Abstract: PUB097
A Decade Later: Persistent Electrolyte Wasting After Cisplatin
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Alam, Mariam, Mercy Health St Rita's Medical Center Internal Medicine Residency Program, Lima, Ohio, United States
- Conlon, Luke, University of Utah Health, Salt Lake City, Utah, United States
- Hartsell, Sydney Elizabeth, University of Utah Health, Salt Lake City, Utah, United States
Introduction
Cisplatin can cause persistent tubular injury and magnesium wasting, though the long-term course remains incompletely understood. We describe prolonged multi-electrolyte wasting with preserved glomerular filtration and complex management.
Case Description
A 23-year-old male with history of childhood osteosarcoma treated at age 11 with cisplatin-based chemotherapy was referred for chronic hypomagnesemia. His history included chemotherapy-induced dilated cardiomyopathy requiring LVAD placement and recurrent driveline infections.
Serum magnesium remained low at 1.0-1.2 mg/dL despite oral magnesium glycinate 600 mg twice daily and SGLT2-i therapy. Fractional excretion of magnesium was elevated at 11.6%, consistent with renal wasting. He also had intermittent hypokalemia, with urine potassium-to-creatinine ratio of 43 mEq/g, consistent with renal potassium wasting. Renal salt wasting was suspected given prior orthostatic hypotension improved with salt tablets, though evaluation was limited by oral sodium use. There was no acidosis or glucosuria. Genetic testing for inherited tubulopathies was negative. Kidney function was preserved, with cystatin C-based eGFR of 111 mL/min/1.73 m2.
IV magnesium was not covered, but inpatient improvement on oral therapy revealed diarrhea-related nonadherence at home; he was transitioned to magnesium malate to improve tolerability. Potassium normalized on spironolactone and Entresto. Amiloride was stopped due to worsened orthostasis and minimal benefit.
Discussion
This case shows cisplatin-associated tubular dysfunction more than 10 years after chemotherapy. Chronic renal magnesium wasting likely contributed to secondary potassium wasting through ROMK dysregulation. Cisplatin-associated salt wasting may also be present.
Prolonged tubular dysfunction after cisplatin is possible but rarely described. Potential risk factors include later childhood chemotherapy and concurrent ifosfamide exposure, both present in this case. Cisplatin may cause genetic changes in tubular cells leading to long-lasting magnesium wasting, though mechanisms remain unclear.
This case supports long-term monitoring for tubular dysfunction in cisplatin-treated childhood cancer survivors, even with preserved kidney function. Management should include screening for oral magnesium side effects, as diarrhea can limit adherence and require a better-tolerated regimen.