Cell biology and molecular mechanisms of injury in ischemic acute renal failure

被引：247

作者：

Sheridan, AM

Bonventre, JV

机构：

[1] Harvard Univ, Sch Med, Dept Med, Charlestown, MA 02129 USA

[2] Harvard MIT Div Hlth Sci & Technol, Charlestown, MA 02129 USA

来源：

CURRENT OPINION IN NEPHROLOGY AND HYPERTENSION | 2000年 / 9卷 / 04期

关键词：

D O I：

10.1097/00041552-200007000-00015

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 pathogenesis of acute renal failure has been attributed to persistent vasoconstriction and leukocyte-endothelial interactions, resulting in inflammation and compromise of local blood flow to the outer medulla, the loss of tubular epithelial cell polarity with multiple functional sequelae, necrosis or apoptosis of epithelial cells, and the de-differentiation, migration and proliferation of surviving cells, In this paper, the authors present their views of pathophysiology of ischemic acute renal failure. Curr Opin Nephrol Hypertens 9:427-434. (C) 2000 Lippincott Williams & Wilkins.

引用

收藏

页码：427 / 434

页数：8

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