Abstract
Platinum-based therapy is currently used in anticancer regimens. Carboplatin [diamine (1,1-cyclobutanedicarboxylato) platinum], one of the second generation platinum compounds (1), has been introduced in clinical use as a less nephrotoxic alternative to cisplatin. The binding of platinum to plasma proteins is less pronounced than for cisplatin, resulting in a higher proportion and a longer half-time of active free platinum in blood. In addition, renal excretion by glomerular filtration is rapid and, unlike cisplatin, occurs without tubular secretion (2). At the conventional dose of 400 mg/m2, carboplatin dose-limiting toxicity is essentially hematologic (neutropenia and thrombocytopenia). This toxicity can be prevented by administration of cytokines such as GM-CSF, G-CSF or IL-3 allowing a dose escalation over 1000 mg/m2. However, at these doses, other signs of toxicity such as nephrotoxicity appear. In this paper, we described the case of a patient with acute renal failure after carboplatin administration.
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Jaumain, H., Bret, M., Accominotti, M., Ardiet, C., Chatelut, E., Moskovtchenko, J. (1996). Pharmacokinetics of Platinum in a Patient Undergoing Hemodialysis after Acute Renal Failure Due to Treatment with Carboplatin. In: Nève, J., Chappuis, P., Lamand, M. (eds) Therapeutic Uses of Trace Elements. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0167-5_41
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DOI: https://doi.org/10.1007/978-1-4899-0167-5_41
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