Seizure-Induced Rhabdomyolysis Complicated by Acute Kidney Injury: A Case Report

BACKGROUND Tonic-clonic seizures can precipitate severe rhabdomyolysis due to sustained muscle activity, leading to release of intracellular contents, including proteins, that can pose an elevated risk for acute kidney injury (AKI). Rhabdomyolysis management centers on aggressive intravenous (IV) fluid resuscitation while the risk of volume overload is vigilantly minimized. Nephrologists regularly assess the need for dialysis while addressing the nuances in each case. This case illustrates the clinical decision-making involved in managing extreme biochemical derangements in seizure-induced rhabdomyolysis with conservative medical management. CASE REPORT A 32-year-old man with a history of seizure disorder presented following a generalized tonic-clonic seizure. Laboratory studies reflected marked abnormalities, including a creatine kinase level of 83 261 u/L, peaking at 133 300 u/L shortly after admission, creatinine of 9.3 mg/dL from baseline of 1.0 mg/dL, aspartate aminotransferase of 819 u/L, and alanine aminotransferase of 192 u/L. Despite significantly elevated creatine kinase and creatinine levels, the patient remained hemodynamically stable, with preserved urine output and no life-threatening electrolyte or acid-base disturbances. He received aggressive IV fluids to enhance kidney perfusion and prevent further myoglobulin induced injury, with intermittent diuretics use to maintain euvolemia. Ultimately, kidney function and laboratory markers improved. CONCLUSIONS Rhabdomyolysis can cause AKI by various mechanisms. This report highlights the importance of timely and appropriate nephrology-guided management. Although aggressive hydration remains the standard of care, careful monitoring is required to prevent fluid overload. Close monitoring and conservative management alone may be sufficient in select patients without life-threatening biochemical derangements, thereby preventing the need for kidney replacement therapy.