IFOSFAMIDE-INDUCED SUBCLINICAL NEPHROTOXICITY AND ITS POTENTIATION BYCISPLATINUM

Citation
R. Rossi et al., IFOSFAMIDE-INDUCED SUBCLINICAL NEPHROTOXICITY AND ITS POTENTIATION BYCISPLATINUM, Medical and pediatric oncology, 22(1), 1994, pp. 27-32
Citations number
30
Categorie Soggetti
Oncology,Pediatrics
ISSN journal
00981532
Volume
22
Issue
1
Year of publication
1994
Pages
27 - 32
Database
ISI
SICI code
0098-1532(1994)22:1<27:ISNAIP>2.0.ZU;2-L
Abstract
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.