Mechanisms in Hyperkalemic Renal Tubular Acidosis

被引：103

作者：

Karet, Fiona E. ^{[1
]}

机构：

[1] Univ Cambridge, Dept Med Genet, Cambridge, England

来源：

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | 2009年 / 20卷 / 02期

基金：

英国惠康基金;

关键词：

THICK ASCENDING LIMB; TRIMETHOPRIM-INDUCED HYPERKALEMIA; AMMONIA PRODUCTION; ALDOSTERONE DEFICIENCY; DISTAL NEPHRON; PSEUDOHYPOALDOSTERONISM TYPE-1; POTASSIUM-TRANSPORT; INTRACELLULAR PH; PROXIMAL TUBULE; NH3; PRODUCTION;

D O I：

10.1681/ASN.2008020166

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

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.

引用

页码：251 / 254

页数：4

共 45 条

[1]

ABBOTT EC, 1966, CAN MED ASSOC J, V94, P1155

[2]

Aker S, 2001, EXP NEPHROL, V9, P332

[3]

ALTENBERG GA, 1990, MINER ELECTROL METAB, V16, P197

[4] HYPERKALEMIA AND RENAL-INSUFFICIENCY - ROLE OF SELECTIVE ALDOSTERONE DEFICIENCY AND TUBULAR UNRESPONSIVENESS TO ALDOSTERONE [J].