Endocrine Abstracts

A 58-year-old presented with a 19 years history of hypertension and hypokalaemia for 10 years. Her diagnostic workup confirmed autonomous hyperaldosteronism with an aldosterone of 400 pmol/l, plasma renin activity <0.2 pmol/ml per h, ratio >2000. Aldosterone failed to suppress at 430 on the saline suppression test. There was a 1.3 cm right adrenal adenoma on CT scan, Hounsfield units 21. Adrenal vein sampling showed a convincing right: left ratio aldosterone: cortisol ratio of 22 with an adequate left adrenal: IVC ratio of <50%. Cortisol suppressed appropriately on the low dose dexamethasone suppression test to 30 nmol/l and urine catecholamines and metanephrines were normal.

Histology after retroperitoneal adrenalectomy confirmed an adrenal cortical adenoma. Soon after the patient was admitted to hospital complaining of palpitations with shortness of breath. CTPA was negative, ECHO showed a LV hypertrophy with a normal EF and a mild multivalve regurgitation. Twenty-four hours ECG showed occasional nocturnal bradycardia, two ventricular ectopics and occasional supraventricular ectopics.

She was then readmitted with an acute kidney injury and hyperkalaemia of 6.6 which was felt to be due to hypoaldosteronism with contralateral adrenal suppression from prolonged hyperaldosteronism. ARBs were then stopped and 300 μg fludrocortisone started.

The β blockers were switched to calcium channel blockers and her renal functions normalised. She remained hypertensive so we titrated the fludrocortisone dose down and the antihypertensives up till we optimised her BP.

This case highlights the fact that the renin–angiotensin aldosterone system feedback system is complex and could be overridden by autonomous aldosterone oversecretion that may need time to recover after the Conn’s adenoma resection.