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Chloride Transport in the Kidney: Lessons from Human Disease and Knockout Mice

Zentrum für Molekulare Neurobiologie (ZMNH), Universität Hamburg, Hamburg, Germany

Address correspondence to: Dr. Thomas J. Jentsch, Zentrum für Molekulare Neurobiologie ZMNH, Universität Hamburg, Falkenried 94, D-20246 Hamburg, Germany. Phone: 49-40-42803-4741; Fax: 49-40-42803-4839; E-mail: jentsch{at}zmnh.uni-hamburg.de

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.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673