Abstract
Cis-dichlorodiammine platinum (II), or cisplatin, has emerged as a principal chemotherapeutic agent in the treatment of otherwise resistant solid tumors and is currently among the most widely used agents in the chemotherapy of cancer. The chief limit to its greater efficacy, however, is its nephrotoxicity, which has made it necessary both to lower its dosage and actively hydrate patients to reduce it. These techniques have proven to be only partially successful as renal failure occurs even at such low doses and especially after its repeated administration (1,2). Use of other means to protect the kidney (3–5) are only partially successful and of uncertain clinical application. It may not be possible to alter or prevent the renal toxicity of cisplatin, however, until a more basic understanding of that toxicity is obtained. This paper summarizes what is known about the biochemical and physiologic aspects of cisplatin nephrotoxicity and gives the results of some recent experiments into its possible mechanism.
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© 1988 Martinus Nijhoff Publishing, Boston
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Safirstein, R., Zelent, A.Z., Gordon, R. (1988). Cisplatin Nephrotoxicity: New Insights Into Mechanism. In: Hacker, M.P., Lazo, J.S., Tritton, T.R. (eds) Organ Directed Toxicities of Anticancer Drugs. Developments in Oncology, vol 53. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2023-4_17
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