R. Rossi et al., IFOSFAMIDE-INDUCED SUBCLINICAL NEPHROTOXICITY AND ITS POTENTIATION BYCISPLATINUM, Medical and pediatric oncology, 22(1), 1994, pp. 27-32
Renal function was assessed in 72 children and adolescents 3.5 to 123
months after completion of chemotherapy employing ifosfamide (n = 39)
or ifosfamide plus cisplatinum (n = 33). No patient had preexisting re
nal parenchymal disease. Whereas reduction in glomerular filtration ra
te was present in six of 69 patients (8.7%), impairment of tubular tra
nsport for phosphate, glucose, and amino acids was more frequent: 32.8
% of the patients showed reduction in phosphate reabsorption, and gluc
ose and amino acid reabsorption was lowered in 16.4% and 55.0%, respec
tively. Elevated sodium excretion was found only occasionally, and the
re was no evidence of renal tubular acidosis. Proximal tubular damage
is related to ifosfamide chemotherapy, but correlation between ifosfam
ide dose and phosphate reabsorption was not linear. The most severe de
pletion of phosphate reabsorption was seen i n patients treated with b
oth ifosfamide and cisplatinum. On reexamination of phosphate reabsorp
tion after a median interval of 8 months, the majority of patients wit
h initially reduced values showed further deterioration of this functi
on. (C) 1994 Wiley-Liss, Inc.