Chloride transport in the kidney: lessons from human disease and knockout mice

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Item Type:	Article
Title:	Chloride transport in the kidney: lessons from human disease and knockout mice
Creators Name:	Jentsch, T.J.
Abstract:	Knockout mouse models and human inherited diseases have provided important new insights into the physiologic role of chloride transport by CLC Cl(-) channels and KCC K-Cl co-transporters. ClC-K/barrtin Cl(-) channels are important for renal salt reabsorption and possibly for acid secretion by intercalated cells. The endosomal ClC-5 protein is crucial for proximal tubular endocytosis. Its disruption in mice and patients with Dent's disease leads to hypercalciuria and kidney stones through a pathologic cascade that may be entirely explained by an impairment of endocytosis. KCC4 is important for recycling Cl(-) for the basolateral anion exchanger in intercalated cells, as is evident from the renal tubular acidosis resulting from its knockout. Finally, both KCC3 and KCC4 are crucial for proximal tubular cell volume regulation.
Keywords:	Chloride Channels, Chlorides, Endocytosis, Ion Transport, Kidney, Kidney Diseases, Kidney Tubules, Membrane Proteins, Symporters, Animal Models, Animals, Mice
Source:	Journal of the American Society of Nephrology
ISSN:	1046-6673
Publisher:	American Society of Nephrology
Volume:	16
Number:	6
Page Range:	1549-1561
Date:	June 2005
Official Publication:	https://doi.org/10.1681/ASN.2005020207
PubMed:	View item in PubMed

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