[Experimental models of acute kidney failure]

Acute renal failure (ARF) is related to reversible tubular necrosis, usually caused by ischemia or toxic substances. Our knowledge of the pathophysiology of ARF stems from the study of animal models which reproduce either an ischemic or a toxic form of ARF. Classical studies using microdissection and micropuncture have characterized the salient mechanisms of ARF: vascular compromise with hypoperfusion and decrease in glomerular filtration rate, and tubular insult with cell necrosis and high intratubular pressure. More recent studies have emphasized the cellular and molecular events occurring during the course of ARF, including changes in cytoskeleton and matrix proteins, apoptosis and the role of Heat Shock Proteins. Endothelin and growth factors such as epidermal growth factor or hepatocyte growth factor seem to be important mediators in the regeneration phase of ARF. In various animal models, EGF, HGF or antagonists of endothelin receptors have a protective effect on renal function. These findings may be of clinical relevance, and suggest future therapeutic approaches in the treatment of ARF.