A mechanism for hyporeninemic hypoaldosteronism in chronic renal disease.
A mechanism for hyporeninemic hypoaldosteronism in chronic renal disease.
复制标题
慢性肾脏病低肾素性低醛固酮增多症的机制。
DOI：
10.1016/0026-0495(74)90032-8
复制
发表时间：
1974
期刊：
影响因子：
--
通讯作者：
E. S. Whang
中科院分区：
文献类型：
--
作者：
M. Oh;H. J. Carroll;J. E. Clemmons;A. Vagnucci;S. Levison;E. S. Whang
Selective aldosterone deficiency in chronic renal disease has been attributed to damage to the renin-producing mechanism. Four patients with selective aldosterone deficiency and chronic renal diseases were studied. These patients had hypertension, increased extracellular fluid volume, and increased total exchangeable sodium, unlikely concomitants of a clinical syndrome in which primary reduction in angiotensin generation led to deficient aldosterone secretion. In two patients who were treated with furosemide to produce sustained diminution in extracellular fluid volume, the gradual increase in plasma renin activity and plasma aldosterone indicated that physiologic suppression, not disease-induced damage, had been preventing elaboration of renin by juxtaglomerular apparatus. Salt and water retention associated with renal disease is proposed as the initial physiologic aberration.
