Abstract: PUB058
Seizures as an Uncommon Presentation of Cisplatin-Induced Nephrotoxicity
Session Information
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Thomas, Taniya, Albany Medical College, Albany, New York, United States
- Ali, Omar, Albany Medical Center, Albany, New York, United States
- Pal, Aman, Albany Medical Center, Albany, New York, United States
- Mehta, Swati, Albany Medical Center, Albany, New York, United States
- Hongalgi, Krishnakumar D., Albany Medical Center, Albany, New York, United States
Introduction
Cisplatin is a platinum-based chemotherapeutic agent which is commonly used for the treatment of solid tumors. Nephrotoxicity is a well-known complication of this medication and thought to occur due to tubular cell injury and death. We report a case of seizures due to cisplatin induced electrolyte derangements in a patient with osteosarcoma.
Case Description
A 21-year-old female presented with a one week history of poor oral intake and muscle weakness followed by a witnessed tonic-clonic seizure, on a pertinent background of osteosarcoma currently being treated with cisplatin and doxorubicin. She was found to have new-onset electrolyte disturbances with serum potassium 2.3 mmol/L, magnesium 0.7 mg/dL, phosphate <1.0 mg/dL, and calcium 6.8 mg/dL. Urine electrolytes revealed elevated potassium and magnesium. There was no evidence of metabolic acidosis (bicarbonate 25mmol/L) or acute kidney injury (AKI) with a creatinine of 0.74mg/dL and urine output of 2L/day. Urine studies were consistent with magnesium and potassium wasting. CT head was unremarkable for gross changes. Cisplatin was discontinued, electrolytes were repleted daily to maintain certain goals, and amiloride was initiated to decrease magnesium and potassium wasting. Over the course of her hospitalization, her oral intake and electrolytes continued to improve, eventually only requiring magnesium supplementation upon discharge after a week.
Discussion
Nephrotoxicity is a well-established side effect of cisplatin chemotherapy, commonly manifesting with AKI and hypomagnesemia. Persistent hypomagnesemia has been shown to inhibit the sodium-potassium pump and inhibit the release of parathyroid hormone (PTH), resulting in hypokalemia, hypophosphatemia and hypocalcemia, respectively. Our case emphasizes routine electrolyte monitoring and prompt medical management of electrolyte disturbances in patients receiving platinum-based chemotherapy to prevent complications.