MON-283 Rhabdomyolysis In A Patient With Primary Hyperaldosteronism: A Clinical Challenge

Abstract Disclosure: M. Lizarazo Jimenez: None. Y. Rodriguez: None. D. Soto Camargo: None. A. Florez: None. L. Kattah Martinez: None. L. Bustamante Gómez: None. Introduction: Rhabdomyolysis is an uncommon but potentially life-threatening complication of severe hypokalemia and may be the initial presentation of underlying endocrine disorders such as primary hyperaldosteronism. Although many patients with hyperaldosteronism are asymptomatic or present with mild hypertension, severe hypokalemia (K⁺ <2 mmol/L) can result in profound muscle injury and rhabdomyolysis, with symptoms including myalgia, weakness, and elevated creatine kinase levels. In this case, rhabdomyolysis was the key clinical manifestation that prompted further investigation. Clinical Case: We report the case of a 52-year-old man with a history of hypertension, admitted with muscle weakness and laboratory-confirmed rhabdomyolysis (CPK: 21,023 U/L; AST: 611 U/L; ALT: 126 U/L; LDH: 767 U/L) with severe hypokalemia (serum potassium: 1.85 mEq/L). Initial screening for primary hyperaldosteronism revealed a negative aldosterone/renin ratio (plasma aldosterone: 8.56 ng/dL; plasma renin concentration: 3.0 ng/L [RR: >5.7]). Further workup revealed elevated urinary cortisol (60 nmol/24h [RR: 20-150]) and ACTH levels >20 pg/mL, suggesting ACTH-dependent hypercortisolism. A pituitary MRI revealed a 13 × 9 mm right paramedian macroadenoma. Inferior petrosal sinus sampling was attempted but was non-diagnostic due to inadequate catheterization, despite elevated basal ACTH gradients (selectivity index left: 17.17; right: 19.38). Confirmatory cortisol suppression tests were normal, ruling out Cushing’s disease (post-dexamethasone cortisol: 0.9 µg/dL [RR: <1.8]; late-night salivary cortisol: <1.5 µg/dL [RR: <1.5]; ACTH: 6.99 pg/mL [RR: 7.2-63.3]). Further evaluation included an adrenal CT, which identified an 18 × 11 mm right adrenal nodule (−4 Hounsfield units, consistent with adenoma). Repeat biochemical testing showed suppressed plasma renin activity (<0.14 ng/mL/h [RR: 0.2-1.6]) and elevated plasma aldosterone (40.8 ng/dL [RR: <15 in normotensive individuals]), with a positive aldosterone/renin ratio (ARR: 291.4; RR: >30 when using PRA). Adrenal vein sampling showed a lateralization index of 21.25 toward the right, confirming a right-sided aldosterone-producing adenoma with no cortisol co-secretion. Adrenalectomy was indicated, resulting in resolution of both hypertension and hypokalemia. Conclusion: This case highlights the diagnostic challenge of severe hypokalemia-induced rhabdomyolysis as an initial manifestation of underlying primary hyperaldosteronism, particularly when confounded by overlapping endocrine abnormalities. Although hypokalemia is a hallmark of hyperaldosteronism, it is not pathognomonic and requires comprehensive clinical and biochemical evaluation. The combination of hormonal assays, imaging, and adrenal vein sampling was essential for diagnosis and management in this complex presentation. Presentation: Monday, July 14, 2025