Abstract
Cancer chemotherapeutic agents classically affect populations of rapidly dividing cells, in both malignant and normal tissue. Hence the most commonly encountered toxic effects are in the bone marrow, gastrointestinal tract, gonadal tissue, and hair follicles. Several drugs in this group also affect other tissues, such as the kidney. This chapter examines those agents which have been implicated in nephrotoxicity in the clinical setting and presents the clinical manifestations and pathogenesis, as well as the effect of drug interactions and clinical methods of blocking the renal toxicity. Four agents (cisplatin, doxorubicin, daunorubicin, and mitomycin C) are examined in more detail to consider the information that has been generated in animal studies that relate to the total picture of nephrotoxicity, as well as the molecular pathogenesis of the renal lesion. Other agents which are known to produce clinical renal toxicity are not covered in detail because: (1) the effect is purely physical and not specific for renal cells (methotrexate; see clinical discussion), (2) the major lesion is in the urinary bladder, rather than the kidney (also the mechanism of action is relatively well understood for cyclophosphamide and ifosfamide), (3) little in-depth experimental work has been conducted in animals, or (4) the drugs represent only a minor clinical problem (nitrosoureas).
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Litterst, C.L., Weiss, R.B. (1987). Clinical and Experimental Nephrotoxicity of Cancer Chemotherapeutic Agents. In: Bach, P.H., Lock, E.A. (eds) Nephrotoxicity in the experimental and clinical situation. Developments in Nephrology, vol 19-20. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-3371-2_12
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