Endocrine Abstracts

Introduction: Prolonged hypoaldosteronism is an uncommon complication following unilateral adrenalectomy for primary aldosteronism. There are only 5 case reports in literature. However, a retrospective series involving 110 patients found that it occurred in 5% of patients. We present our experience with two patients.

Case presentation: Patient 1 was a 51-year-old male presenting with a 7-year history of difficult-to-manage hypertension. He was intolerant to many antihypertensives and had undergone bilateral renal denervation. Despite this intervention, blood pressure remained poorly controlled. He was found to have primary aldosteronism. No adenoma was detected on CT, but adrenal venous sampling lateralized to the left gland, with contralateral suppression. He underwent left adrenalectomy where primary adrenal hyperplasia was found. Postoperatively, blood pressure was good requiring no medications. However he developed hyperkalemia and doubling of his baseline creatinine. Renin was undetected at 2 months. Subsequent renin levels were detectable but low. Aldosterone levels monitored until 30 months postop were borderline low, and hyperkalemia and raised creatinine levels persisted. Mineralocorticoid replacement was initiated, but then discontinued by the patient who remained well. Patient 2 was a 50-year-old male with 16 years of hypertension. Blood pressure was poorly controlled on 3 agents and he had severe spontaneous hypokalemia. Workup confirmed primary aldosteronism. CT showed a 3.0 cm hypodense adenoma in the right adrenal with nodular thickening of the left gland. Adrenal venous sampling lateralized to the right, with contralateral suppression. Immediately following right adrenalectomy, blood pressure improved. However at 2 months, he had to restart nifedipine. He was also noted to have hyperkalemia, elevated creatinine with borderline low renin and aldosterone levels. This persisted at 9 months postop. He was initially treated with salt tablets. As the patient was asymptomatic, mineralocorticoid therapy was not instituted.

Discussion: The etiology of prolonged post-adrenalectomy hypoaldosteronism is unclear. It has been proposed to be due to atrophy of the zona glomerulosa resulting in suppressed aldosterone synthesis and insufficiency—a functional primary hypoaldosteronism. Conversely, hyporeninemic hypoaldosteronism which both our cases had is very rare, occurring in only 1.8% of cases in the above series. Interestingly, impaired renin response following renal denervation may play a role in our first patient.

Conclusion: Post-adrenalectomy hypoaldosteronism may be more common than appreciated. Monitoring of patients’ wellbeing, blood pressure, electrolytes, renal function and recovery of the renin-aldosterone system is important as the entity may result in hypotension and hyperkalemia with potentially severe consequences.