17 June 2026
: Case report
[In Press] Seizure-Induced Rhabdomyolysis Complicated by Acute Kidney Injury: A Case Report
Unusual or unexpected effect of treatment, Educational Purpose (only if useful for a systematic review or synthesis)
Harsimranjit Kaur1ABCDEF, Huma Hasnain Kennedy1EF, Niloofar NobakhtDOI: 10.12659/AJCR.951097
Am J Case Rep In Press; DOI: 10.12659/AJCR.951097
Available online: 2026-06-17, In Press, Corrected Proof
Publication in the "In-Press" formula aims at speeding up the public availability of the pending manuscript while waiting for the final publication. The assigned DOI number is active and citable. The availability of the article in the Medline, PubMed and PMC databases as well as Web of Science will be obtained after the final publication according to the journal schedule
Abstract
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.
Keywords: Acute Kidney Injury; Dialysis; Rhabdomyolysis
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