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-alpha (TNF-alpha) in mediating the inflammatory injury in cisplatin-induced acute renal failure has recently been established. Cisplatin induces the expression of TNF-alpha and TNF receptor subtype 2 (TNFR2) within the kidney. Genetic deletion of either TNF-alpha 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-alpha might reduce cisplatin-induced renal failure in humans.
Division of Nephrology, Department of Medicine, Penn State College of Medicine, Milton S. Hershey Medical Center, Hershey, PA 17033, USA.
Ganesan
G
Ramesh
W Brian
WB
Reeves
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000378:metabolism*; D002945:Cisplatin / Q000633:toxicity; D016207:Cytokines / Q000378:metabolism*; D006801:Humans; D007249:Inflammation; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000502:physiology; D015427:Reperfusion Injury / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D016207:Cytokines; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; D002945:Cisplatin