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


Luft, Friedrich C; Wagner, Carsten A (2018). Pendred, pendrin, pseudohypoaldosteronism type II, and renal tubular acidosis. Kidney International, 94(3):457-459.

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.

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.

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Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Physiology
07 Faculty of Science > Institute of Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:September 2018
Deposited On:11 Sep 2018 14:49
Last Modified:11 Sep 2018 15:00
Publisher:Elsevier
ISSN:0085-2538
OA Status:Closed
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1016/j.kint.2018.05.024
PubMed ID:30143066

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