Carboplatin-related hematuria and acute renal failure

Cisplatin is a potent tubular toxin with a high incidence of nephrotoxicity. Carboplatin is considered less nephrotoxic but can still cause tubular injury and interstitial nephritis in patients who have been previously treated with cisplatin. The affected individuals usually have nonoliguric renal failure with a urine output of more than a liter per day. We present a 57-year-old white woman with no history of renal disease who underwent a total abdominal hysterectomy and bilateral salpingo-oophorectomy for stage IC ovarian carcinoma. One month later, she received chemotherapy with paclitaxel (Taxol) and carboplatin. On the following day, she developed frank hematuria and flank pain associated with a diminished urine output. Intravenous pyelogram (IVP) showed bilateral hydronephrosis with a total blockage of dye flow at the level of intraureteral lucencies consistent with bilateral blood clots. Her coagulation profile and uric acid was normal. Her acute renal failure (ARF) spontaneously resolved in the following 24 hours, with a brisk diuresis presumably due to clot lysis. The follow-up IVP showed a resolution of obstructive changes. A review of the literature shows a previous case in which high doses of carboplatin were implicated as the cause of hemorrhagic cystitis, presumably by toxicity to transitional epithelium of the bladder. We believe that the current case represents carboplatin-induced damage to the transitional epithelium in the renal pelvi and ureters causing gross hematuria and blood clots, resulting in bilateral ureteral obstruction and hydronephrosis.