MON-278 Forty-Year Clinical Course of a Patient With Bilateral Primary Aldosteronism Who Underwent Dominant-Side Unilateral Adrenalectomy: The Importance of Sustained Treatment With Mineralocorticoid Receptor Blocking Agent

Abstract Disclosure: J.V. Chua: None. J.G. Sazon: None. L.B. Mercado-Asis: None. Background: Primary aldosteronism (PA) is a major cause of secondary hypertension, commonly caused by bilateral adrenal hyperplasia (BAH). It is characterized by hypertension, hypokalemia, and suppressed renin activity. Systemic hormonal unloading (SHU) through dominant-side unilateral adrenalectomy is a well-established treatment for BAH, significantly improving clinical outcomes. However, the risk of recurrence due to compensatory excess aldosterone secretion in the remaining adrenal gland highlights the critical need for long-term monitoring and compliance to medical therapy, specifically the continuous blocking of mineralocorticoid receptors, which in our case is spironolactone. Case Presentation A 67-year-old woman initially presented at age 27 with generalized weakness, persistent hypokalemia, and resistant hypertension. Work-up revealed primary aldosteronism with bilateral adrenal nodularity on CT and bilateral aldosterone secretion on adrenal venous sampling, more dominant on the left. She underwent SHU via left unilateral adrenalectomy, leading to symptom resolution, normokalemia, and better blood pressure control while being maintained on spironolactone. However, noncompliance with consult visits and discontinuation of spironolactone led to symptom recurrence, such as uncontrolled hypertension and hypokalemia, respectively. Initial repeat work-up showed a low ARR, inconsistent with clinical findings. With a positive confirmatory saline infusion test, a diagnosis of primary hyperaldosteronism was obtained. Resumption of spironolactone led to sustained normalization of her potassium levels and stabilized her blood pressure on regular consult visits. Further, in forty years post-SHU with unilateral adrenalectomy, a recent 2D echocardiogram showed only concentric left ventricular hypertrophy with normal wall motion, contractility, and systolic function, reflecting the protective effect of SHU on adverse complications of long-term excess hyperaldosteronism, such as cardiomyopathy. Conclusion: This case highlights key aspects of PA management: the progressive nature of BAH requiring lifelong follow-up with sustained blocking of mineralocorticoid receptors, the long-term benefits of SHU via unilateral adrenalectomy, and utilization of confirmatory testing in equivocal initial hormonal work-up. The patient’s discontinuation of spironolactone was a pivotal factor leading to the recurrence of symptoms, reinforcing the need for compliance and regular consult visits. Presentation: Monday, July 14, 2025