Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Mediators of Ischemic Renal Injury

Mediators of Ischemic Renal Injury Acute renal failure is a serious consequence of renal ischemia. The diagnosis carries an associated high mortality rate. When blood flow to the kidneys is inadequate to supply metabolic demands, a number of pathophysiological changes occur that ultimately result in cell death and tissue dysfunction, characterized by a marked reduction in glomerular filtration rate and associated accumulation of systemic toxins and disorders of fluid and electrolyte metabolism. In this chapter we review the factors that have been implicated as mediators of the renal tissue damage associated with ischemia and reperfusion. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Medicine Annual Reviews

Mediators of Ischemic Renal Injury

Annual Review of Medicine , Volume 39 (1) – Feb 1, 1988

Loading next page...
 
/lp/annual-reviews/mediators-of-ischemic-renal-injury-FTD8kY7ktU

References (52)

Publisher
Annual Reviews
Copyright
Copyright 1988 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0066-4219
eISSN
1545-326X
DOI
10.1146/annurev.me.39.020188.002531
pmid
3285790
Publisher site
See Article on Publisher Site

Abstract

Acute renal failure is a serious consequence of renal ischemia. The diagnosis carries an associated high mortality rate. When blood flow to the kidneys is inadequate to supply metabolic demands, a number of pathophysiological changes occur that ultimately result in cell death and tissue dysfunction, characterized by a marked reduction in glomerular filtration rate and associated accumulation of systemic toxins and disorders of fluid and electrolyte metabolism. In this chapter we review the factors that have been implicated as mediators of the renal tissue damage associated with ischemia and reperfusion.

Journal

Annual Review of MedicineAnnual Reviews

Published: Feb 1, 1988

There are no references for this article.