Abstract: FR-PO0891
Hyperkalemia as a Harbinger: More Than Meets the Muscle
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Wong, Mike, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
- Chatterjee, Totini S., The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
Introduction
Hyperkalemia is a common indication for nephrology consultation requiring evaluation to identify the etiology. Causes include medications, hypoaldosteronism, diet, tumor lysis syndrome, pseudohyperkalemia, and rhabdomyolysis. While statins commonly cause muscle injury, persistence after stopping the drug suggests other diagnoses. We present a case initially attributed to statins, but further investigation revealed immune-mediated necrotizing myopathy (IMNM). This highlights the need for a broad differential when evaluating hyperkalemia and elevated creatine kinase (CK).
Case Description
A 68-year-old man with type 2 diabetes mellitus, hypertension, and hypothyroidism was referred to nephrology clinic for evaluation of persistent hyperkalemia and progressive proximal muscle weakness. Potassium levels had averaged approximately 5.0 mmol/L across ten outpatient laboratory measurements over several months. Given this, a CK level was obtained and found to be markedly elevated at 9,000 U/L, prompting referral to the emergency department. On admission, repeat CK was 8,000 U/L with preserved kidney function (creatinine 0.85 mg/dL; baseline 0.8 mg/dL). The patient was initially presumed to have statin-associated rhabdomyolysis and intravenous (IV) fluids were initiated. Notably, he had been hospitalized one month earlier for a similar presentation with CK exceeding 10,000 U/L, at which his statin therapy of three years was discontinued. This prompted an autoimmune workup and empiric IV steroids. Testing confirmed anti–3-hydroxy-3-methylglutaryl coenzyme A reductase (anti-HMGCR) antibodies, diagnosing IMNM. Following treatment with mycophenolate mofetil and corticosteroids, his CK improved to 4,000 U/L, potassium normalized, and weakness resolved.
The patient was discharged on mycophenolate mofetil with gradual prednisone taper.
Discussion
Hyperkalemia with preserved kidney function and proximal muscle weakness suggests active muscle injury. While statins are common culprits, persistent CK elevation after stopping the drug warrants investigation into autoimmune myopathies. IMNM is a rare condition associated with anti-HMGCR antibodies. It mimics toxic statin myopathy with myalgias and high CK, but management is vastly different. Unlike toxic myopathy, IMNM requires aggressive immunosuppression to prevent respiratory or cardiac involvement. This case shows how electrolyte imbalances can serve as vital clues to occult systemic disease.