Rhabdomyolysis-Associated Acute Kidney Injury: A Three-Patient Case Series Illustrating Different Precipitants, Biochemical Trajectories and Renal Outcomes

Abstract

Background: Rhabdomyolysis results from skeletal muscle injury with release of intracellular contents into the circulation. It can lead to acute kidney injury (AKI), electrolyte and acid-base disturbances, and, in severe cases, multiorgan dysfunction. The clinical course is heterogeneous, and the extent of CK elevation does not necessarily reflect the severity of kidney injury.

Case presentation: We describe three adult cases of rhabdomyolysis-associated AKI arising from distinctly different clinical circumstances. The first patient, a 27-year-old man, developed exertional rhabdomyolysis following an unusually intense gym workout. His CK concentration peaked at 46,780 U/L, while serum creatinine increased from 0.9 to 3.2 mg/dL. He responded to early intravenous crystalloid therapy and did not require kidney replacement therapy. The second patient was a 41-year-old man admitted after a generalized tonic-clonic seizure followed by prolonged immobilization. He developed severe rhabdomyolysis, hyperkalemia, metabolic acidosis and oligo-anuric AKI, with CK peaking at 132,400 U/L and creatinine reaching 7.8 mg/dL. Intermittent hemodialysis was required for six sessions, followed by gradual renal recovery. The third patient, a 58-year-old woman receiving high-dose statin therapy, presented after several days of fever, poor oral intake and progressive proximal muscle weakness. Her initial CK was 18,940 U/L, but she developed marked AKI with creatinine rising to 6.4 mg/dL in the setting of volume depletion and delayed presentation. She required four hemodialysis sessions and subsequently recovered to a creatinine of 1.3 mg/dL at 3-month follow-up.

Conclusion: These cases show the clinical heterogeneity of rhabdomyolysis-associated AKI. Severe kidney injury may result from the combined effects of muscle injury, hypovolemia, acidemia, and other patient factors rather than from CK elevation alone. Management rests on early recognition, treatment of theprecipitating cause, appropriate crystalloid therapy, close biochemical monitoring, and kidney replacement therapy when standard indications arise. CK should therefore be interpreted alongside the overall clinical and biochemical picture.