A Case of Cisplatin-Induced Tubulopathy (Fanconi-Like Syndrome)

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Introduction: Proximal tubulopathy is characterized by proteinuria, hypophosphatemia, hypokalemia, hypouricemia, renal acidosis, glucosuria with normal blood glucose level. Cisplatin is a potent and valuable chemotherapy agent used to treat a broad spectrum of malignancies and Cisplatin-mediated nephrotoxicity is accompanied by the development of a Fanconi-like syndrome. We are presenting a case of Cisplatin induced tubulopathy in a 33-year-old female. Case Description: 33 yo F with PMH of stage III cervical cancer undergoing cisplatin based chemo + RT, HTN, anemia, recent PE on Eliquis, referred to ED for febrile neutropenia. Vitals were significant for fever of 101 *F and tachycardia with HR 110. Labs were significant for HGB 6.3, WBC 0.79 with ANC of 0.31, Plts 104, Cre 1.8 (baseline 0.9), Na 126, K 2.7, PO4 1.7, Mag 0.96, uric acid 2.7 and tCO2 of 19. Imaging showed RLL pneumonia and UA was positive for proteinuria and glucosuria despite A1C of <4.2 and plasma glucose 99 and urinary pH of 7.0. Further testing revealed FEPhos 85.7%, uK/uCr ratio 21.3 mEq/g. Patient was treated with IVF, broad spectrum abx and neupogen. During her hospital stay Patient’s electrolytes continued to remain low despite aggressive IV repletion suggestive of cisplatin induced proximal tubulopathy and renal wasting of phosphorous, potassium, magnesium and bicarbonate. Recommendations were made to switch her chemotherapy to non-platinum based therapy upon discharge. Discussion: Cisplatin-mediated nephrotoxicity is accompanied by the development of a Fanconi-like syndrome, with increased urinary excretion of glucose, phosphate, bicarbonate, uric acid and amino acids. Tubular disorders are frequently underdiagnosed, probably due to the relative absence of specific symptoms that may be related to tubular dysfunction. Timely recognition will allow a multidisciplinary approach for an accurate assessment that improves the long-term results of patients.

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