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高钾性肾小管酸中毒的机制。

Mechanisms in hyperkalemic renal tubular acidosis.

作者信息

Karet Fiona E

机构信息

Cambridge Institute for Medical Research (Room 4.3), Addenbrooke's Hospital Box 139, Hills Road, Cambridge, CB2 0XY, UK.

出版信息

J Am Soc Nephrol. 2009 Feb;20(2):251-4. doi: 10.1681/ASN.2008020166. Epub 2009 Feb 4.

Abstract

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.

摘要

与高钾血症相关的肾小管酸中毒形式通常归因于真性或假性醛固酮减少症。因此,它是糖尿病以及其他一些与肾素或醛固酮生成不足相关疾病的常见特征。此外,钾水平与氨生成之间的密切关系表明,高钾血症本身可导致酸中毒。在此,我描述了肾单位远端的分子功能、氨生成途径和高钾血症之间的现代关系。

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