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Cellular Mechanisms of Acute Ischemic Injury in the Kidney

Cellular Mechanisms of Acute Ischemic Injury in the Kidney Hypoxic injury to tubular cells represents an early event in acute renal failure. Although important advances have been made in the understanding of hypoxic injury at the cellular level (e.g. loss of cell polarity, production of free radicals, calcium entry, and the activation of genes for protection or regeneration), the basic mechanisms responsible for organ failure remain elusive. The renal medulla, working on the brink of anoxia and being the site of concentration for many toxins, may be an important target for the synergistic events of hypoperfusion and nephrotoxic exposure that often precede human acute renal failure. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Medicine Annual Reviews

Cellular Mechanisms of Acute Ischemic Injury in the Kidney

Annual Review of Medicine , Volume 44 (1) – Feb 1, 1993

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References (22)

Publisher
Annual Reviews
Copyright
Copyright 1993 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0066-4219
eISSN
1545-326X
DOI
10.1146/annurev.me.44.020193.000331
pmid
8476249
Publisher site
See Article on Publisher Site

Abstract

Hypoxic injury to tubular cells represents an early event in acute renal failure. Although important advances have been made in the understanding of hypoxic injury at the cellular level (e.g. loss of cell polarity, production of free radicals, calcium entry, and the activation of genes for protection or regeneration), the basic mechanisms responsible for organ failure remain elusive. The renal medulla, working on the brink of anoxia and being the site of concentration for many toxins, may be an important target for the synergistic events of hypoperfusion and nephrotoxic exposure that often precede human acute renal failure.

Journal

Annual Review of MedicineAnnual Reviews

Published: Feb 1, 1993

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