Abstract

The clinical condition of acute renal failure (ARF) can be caused by a diverse number of renal injuries, but it is generally characterized by a sharp reduction in the glomerular filtration rate (GFR). A lipid mediator, platelet activating factor (PAF), may be one of the entities responsible for causing the hemodynamic changes in the ARF kidney because it can act as a vasodilator or vasoconstrictor, depending upon its concentration. This review examines the action and mechanisms of PAF in experimental animal models of ischemia and nephrotoxicity, as well as renal failure associated with extrarenal disease. While further research is necessary before extrapolating our current knowledge of PAF into the prevention of renal failure of therapeutic intervention using PAF antagonists in human ARF, there is reasonable evidence to support its role as a mediator of the decrease in GFR characteristic of ARF.

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