[Nephrotoxicity of cytostatic drugs. Pathogenesis, prevention, therapy]

Tumourous diseases can damage the kidneys by different mechanisms, e.g. by infiltration of the kidneys, by obstruction of the urinary pathways or the syndrome of acute tumour lysis after aggressive cytostatic treatment. Moreover, there may be be even direct renal damage caused by cytostatic treatment. Serious nephrotoxicity with development of acute renal failure, Mg depletion and possibly chronic renal failure may be caused in particular by cisplatinum and less by its more recent derivatives. Nephrotoxicity of cisplatinum derivatives can be effectively mitigated by hydratation regimens and the administration of hypertonic NaCl. More recent findings on the nephrotoxicity of cisplatinum will certainly make possible the development of less toxic derivatives as well as more effective prevention and treatment of cisplatinum nephrotoxicity. Large-dose vaginous with iphosphamide may cause in addition to urotoxicity, common in all oxazaposphorins, the development of renal insufficiency and serious forms of acquired Fanconi's syndrome. The uro- and nephrotoxicity of iphosphamide can be reduced, but not entirely eliminated by administration of mesna. Large doses of metothrexate can precipitate in the tubules and induce acute renal failure. The nephrotoxicity of metothrexate can be prevented by alkalinisation and hydration regimes. Less common are other forms of nephrotoxicity e.g. tubulointerstitial nephritis induced by derivatives of hydroxyurea or the haemolytic-uraemic syndrome in conjunction with treatment with mitomycin C.