Ischemic acute renal failure: An inflammatory disease?

被引：692

作者：

Bonventre, JV

Zuk, A

机构：

[1] Brigham & Womens Hosp, Med Serv, Charlestown, MA USA

[2] Harvard Med Sch, Charlestown, MA USA

[3] Harvard Massachusetts Inst Technol, Div Hlth Sci & Technol, Charlestown, MA USA

[4] Beth Israel Deaconess Med Ctr, Ctr Matrix Biol, Boston, MA 02215 USA

[5] Beth Israel Deaconess Med Ctr, Dept Surg, Boston, MA 02215 USA

[6] Harvard Med Sch, Boston, MA 02215 USA

来源：

KIDNEY INTERNATIONAL | 2004年 / 66卷 / 02期

关键词：

acute kidney failure; injury; endothelium; epithelium; leukocyte; inflammatory mediators; preconditioning;

D O I：

10.1111/j.1523-1755.2004.761_2.x

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 [临床医学]; 100201 [内科学];

摘要：

Inflammation plays a major role in the pathophysiology of acute renal failure resulting from ischemia. In this review, we discuss the contribution of endothelial and epithelial cells and leukocytes to this inflammatory response. The roles of cytokines/chemokines in the injury and recovery phase are reviewed. The ability of the mouse kidney to be protected by prior exposure to ischemia or urinary tract obstruction is discussed as a potential model to emulate as we search for pharmacologic agents that will serve to protect the kidney against injury. Understanding the inflammatory response prevalent in ischemic kidney injury will facilitate identification of molecular targets for therapeutic intervention.

引用

页码：480 / 485

页数：6

共 70 条

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MECHANISMS OF FILTRATION FAILURE DURING POSTISCHEMIC INJURY OF THE HUMAN KIDNEY - A STUDY OF THE REPERFUSED RENAL-ALLOGRAFT [J].