Abstract: TH-PO0716
From Myalgias to Dialysis: Oxaliplatin-Associated Rhabdomyolysis Causing Anuric AKI
Session Information
- AKI: Prevention, Diagnostics, and Management
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Nasrin, Sharmila, Henry Ford Macomb Hospital, Charter Township of Clinton, Michigan, United States
- Alali, Mohammad, Henry Ford Macomb Hospital, Charter Township of Clinton, Michigan, United States
- Tahir, Hebah, Henry Ford Macomb Hospital, Charter Township of Clinton, Michigan, United States
- Al-Antary, Nada, Henry Ford Macomb Hospital, Charter Township of Clinton, Michigan, United States
- Asad, Ismail, Henry Ford Macomb Hospital, Charter Township of Clinton, Michigan, United States
- Sreenivasan, Anuradha, Henry Ford Macomb Hospital, Charter Township of Clinton, Michigan, United States
Introduction
Rhabdomyolysis is a life-threatening syndrome of skeletal muscle breakdown leading to electrolyte derangements and acute kidney injury (AKI). While trauma and immobilization are common causes, drug-induced etiologies are increasingly recognized. Oxaliplatin, widely used in gastrointestinal malignancies, is typically associated with peripheral neuropathy; however, oxaliplatin-associated rhabdomyolysis is exceedingly rare, with few reported cases. Early manifestations may include progressive myalgias and weakness preceding severe muscle injury and renal failure.
Case Description
A 68-year-old male with metastatic rectal adenocarcinoma on oxaliplatin-based chemotherapy presented with recurrent falls, progressive weakness, diffuse myalgias, fatigue, and dark urine. After an unwitnessed fall with prolonged immobilization, he was brought for evaluation.
Laboratory studies demonstrated severe rhabdomyolysis with creatine phosphokinase (CPK) peaking at 76,219 U/L. He developed rapidly progressive anuric AKI with significant electrolyte abnormalities, including hyperkalemia, hyperphosphatemia, hypomagnesemia, and hyperuricemia. Despite aggressive intravenous fluids and diuretic challenge, he remained anuric with worsening renal function, requiring emergent intermittent hemodialysis.
CPK levels declined without evidence of ongoing muscle injury; however, renal recovery did not occur, and the patient remained dialysis-dependent. Management included renal replacement therapy, electrolyte correction, and discontinuation of oxaliplatin.
Discussion
This case highlights severe rhabdomyolysis complicated by dialysis-dependent anuric AKI following recent oxaliplatin exposure. Although prolonged immobilization likely contributed, preceding symptoms of myalgias, weakness, and fatigue raise concern for oxaliplatin-associated myotoxicity as a precipitating factor. Similar cases describe early muscle symptoms preceding marked CPK elevation and AKI.
Given the widespread use of oxaliplatin, clinicians should remain vigilant for this rare but catastrophic complication. Early recognition of unexplained myalgias, weakness, falls, or dark urine in patients receiving oxaliplatin should prompt evaluation for rhabdomyolysis, as delayed diagnosis may result in severe electrolyte derangements and dialysis-dependent renal failure.