: stage 1: 19 patients, stage 2: 35 patients, stage 3: 67 patients, stage 4: 68 patients, and stage 5: 61 patients. The composite of proteinuria and abnormal imaging in stages 1 and 2 was satisfied in 100% of the cases. The prevalence of anemia was elevated for the hemoglobin levels below 12 g/dL (the level at which the evaluation of anemia in CKD should be initiated in the different stages of CKD, that is, 42%, 33%, 48%, 71%, and 82% in the stages from 1 to 5, respectively. The prevalence was also elevated for the hemoglobin levels below 11 g/dL (the minimum hemoglobin level at which therapy should be initiated with erythropoietin, that is, 21%, 17%, 31%, 49%, and 72%, respectively for stages from 1 to 5. In conclusion, we found a large prevalence of anemia among the CKD population in Saudi Arabia, and the burden of patients who require treatment with erythropoietin is considerably large. However, the response to therapy will not require large doses according to the availability of long-acting erythropoiesis stimulating agents, which will render the therapy more convenient and less expensive.

  4. Diet and polycystic kidney disease: A pilot intervention study.

    Science.gov (United States)

    Taylor, Jacob M; Hamilton-Reeves, Jill M; Sullivan, Debra K; Gibson, Cheryl A; Creed, Catherine; Carlson, Susan E; Wesson, Donald E; Grantham, Jared J

    2017-04-01

    Dietary sodium, protein, acid precursors, and water have been linked to cyst growth in polycystic kidney disease; yet, no studies in patients have examined the feasibility of using a dietary intervention that controls all of these factors. The aim of this study was to determine if a diet, appropriate for persons of most ages, reduces the excretion of sodium, urea, acid, and decreases mean urine osmolality while gaining acceptance by patients with autosomal dominant polycystic kidney disease (ADPKD). Twelve adults with ADPKD enrolled in a pre-post pilot feasibility study and served as their own controls. Individuals consumed their usual diet for one week then for four weeks followed an isocaloric diet lower in sodium and protein and higher in fruits, vegetables, and water. Three-day diet records and two 24-h urine samples were collected at baseline, week 2, and week 4 visits; blood pressure, weight, and serum were obtained at all three visits. A modified nutrition hassles questionnaire was completed on the last visit. During the dietary intervention, subjects (n = 11) consumed less sodium, protein, and dietary acid precursors 36%, 28%, and 99%, respectively, and increased fluid intake by 42%. Urinary sodium, urea, net acid excretion, osmoles, and osmolality decreased 20%, 28%, 20%, 37%, and 15%, respectively; volume increased 35%. Urine changes were in accord with the diet record. Ninety-one percent of participants reported that none of the hassles were worse than "somewhat severe", and most participants felt "somewhat confident" or "very confident" that they could manage the new diet. A majority of adult patients with ADPKD successfully prepared and followed a composite diet prescription with decreased sodium, protein, acid precursors, and increased fluid intake. This trail was registered at ClinicalTrials.gov (NCT01810614). Copyright © 2016 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

  5. Renal function trajectory is more important than chronic kidney disease stage for managing patients with chronic kidney disease.

    Science.gov (United States)

    Rosansky, Steven J

    2012-01-01

    Management of patients with chronic kidney disease (CKD) emphasizes a current level of function as calculated from the modification of diet in renal disease glomerulofiltration rate equations (eGFR) and proteinuria for staging of CKD. Change in a patient's eGFR over time (renal function trajectory) is an additional and potentially more important consideration in deciding which patients will progress to the point where they will require renal replacement therapy (RRT). Many patients with CKD 3-5 have stable renal function for years. Proteinuria/albuminuria is a primary determinant of renal trajectory which may be slowed by medications that decrease proteinuria and/or aggressively lower blood pressure. A renal trajectory of >3 ml/min/1.73 m(2)/year may relate to a need for closer renal follow-up and increased morbidity and mortality. Additional CKD population-based studies need to examine the relationship of renal trajectory to: baseline renal function; acute kidney injury episodes; age, race, sex and primary etiologies of renal disease; blood pressure control and therapies; dietary protein intake; blood glucose control in diabetics and the competitive risk of death versus the requirement for renal replacement therapy. In the elderly CKD 4 population with significant comorbidities and slow decline in renal function, the likelihood of death prior to the need for RRT should be considered before placing AV access for dialysis. Prediction models of renal progression must account for the competitive risk of death as well as stable or improved renal function to be clinically useful. Copyright © 2012 S. Karger AG, Basel.

  6. 76 FR 64358 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting

    Science.gov (United States)

    2011-10-18

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, PAR09-247: Ancillary Studies in Liver... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting Pursuant to section 10(d) of the... Assistance Program Nos. 93.847, Diabetes, [[Page 64359

  7. 75 FR 38817 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting

    Science.gov (United States)

    2010-07-06

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, Acute Liver Failure Study. Date: July 22... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meeting Pursuant to section 10(d) of the... Domestic Assistance Program Nos. 93.847, Diabetes, Endocrinology and Metabolic Research; 93.848, Digestive...

