2012•UBC Faculty of Medicine medical journalRequires access

Rhabdomyolysis causing acute kidney injury in a patient with multiple risk factors and an underlying inflammatory muscle disease: A Case Report

Chris Little, John Shik, Sean Hamilton

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Abstract

A 33 year-old Caucasian male with underlying type one diabetes mellitus, dyslipidemia, hypothyroidism and nephrotic syndrome secondary to membranous glomerulonephropathy (GN), presented with new onset tonic-clonic seizures (lasting one minute) after an episode of binge drinking in which there was a considerable period of immobilization. The patient was taking 80 mg of Atorvastatin daily at the time of presentation. The patient was intubated and ventilated and initial laboratory investigations confirmed a creatine kinase (CK) of 12,000 U/L (Normal 20-220 U/L) and creatinine of 3.1 mg/dL (Normal 0.7 – 1.3 mg/dL) and associated hyperkalemia of 5.6-5.9 mmol/L (Normal 2.5-5.0 mmol/L) The patient developed acute kidney injury (AKI) presumed secondary to rhabdomyolysis, and required renal replacement therapy.  His CK eventually peaked at 153,741 U/L on the seventh day of admission. The patient regained consciousness and improved clinically over the following weeks. A muscle biopsy performed on the 29th day of admission showed changes consistent with polymyositis. On follow up testing the patient’s TSH was noted to be 101.99 mIU/L (Normal 0.5-5.0 mIU/L ) with a T4 of 5.5 pmol/L (Normal 8.5-15.2 pmol/L) indicating uncontrolled hypothyroidism. This case highlights multiple potential etiologies causing rhabdomyolysis that may occur concurrently in a patient and contribute to AKI.

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What this paper is about

A 33 year-old Caucasian male with underlying type one diabetes mellitus, dyslipidemia, hypothyroidism and nephrotic syndrome secondary to membranous glomerulonephropathy (GN), presented with new onset tonic-clonic seizures (lasting one minute) after an episode of binge drinking in which there was a considerable period of immobilization. The patient was taking 80 mg of Atorvastatin daily at the time of presentation. The patient was intubated and ventilated and initial laboratory investigations confirmed a creatine kinase (CK) of 12,000 U/L (Normal 20-220 U/L) and creatinine of 3.1 mg/dL (Normal 0.7 – 1.3 mg/dL) and associated hyperkalemia of 5.6-5.9 mmol/L (Normal 2.5-5.0 mmol/L) The patient developed acute kidney injury (AKI) presumed secondary to rhabdomyolysis, and required renal replacement therapy.  His CK eventually peaked at 153,741 U/L on the seventh day of admission. The patient regained consciousness and improved clinically over the following weeks. A muscle biopsy performed on the 29th day of admission showed changes consistent with polymyositis. On follow up testing the patient’s TSH was noted to be 101.99 mIU/L (Normal 0.5-5.0 mIU/L ) with a T4 of 5.5 pmol/L (Normal 8.5-15.2 pmol/L) indicating uncontrolled hypothyroidism. This case highlights multiple potential etiologies causing rhabdomyolysis that may occur concurrently in a patient and contribute to AKI.

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Available abstract

A 33 year-old Caucasian male with underlying type one diabetes mellitus, dyslipidemia, hypothyroidism and nephrotic syndrome secondary to membranous glomerulonephropathy (GN), presented with new onset tonic-clonic seizures (lasting one minute) after an episode of binge drinking in which there was a considerable period of immobilization. The patient was taking 80 mg of Atorvastatin daily at the time of presentation. The patient was intubated and ventilated and initial laboratory investigations confirmed a creatine kinase (CK) of 12,000 U/L (Normal 20-220 U/L) and creatinine of 3.1 mg/dL (Normal 0.7 – 1.3 mg/dL) and associated hyperkalemia of 5.6-5.9 mmol/L (Normal 2.5-5.0 mmol/L) The patient developed acute kidney injury (AKI) presumed secondary to rhabdomyolysis, and required renal replacement therapy.  His CK eventually peaked at 153,741 U/L on the seventh day of admission. The patient regained consciousness and improved clinically over the following weeks. A muscle biopsy performed on the 29th day of admission showed changes consistent with polymyositis. On follow up testing the patient’s TSH was noted to be 101.99 mIU/L (Normal 0.5-5.0 mIU/L ) with a T4 of 5.5 pmol/L (Normal 8.5-15.2 pmol/L) indicating uncontrolled hypothyroidism. This case highlights multiple potential etiologies causing rhabdomyolysis that may occur concurrently in a patient and contribute to AKI.

Key concepts: Rhabdomyolysis, Medicine, Acute kidney injury, Hyperkalemia, Creatine kinase, Internal medicine, Dyslipidemia, Etiology

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