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Published in: Current Urology Reports 1/2013

01-02-2013 | Kidney Diseases (G Ciancio, Section Editor)

The Role of Claudin in Hypercalciuric Nephrolithiasis

Author: Jianghui Hou

Published in: Current Urology Reports | Issue 1/2013

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Abstract

Calcium nephrolithiasis is a common condition. Family-based genetic linkage studies and genome-wide association studies (GWASs) have uncovered a run of important candidate genes involved in renal Ca++ disorders and kidney stone diseases. The susceptible genes include NKCC2, ROMK and ClCkb/Barttin that underlie renal salt excretion; claudin-14, -16 and -19 that underlie renal Ca++ excretion; and CaSR that provides a sensing mechanism for the kidney to regulate salt, water and Ca++ homeostasis. Biological and physiological analyses have revealed the cellular mechanism for transepithelial Ca++ transport in the kidney that depends on the concerted action of these gene products. Although the individual pathogenic weight of the susceptible genes in nephrolithiasis remains unclear, perturbation of their expression or function compromises the different steps within the integrated pathway for Ca++ reabsorption, providing a physiological basis for diagnosing and managing kidney stone diseases.
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Metadata
Title
The Role of Claudin in Hypercalciuric Nephrolithiasis
Author
Jianghui Hou
Publication date
01-02-2013
Publisher
Current Science Inc.
Published in
Current Urology Reports / Issue 1/2013
Print ISSN: 1527-2737
Electronic ISSN: 1534-6285
DOI
https://doi.org/10.1007/s11934-012-0289-2

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