Summary
The kidney plays a critical role in regulating water homeostasis through specific
proteins highly expressed in the kidney, called aquaporins, allowing water permeation at a high rate. This brief review focuses on some nephropathies
associated with impaired urinary concentrating ability and in particular analyzes
the role of aquaporin 2 in hypercalciuria, the most common metabolic abnormality in
patients with nephrolithiasis. Specifically, this review discusses the relationship
between hypercalciuria and impaired aquaporin 2−mediated water handling in both acquired
and inherited disorders characterized by hypercalciuria, including those affecting
the sensor of extracellular calcium concentration, the calcium-sensing receptor, which
represents the principal target for extracellular calcium regulation of several tissues
including parathyroid glands and kidney. In the kidney, the calcium-sensing receptor
regulates renal calcium excretion and influences the transepithelial movement of water
and other electrolytes. Understanding the molecular basis of alteration of kidney
concentrating ability found in hypercalciuria will help for devising strategies for
reducing the risk of nephrocalcinosis, nephrolithiasis, and renal insufficiency.
Keywords
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Article info
Footnotes
Supported by grants from Telethon (GGP04202 to G.V.), PRIN (Research Program of National Interest to G.V.), Centro di Eccellenza di Genomica in campo Biomedico ed Agrario (CEGBA), and from the Regional Project 2007 (G.V.).
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© 2008 Elsevier Inc. Published by Elsevier Inc. All rights reserved.