Reactive oxygen species and acute renal failure

Karl A. Nath, Suzanne M. Norby

Research output: Contribution to journalComment/debate

313 Scopus citations

Abstract

Acute renal failure is commonly due to acute tubular necrosis (ATN), the latter representing an acute, usually reversible loss of renal function incurred from ischemic or nephrotoxic insults occurring singly or in combination. Such insults instigate a number of processes - hemodynamic alterations, aberrant vascular responses, sublethal and lethal cell damage, inflammatory responses, and nephron obstruction - that initiate and maintain ATN. Eventually, reparative and regenerative processes facilitate the resolution of renal injury and the recovery of renal function. Focusing mainly on ischemic ATN, this article reviews evidence indicating that the inordinate or aberrant generation of reactive oxygen species (ROS) may contribute to the initiation and maintenance of ATN. This review also discusses the possibility that ROS may instigate adaptive as well as maladaptive responses in the kidney with ATN, and raises the possibility that ROS may participate in the recovery phase of ATN. (C) 2000 by Excerpta Medica, Inc.

Original languageEnglish (US)
Pages (from-to)665-678
Number of pages14
JournalAmerican Journal of Medicine
Volume109
Issue number8
DOIs
StatePublished - Dec 1 2000

ASJC Scopus subject areas

  • Medicine(all)

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