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Mechanisms in Hyperkalemic Renal Tubular Acidosis

Department of Medical Genetics, University of Cambridge, Cambridge, United Kingdom

Correspondence: Prof. Fiona E. Karet, Cambridge Institute for Medical Research (Room 4.3), Addenbrooke's Hospital Box 139, Hills Road, Cambridge, CB2 0XY, UK. Phone: +44-1223-762617; Fax: +44-1223-331206; E-mail: fek1000{at}cam.ac.uk

The form of renal tubular acidosis associated with hyperkalemia is usually attributable to real or apparent hypoaldosteronism. It is therefore a common feature in diabetes and a number of other conditions associated with underproduction of renin or aldosterone. In addition, the close relationship between potassium levels and ammonia production dictates that hyperkalemia per se can lead to acidosis. Here I describe the modern relationship between molecular function of the distal portion of the nephron, pathways of ammoniagenesis, and hyperkalemia.

Copyright © 2009 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673