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

Friedrich C. Luft | Zendy; Carsten A. Wagner | Zendy

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

Author(s) -

Friedrich C. Luft,

Carsten A. Wagner

Publication year - 2018

Publication title -

kidney international

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.499

H-Index - 276

eISSN - 1523-1755

pISSN - 0085-2538

DOI - 10.1016/j.kint.2018.05.024

Subject(s) - pseudohypoaldosteronism , pendrin , medicine , renal tubular acidosis , endocrinology , acidosis , distal renal tubular acidosis , metabolic acidosis , hyperkalemia , chemistry , biochemistry , transporter , gene

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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