ArticleProceedings of the National Academy of Sciences of the United States of America1999
Diet-dependent hypercalciuria in transgenic mice with reduced CLC5 chloride channel expression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 67 citations in OpenAlex.
- Lentiviral vector mediated gene therapy for type I Dent disease ameliorates Dent disease-like phenotypes for three months in ClC-5 null mice.Molecular therapy. Methods & clinical development · 2022Article
- Albumin uptake and processing by the proximal tubule: physiological, pathological, and therapeutic implications.Physiological reviews · 2022Review
- Genetics and phenotypic heterogeneity of Dent disease: the dark side of the moon.Human genetics · 2021Review
- Comparison of clinical and genetic characteristics between Dent disease 1 and Dent disease 2.Pediatric nephrology (Berlin, Germany) · 2020Article
- Dent disease: A window into calcium and phosphate transport.Journal of cellular and molecular medicine · 2019Review
- Complexity of the 5'UTR region of the CLCN5 gene: eleven 5'UTR ends are differentially expressed in the human kidney.BMC medical genomics · 2014Article
- The proximal tubule and albuminuria: really!Journal of the American Society of Nephrology : JASN · 2014Review
- Receptor-mediated endocytosis and endosomal acidification is impaired in proximal tubule epithelial cells of Dent disease patients.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Suppression of intestinal calcium entry channel TRPV6 by OCRL, a lipid phosphatase associated with Lowe syndrome and Dent disease.American journal of physiology. Cell physiology · 2012Article
- Dent's disease: clinical features and molecular basis.Pediatric nephrology (Berlin, Germany) · 2011Article
- Hypercalciuria in patients with CLCN5 mutations.Pediatric nephrology (Berlin, Germany) · 2006Article
- Use of knock-out mouse models for the study of renal ion channels.The Journal of membrane biology · 2004Review
- The voltage-dependent Cl(-) channel ClC-5 and plasma membrane Cl(-) conductances of mouse renal collecting duct cells (mIMCD-3).The Journal of physiology · 2001Article
- Functional inhibition of native volume-sensitive outwardly rectifying anion channels in muscle cells and Xenopus oocytes by anti-ClC-3 antibody.The Journal of physiology · 2001Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dent's disease is an X-linked inherited disorder characterized by hypercalciuria, nephrocalcinosis, nephrolithiasis, low molecular weight proteinuria, Fanconi's syndrome, and renal failure. It is caused by inactivating mutations in CLC5, a member of the CLC voltage-gated chloride channel family. CLC5 is known to be expressed in the endosomal compartment of the renal proximal tubule, where it may be required for endosomal acidification and trafficking. Although the Fanconi's syndrome and low molecular weight proteinuria in Dent's disease can be explained by disruption of endosomal function in this nephron segment, the pathogenesis of the hypercalciuria in this disease is unknown. We have generated transgenic mice (RZ) with reduced CLC5 expression by introduction of an antisense ribozyme targeted against CLC5. RZ mice are markedly hypercalciuric compared with nontransgenic control mice, at a time when their serum electrolytes and renal function are otherwise normal. This suggests that hypercalciuria in Dent's disease is a direct consequence of CLC5 hypofunction and is not attributable to a gain of function by mutant CLC5, an effect of modifier genes, or a secondary result of nonspecific renal injury. Surprisingly, hypercalciuria in RZ mice is abolished by dietary calcium deprivation, suggesting that the hypercalciuria may be attributable to gastrointestinal hyperabsorption of calcium rather than a renal calcium leak.
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