Pathogenetic mechanisms in nephrotoxic acute renal failure.
Despite marked variations in the chemical nature of nephrotoxic agents, most probably trigger lethal tubular injury via activation of a limited number of pathogenetic pathways. Elucidation of these pathways has been an area of intense investigation, with the hope that the knowledge obtained might lead to new interventions for preventing acute renal failure. The roles of altered cellular energetics, oxidant stress, cellular calcium overload, and deranged phospholipid homeostasis have undergone intense scrutiny. Recently, the participation of cytoskeletal rearrangements and apoptosis have been increasingly assessed. The purpose of this article is to provide a brief overview of this broad and evolving area of investigation.
Zager
R A
RA
Department of Medicine, the University of Washington, Seattle 98104, USA.
D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D017209:Apoptosis; D002118:Calcium / Q000378:metabolism; D064420:Drug-Related Side Effects and Adverse Reactions; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D010743:Phospholipids / Q000378:metabolism
D010743:Phospholipids; D002118:Calcium