title: Emerging therapies for acute renal failure.
abstract: Ischemia is the most common cause of acute renal failure (ARF). In the last decade, several new and important pathophysiological mechanisms that underlie the renal dysfunction have been discovered. These pathophysiological mechanisms include the role of both calcium and calcium-dependent enzymes, oxidant stress, loss of polarity of the tubular cell, tubular obstruction and arginine-glycine-aspartic acid (RGD) peptides, neutrophils, intracellular adhesion molecules (ICAM), and growth factors. A better understanding of tubular and vascular mechanisms has led to therapeutic studies in animals and clinical trials in humans. In this review, the pathophysiology of ischemic ARF will be correlated with the rationale for both current and future therapies.
authors.affiliation: Department of Medicine, University of Colorado School of Medicine, Denver 80262, USA.
authors.forename: C L
authors.initials: CL
authors.lastname: Edelstein
authors.forename: H
authors.initials: H
authors.lastname: Ling
authors.forename: A
authors.initials: A
authors.lastname: Wangsiripaisan
authors.forename: R W
authors.initials: RW
authors.lastname: Schrier
mesh_terms: D058186:Acute Kidney Injury / Q000503:physiopathology* / Q000628:therapy*; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000502:physiology; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002154:Calpain / Q000378:metabolism; D006133:Growth Substances / Q000627:therapeutic use; D006801:Humans; D007684:Kidney Tubules / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D010084:Oxidation-Reduction
chemical_list: D002121:Calcium Channel Blockers; D006133:Growth Substances; D009569:Nitric Oxide; D009320:Atrial Natriuretic Factor; D002154:Calpain