Abstract Rhabdomyolysis usually present with hyperkalemia, hyperphosphatemia, metabolic acidosis and AKI. Here we describe a patient who presented with hypokalemia, normal phosphate, metabolic alkalosis and normal renal function. Case Presentation A 69-year-old male, a professional boxing instructor with a history of sick sinus syndrome (status post pacemaker placement) and remote seizure disorder, presented with bilateral lower extremity weakness and pain for two weeks and reddish urine for one day. He reported poor oral intake and regular alcohol consumption but denied trauma, excessive exertion, or medication or drug use. Vitals were stable on admission On examination, he had bilateral lower limb weakness (grade 2/5) and diffuse muscle tenderness. Initial labs revealed severe hypokalemia (K 1.7 mEq/L), hypomagnesemia (Mg 0.8 mg/dL), markedly elevated Creatine Kinase (CK) (37,000 U/L), bicarbonate (40) and transaminitis with aspartatate aminotransferase (AST) 656 U/L, alanine aminotransferase (ALT) 187 U/L, consistent with rhabdomyolysis. Liver function and renal parameters were otherwise normal, with mild lactic acidosis. Aggressive IV fluid resuscitation and electrolyte repletion were initiated. The hypokalemia and hypomagnesemia were refractory to resuscitation for the first 72 hours. The CK continued to peak despite fluids until 98K on the 5th day and the transaminitis also continued to trend up with the CK reaching AST- 1845 and ALT- 431. On day 5 he also started getting volume overloaded and was complaining of difficulty breathing with B-lines noted on bedside ultrasound, so we treated him with Lasix PRN and continued with fluids. following which his labs started trending down and his symptoms also gradually resolved over the course of the next 1 week. Comprehensive workup for secondary causes, including autoimmune, endocrine, infectious, and toxic etiologies, were negative. Throughout his hospital course he did not develop hyperkalemia and hyperphospatemia. His blood calcium levels remained steady and renal function was within normal limits. Given the lack of a common underlying etiology of rhabdomyolysis and the improvement of CK only after correction of the potassium we can attribute the etiology of the rhabdomyolysis to hypomagnesemia induced hypokalemia. Normal potassium levels are required for optimal functioning of the muscles. Though uncommon hypokalemia can induce severe rhabdomyolysis through the following mechanisms. Impaired muscle perfusion due to loss of potassium-mediated vasodilation. Membrane instability, leading to calcium influx, protease activation, and myocyte necrosis. Conclusion This case shows an extreme presentation of severe hypokalemia and hypomagnesemia induced rhabdomyolysis leading to markedly elevated CK level and absence of hyperkalemia or hyperphosphatemia throughout the hospital course. This abstract is funded by: None
Reddy et al. (2026) studied this question.