Author/Authors :
Ghane Sharbaf, Fatemeh Department of Pediatric - Division of Nephrology - Dr. Sheikh Hospital - Mashhad University of Medical Sciences, Mashhad , Farhangi, Hamid Department of Pediatric - Division of Nephrology - Dr. Sheikh Hospital - Mashhad University of Medical Sciences, Mashhad , Assadi, Farahnak Department of Pediatrics - Division of Nephrology - Rush University Medical Center, Chicago, Illinois United States
Abstract :
Children with cancer treated with cytotoxic drugs are frequently at risk of developing renal dysfunction. The cytotoxic drugs that are widely used for cancer treatment in children are cisplatin (CPL), ifosfamide (IFO), carboplatin, and methotrexate (MTX). Mechanisms of anticancer
drug‑induced renal disorders are different and include acute kidney injury (AKI), tubulointerstitial disease, vascular damage, hemolytic uremic syndrome (HUS), and intrarenal obstruction. CPL nephrotoxicity is dose‑related and is often demonstrated with hypomagnesemia, hypokalemia, and impaired renal function with rising serum creatinine and blood urea nitrogen levels. CPL, mitomycin C, and gemcitabine treatment cause vascular injury and HUS. High‑dose IFO, streptozocin, and azacitidine cause renal tubular dysfunction manifested by Fanconi syndrome, rickets, and osteomalacia. AKI is a common adverse effect of MTX, interferon‑alpha, and nitrosourea compound treatment. These strategies to reduce the cytotoxic drug‑induced nephrotoxicity should include adequate hydration, forced diuresis, and urinary alkalization. Amifostine, sodium thiosulfate, and diethyldithiocarbamate provide protection against CPL‑induced renal toxicity.
Keywords :
Acute kidney injury , anti‑cancer drugs , chemotherapy , glomerular fltration rate , nephrotoxicity