SUN-189 A Case of Delayed Hypoaldosteronism Following Unilateral Adrenalectomy for Primary Aldosteronism

Abstract

BACKGROUND: Hypoaldosteronism occurs in 6–30% of patients following unilateral adrenalectomy for primary aldosteronism. The Endocrine Society guidelines recommend discontinuing potassium supplementation and spironolactone postoperatively with repeat renin and aldosterone after surgery to monitor for cure. Clinical Case: A 69-year-old male with a 15-year history of hypertension on amlodipine 10 mg daily, atenolol 100 mg daily, terazosin 5 mg daily, valsartan 160 mg daily, spironolactone 50 mg three times daily, with longstanding hypokalemia on potassium chloride 20 mEq four times daily presented with an ischemic stroke and persistent hypertension (BP 182/79). Following discontinuation of spironolactone, evaluation revealed aldosterone concentration of 214 ng/dL (normal 4.0 - 31) and plasma renin activity of 0.1 ng/mL/hr (normal 0.5 - 4.0), giving an aldosterone-to-renin ratio of 2,140. CT of the abdomen showed a 3 cm right adrenal mass. He underwent uncomplicated right adrenalectomy for primary aldosteronism. Postoperative potassium was 3.4 mEq/L (normal 3.5–5.0) and hypertension persisted, so he was discharged on potassium chloride 10 mEq, losartan 100 mg daily, amlodipine 10 mg daily, and labetalol 200 mg twice daily. Two weeks later potassium level was 5.1 mEq/L and potassium chloride supplement was discontinued. Six months postoperatively, potassium was 5.7 mEq/L with well-controlled blood pressure, so losartan was discontinued. Labs over the subsequent several weeks showed persistent hyperkalemia up to 6.2 mEq/L and new hyponatremia to 128 mEq/L (normal 134 - 150). Repeat plasma renin activity was 0.51 ng/mL/hr and aldosterone concentration <1.0 ng/dL. Morning cortisol concentration was 18.3 ug/dL (normal 6.7 - 22.6) and ACTH 38 pg/mL (normal 6.0 - 50 pg/mL). He was diagnosed with postsurgical hypoaldosteronism. Potassium stabilized at 5.1 mEq/L and sodium stabilized at 134 mEq/L, so he was monitored without treatment for hypoaldosteronism. One year postoperatively his labs showed: potassium 5.1 mEq/L, sodium 135 mEq/L, renin 1.0 ng/mL/hr, and aldosterone 5.7 ng/dL. Conclusion: This patient had primary aldosteronism leading to suppression of aldosterone secretion from the contralateral healthy adrenal gland. This resulted in postoperative hypoaldosteronism once the affected adrenal gland was resected. This case demonstrates the need for continued monitoring of potassium, sodium, renin, and aldosterone following unilateral adrenalectomy for primary aldosteronism, especially in the setting of postoperative angiotensin receptor blocker use or other medications which can affect the renin-angiotensin-aldosterone system.