Division of Nephrology, Department of Medicine, Penn State College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania

Correspondence: W. Brian Reeves, M.D., Division of Nephrology, 500 University Dr., Hershey, PA 17033. E-mail: wreeves@psu.edu

Abstract

Inflammatory cytokines in acute renal failure. A growing body of evidence indicates that inflammatory mechanisms contribute to toxin-induced acute renal failure as well as ischemia/reperfusion injury. A role for tumor necrosis factor- (TNF-) in mediating the inflammatory injury in cisplatin-induced acute renal failure has recently been established. Cisplatin induces the expression of TNF- and TNF receptor subtype 2 (TNFR2) within the kidney. Genetic deletion of either TNF- or TNFR2 substantially reduces cisplatin-induced renal failure and also necrosis and apoptosis within the kidney. Studies will be required to determine if pharmacologic inhibition of TNF- might reduce cisplatin-induced renal failure in humans.