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Pendred, pendrin, pseudohypoaldosteronism type II, and renal tubular acidosis

Item Type:Editorial
Title:Pendred, pendrin, pseudohypoaldosteronism type II, and renal tubular acidosis
Creators Name:Luft, F.C. and Wagner, C.A.
Abstract:The sodium chloride cotransporter is regulated by the with-no-lysine kinases 1 and 4. Mutations in these genes are responsible for Mendelian hypertension, increased sodium chloride cotransporter activity, metabolic acidosis, and hyperkalemia. Explaining metabolic acidosis and hyperkalemia has been difficult. We now learn that the versatile bicarbonate-chloride exchanger, pendrin, is important in the process. As a result, we are confronted with still another mechanism causing renal tubular acidosis.
Keywords:Hyperkalemia, Hypertension, Pseudohypoaldosteronism, Renal Tubular Acidosis, Sodium Chloride Symporters, Animals, Mice
Source:Kidney International
ISSN:0085-2538
Publisher:Elsevier (U.S.A.)
Volume:94
Number:3
Page Range:457-459
Date:September 2018
Official Publication:https://doi.org/10.1016/j.kint.2018.05.024
PubMed:View item in PubMed

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