Potential Deleterious Effects of Vasopressin in Chronic Kidney Disease and Particularly Autosomal Dominant Polycystic Kidney Disease

被引：28

作者：

Meijer, E. ^{[1
]}

Boertien, W. E. ^{[1
]}

Zietse, R. ^{[2
]}

Gansevoort, R. T. ^{[1
]}

机构：

[1] Univ Groningen, Univ Med Ctr Groningen, Dept Internal Med, Div Nephrol, Groningen, Netherlands

[2] Erasmus MC, Dept Nephrol, Rotterdam, Netherlands

来源：

KIDNEY & BLOOD PRESSURE RESEARCH | 2011年 / 34卷 / 04期

关键词：

Vasopressin; Copeptin; Chronic kidney disease; Autosomal dominant polycystic kidney disease; Albuminuria; Proteinuria; Glomerular filtration rate; RENAL CONCENTRATING CAPACITY; GLOMERULAR-FILTRATION-RATE; RENIN-ANGIOTENSIN SYSTEM; RECEPTOR ANTAGONISTS; DIABETES-MELLITUS; ANTIDIURETIC ACTION; PLASMA VASOPRESSIN; SURROGATE MARKER; BRATTLEBORO RATS; SODIUM-EXCRETION;

D O I：

10.1159/000326902

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

The antidiuretic hormone vasopressin is crucial for regulating free water clearance in normal physiology. However, it has also been hypothesized that vasopressin has deleterious effects on the kidney. Vasopressin is elevated in animals and patients with chronic kidney disease. Suppression of vasopressin activity reduces proteinuria, renal hypertrophy, glomerulosclerosis and tubulointerstitial fibrosis in animal models. The potential detrimental influence of vasopressin is probably mediated by its effects on mesangial cell proliferation, renin secretion, renal hemodynamics, and blood pressure. In this review, we discuss the increasing body of evidence pointing towards the contribution of vasopressin to chronic kidney disease progression in general and to autosomal dominant polycystic kidney disease in particular. These data allude to the possibility that interventions directed at lowering vasopressin activity, for example by the administration of vasopressin receptor antagonists or by drinking more water, may be beneficial in chronic kidney disease. Copyright (C) 2011 S. Karger AG, Basel

引用

页码：235 / 244

页数：10

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