Abstract: SA-PO0349
Beyond Hydration and Dialysis: A Case of Steroid-Responsive Refractory Rhabdomyolysis
Session Information
- AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Mhannayeh, Hayat, The University of Alabama at Birmingham, Birmingham, Alabama, United States
- Maheshwari, Surabhi, The University of Alabama at Birmingham, Birmingham, Alabama, United States
- Garapati, Hari Naga, Baptist Medical Center South, Montgomery, Alabama, United States
Introduction
Rhabdomyolysis is skeletal muscle injury with massive release of intracellular contents (CK, myoglobin) into circulation, leading to multisystem complications, most notably acute kidney injury (AKI), historically in 7–10% of cases. It is typically managed with aggressive IV fluids and removal of triggers. A small subset develops refractory rhabdomyolysis with persistently elevated CK despite maximal supportive care. In such cases, high-dose corticosteroids may be considered as rescue therapy.
Case Description
A 62-year-old Caucasian male with a history of atrial fibrillation, coronary artery disease, immune thrombocytopenia, and chronic alcohol use presented with severe generalized weakness and multiple recent falls. On examination, he had muscle tenderness but preserved motor strength in all extremities. Laboratory studies revealed markedly elevated creatine kinase (CK) of 247,667 IU/L, severe acute kidney injury (BUN 80, creatinine 12.5, GFR 4), hypocalcaemia (5.9), AG=20, and significant transaminitis (AST 2534, ALT 308). Statin use was noted but anti-HMG-CoA reductase antibody was negative. Extensive infectious, autoimmune, and toxic workup was negative. He became anuric on IV fluids requiring hemodialysis. Despite dialysis, CK peaked at 338,439 IU/L on hospital day 4 with minimal clinical improvement. Given refractory rhabdomyolysis, he received three doses of intravenous methylprednisolone (125 mg). Within 24 hours, he demonstrated marked clinical improvement with rapid and sustained decline in CK levels. By day 3 post-steroids, CK decreased to 34,797 IU/L and normalized to 470 IU/L by day 13. Unfortunately, despite resolution of rhabdomyolysis, he developed fatal Clostridium difficile infection and progressive multiorgan failure.
Discussion
Rhabdomyolysis ranges from mild enzyme elevation to severe multisystem failure. Myoglobin-mediated renal injury occurs via vasoconstriction, tubular obstruction, and oxidative damage. This case suggests a severe inflammatory process driving persistent muscle injury. The rapid CK decline after corticosteroids supports inflammation as a key mechanism. Steroids likely reduce ongoing muscle damage by inhibiting vasodilation, permeability, and leukocyte migration. High-dose corticosteroids may be a potential rescue option in refractory severe rhabdomyolysis unresponsive to standard therapy.
Acknowledgment
We sincerely thank the healthcare team for their dedicated care of the patient.