A 69-year-old retired pharmacist was referred to our endocrine clinic with an incidental finding of hypokalaemia noted during recent spinal fusion surgery. He has been hypertensive for 6 years. His blood pressure was well controlled on Diltiazem 240 mg and Doxazosin 4 mg, but required 8 tablets of SandoK daily to maintain normokalaemia. His past medical history includes type 2 diabetes, diabetic retinopathy, chronic kidney disease, hypercholesterolaemia and benign prostatic hypertrophy. A diagnosis of Primary Hyperaldosteornism was made on the basis of a high aldosterone: 2684 pmol/l and suppressed renin <0.2 nmol/l/h. CT adrenals revealed a 30×28 mm left adrenal adenoma. He underwent adrenal vein sampling. Cortisol levels in the IVC, right and left adrenal veins were 1439 nmol/l, 1486 nmol/l and 16 840 nmol/l respectively, suggesting unsuccessful cannulation of the right adrenal vein. He therefore underwent a metomidate PET CT scan which suggested not one, but two, aldosterone-producing adenomas (APA) in his left adrenal gland. He successfully underwent a laparoscopic left adrenalectomy. Blood pressure and potassium levels normalised post-operatively. He was however discharged home on hydrocortisone replacement (10/5/5 mg), in view of a non-suppressed cortisol (60 nmol/l) after a LDDST performed pre-operatively. On reassessment 9am cortisol was 393 nmol/l, hence hydrocortisone replacement was stopped. At 1-month follow-up, he reported a 1-week history of feeling generally unwell with symptoms suggestive of viral gastroenteritis. Although the diarrhoea had settled he was still extremely lethargic. Blood tests revealed an acute on chronic renal failure, Na128 mmol/l, K7.4 mmol/l. He was urgently admitted for IV fluids, insulin-dextrose and IV hydrocortisone. Originally we presumed this gentleman had adrenal insufficiency due to cortisol co-secretion from his APAs which were suppressing his contralateral adrenal. However cortisol levels were reasonable: 625 nmol/l (01100 h sample). Most likely this gentleman has hyporeninaemic hypoaldosteronism as a result of his longstanding diabetes. Removal of his left APA(s) unmasked his underlying mineralocorticoid deficiency. Clinically and biochemically he responded promptly to fludrocortisone replacement (50 μg BD). Isolated mineralocorticoid deficiency post adrenalectomy is rare, observed in <5% of studied populations, but usually associated with high renin levels. However awareness of this complication is vital due to its potentially life-threatening consequences. In retrospect, when our patient was started on spironolactone pre-operatively, deterioration in his renal function, associated with a mild hyperkalaemia and hyponatraemia, was noted. This resolved promptly on reducing the dose of spironolactone. Was this a warning sign of the impending problems to come?