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Cisplatin is a potent chemotherapy agent which is used to treat a broad spectrum of solid cancers. However, its clinical use is limited due to its nephrotoxicity with a decline in the glomerular filtration rate that occur in 15-30% of patients. Multiple mechanisms contribute to renal dysfunction following exposure to cisplatin include tubular epithelial cell toxicity, vasoconstriction in the renal microvasculature, and increase the expression of proinflammatory cytokines. The most important manifestations of cisplatin nephrotoxicity are non oliguric acute renal failure (ARF) which can be progressive, hypomagnesemia, fanconi-like syndrome, and anemia. An increasing risk of ARF is associated with higher doses of cisplatin, previous cisplatin chemotherapy, underlying kidney dysfunction, and the concomitant use of other nephrotoxic agents. The standard approach to prevent cisplatin-induced nephrotoxicity is the administration of lower doses of cisplatin in combination with the administration of full intravenous isotonic saline before and after cisplatin administration. Although a number of pharmacologic agents including sodium thiosulfate, N-acetylcysteine, theophylline and glycine have been evaluated for prevention of nephrotoxicity, none have proved to have an established role, thus, additional clinical studies will be required to confirm their probable effects.

Keywords: Cisplatin, Cisplatin nephrotoxicity, chemotherapy

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