Cisplatin treatment causes tubulointerstitial injury to the kidneys. Common clinical syndromes associated with its use include acute renal failure and a magnesium wasting state. Routine fluid infusion therapy has markedly reduced the incidence of acute renal failure. However, methodologic limitations of most recent studies preclude confident conclusions regarding long-term effects of cisplatin treatment on renal function. Experimental and clinical evidence suggests that sulfhydryl metabolism and oxidative stress are central to cisplatin renal injury. Both in animals and humans, a variety of agents appear to alter renal uptale of cisplatin and its hemodynamic consequences, thus modulating nephrotoxicity. Thiosulfates and related agents have received most study. Other agents examined have included calcium channel blockers, bismuth, selenium, glycine, cimetidine, and probenecid.