  8. Inclusion of methods for early detection of chronic kidney disease in ...

    African Journals Online (AJOL)

    Background The burden and magnitude of chronic kidney disease (CKD) are enormous. The incidence and prevalence of chronic kidney disease are rising all over the world. Thus, there is the urgent and pressing need for methods of early detection of CKD, to be included in guidelines for management of noncommunicable ...

  9. The renal arterial resistive index and stage of chronic kidney disease in patients with renal allograft

    DEFF Research Database (Denmark)

    Winther, Stine O; Thiesson, Helle C; Poulsen, Lene N

    2012-01-01

    The study investigated the optimal threshold value of renal arterial resistive index as assessed by Doppler ultrasonography determining chronic kidney disease stage 4 or higher in patients with renal allograft.......The study investigated the optimal threshold value of renal arterial resistive index as assessed by Doppler ultrasonography determining chronic kidney disease stage 4 or higher in patients with renal allograft....

  10. How to preserve residual renal function in patients with chronic kidney disease and on dialysis?

    NARCIS (Netherlands)

    Krediet, Raymond T.

    2006-01-01

    A review is given on various aspects of GFR in patients with chronic kidney disease and in dialysis patients. These include the measurement of GFR, measures to preserve GFR in chronic kidney disease and dialysis, the importance of residual GFR in dialysis patients and factors that influence GFR in

  11. The challenges of chronic kidney disease in Nigeria and the way ...

    African Journals Online (AJOL)

    Background: Chronic kidney disease (CKD), is a worldwidehealth problem with a great burden and high cost of care mostly in developing countries like Nigeria. Chronic kidney disease is increasingworldwide at an annual incidence of 8%1. Amid rapid urbanization and adoption of western lifestyles, increasing rates of ...

  12. 78 FR 34663 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2013-06-10

    ... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, PAR-12-265 Ancillary Studies: The Microbiome in Child Health, Development and Obesity. Date: June 21, 2013. Time: 1:30 p.m. to 3:00 p.m. Agenda...

  13. 77 FR 36564 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2012-06-19

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Clinical Trial Planning Grants in Type 1 Diabetes. Date: July 12, 2012. Time: 4:00 p.m. to 5:30 p.m. Agenda: To review and evaluate grant... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the...

  14. 78 FR 36554 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2013-06-18

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Clinical Trials in Type 1 Diabetes (UC4) Meeting A. Date: July 17, 2013. Time: 1:30 p.m. to 2:30 p.m. Agenda: To review and evaluate grant... Institute of Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Clinical Trials in Type 1...

  15. 76 FR 30370 - National Institute of Diabetes and Digestive and Kidney Diseases; Meetings

    Science.gov (United States)

    2011-05-25

    ... Emphasis Panel; RFA-DK-10-012 Type 1 Diabetes Impact Award (DP3). Date: July 11, 2011. Time: 8 a.m. to 6 p... Institute of Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; NIDDK KUH-Fellowship Review... Diabetes and Digestive and Kidney Diseases; Meetings Notice of Closed Meetings Pursuant to section 10(d) of...

  16. 77 FR 28396 - National Institute of Diabetes and Digestive and Kidney Diseases Notice of Closed Meetings

    Science.gov (United States)

    2012-05-14

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, Training in Behavioral Research in Type 1 Diabetes. Date: June 11, 2012. Time: 9:00 a.m. to 11:30 a.m. Agenda: To review and evaluate grant... of Diabetes and Digestive and Kidney Diseases Special Emphasis Panel, Improving Adherence in Type 1...

  17. 77 FR 38075 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2012-06-26

    ... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Type 1 Diabetes Mouse Resource. Date: July 23, 2012. Time: 1 p.m. to 3 p.m. Agenda: To review and evaluate grant applications. Place... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the...

  18. 78 FR 18358 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2013-03-26

    ... Emphasis Panel; Biomarkers in Type 1 Diabetes. Date: April 10, 2013. Time: 4:30 p.m. to 5:30 p.m. Agenda... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Review of U34 Clinical Trial Planning... of Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; Review of U34 Clinical Trial...

  19. 76 FR 11501 - National Institute of Diabetes and Digestive and Kidney Diseases

    Science.gov (United States)

    2011-03-02

    ... DEPARTMENT OF HEALTH AND HUMAN SERVICES National Institutes of Health National Institute of Diabetes and Digestive and Kidney Diseases Amended Notice of Meeting Notice is hereby given of a change in the meeting of the National Institute of Diabetes and Digestive and Kidney Diseases Special Emphasis...

  20. 76 FR 12125 - National Institute of Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings

    Science.gov (United States)

    2011-03-04

    ... Diabetes and Digestive and Kidney Diseases; Notice of Closed Meetings Pursuant to section 10(d) of the... Diabetes and Digestive and Kidney Diseases Special Emphasis Panel; GenitoUrinary Development Molecular Anatomy Project (GUDMAP) Date: March 23, 2011. Time: 12 p.m. to 1 p.m. Agenda: To review and evaluate...