Endocrine Abstracts

Introduction: Primary aldosteronism (PA) is a common and potentially reversible cause of secondary hypertension, characterised by resistance to standard antihypertensive therapy and possible hypokalaemia. Lateralisation investigations, including adrenal vein sampling (AVS), are required to distinguish between unilateral or bilateral disease, with unilateral disease representing a potentially surgically curable form of PA. The majority of patients proceeding to adrenalectomy remain well postoperatively, with complete resolution of hypokalaemia. Rarely, patients can develop hypoaldosteronism postoperatively, due to prolonged suppression of the contralateral zona glomerulosa. There remains a lack of guidance on how to predict and monitor hypoaldosteronism in PA patients undergoing adrenalectomy. We will illustrate these challenges within two cases.

Cases: Case 1: A 58-year-old fit and otherwise healthy female was referred with a 20-year history of hypertension (on three antihypertensive agents) and unprovoked hypokalaemia (K=2.9 mmol/l). Following diagnosis of PA, lateralisation studies confirmed unilateral left adrenal disease. She underwent an uncomplicated left adrenalectomy. At her 1-month postoperative review, she reported symptoms of postural hypotension with fatigue. A short synacthen test (SST) was normal. However, serum electrolytes revealed hyperkalaemia (K=6.1 mmol/l), hyponatraemia (Na=129 mmol/l) and renal impairment (creatinine=129 μmol/l). Additional biochemical testing revealed plasma renin concentration (PRC) 62 mU/L and plasma aldosterone concentration (PAC) 104 pmol/l. Following commencement of fludrocortisone, there was significant clinical and biochemical improvement (serum K=4.9 mmol/l, Na=135 mmol/l, creatinine=84 μmol/l). A subsequent attempt to withdraw fludrocortisone therapy was associated with recurrence of hypoaldosteronism. Case 2: A 55-year-old male was referred with a 10-year history of hypokalaemia and resistant hypertension (average BP 170/11 mmHg on four antihypertensive agents). He had a history of mild renal impairment (baseline creatinine 107 μmol/l). Following diagnosis of PA, he was commenced on Eplerenone which successfully achieved a normotensive state. Lateralisation studies confirmed unilateral left adrenal disease, and the patient proceeded to left adrenalectomy without complication. At his 1-month postoperative review, he was found to be hyperkalaemic with renal impairment (creatinine 176 μmol/l). His PAC was undetectable (<70 pmol/l); SST was normal. Following commencement of fludrocortisone, there was a rapid improvement in his biochemistry (K=5.1 mmol/l, Na=141 mmol/, creatinine 113 μmol/l).

Conclusion: Although considered to be a relatively rare (~5%) complication in patients with PA undergoing unilateral adrenalectomy, hypoaldosteronism is a potentially serious manifestation. Factors that may predict its development include severity of PA (e.g. presence of hypokalaemia). Our cases highlight the importance of attempting to identify those patients who are at higher risk of postoperative hypoaldosteronism, ensuring that there is a strategy for close biochemical surveillance postoperatively in these patients.