Endocrine Abstracts (2018) 55 WE14 | DOI: 10.1530/endoabs.55.WE14

Hyporeninaemic hypoaldosteronism in surgically cured Conn's syndrome

James Pittaway, Simon Coppack, Rob Carpenter & William Drake


St Bartholomew’s Hospital, London, UK.


A 53 year old gentleman from Ghana was referred to our clinic for further management of his Conn’s syndrome. This had been diagnosed at another hospital 3 years previously when he presented with hypertension and hypokalaemia on the back of 14 years of poorly controlled hypertension. Serum aldosterone was raised at 3178 pmol/l and serum renin mass was 3.9 mU/l. MRI revealed a 5 mm nodule in the medial limb of the right adrenal gland. He was initially commenced on medical treatment with spironolactone and then eplerenone but although these medications controlled his blood pressure and hypokalaemia well, caused him troublesome gynaecomastia. Repeat biochemistry, imaging and adrenal venous catheter studies re-affirmed the diagnosis and strongly pointed to the right adrenal lesion as the source of his hyperaldosteronism without evidence of cortisol co-secretion. Referral was made to the endocrine surgical service for consideration of adrenalectomy. However given this gentleman’s morbid obesity with a BMI >50 kg/m2 with uncontrolled OSA, the anaesthetic and surgical risk was considered too great in the context of a medically controllable condition (albeit with averse side-effects). He was seen in the obesity clinic and with little improvement on oral weight control agents went on to have a gastric banding procedure. This precipitated weight loss of 40 kg and enabled a successful laparoscopic right adrenalectomy the following year. Post-operatively he still required two antihypertensive agents for presumed non-aldosterone mediated hypertension. In the follow up to this, he was admitted to our hospital from clinic when follow up biochemistry revealed hyperkalaemia of 7.7 mmol/l. Venous blood gases revealed a normal anion gap metabolic acidosis (HCO3 17 mmol/l, pH 7.306). Reassessment of his renin-aldosterone axis showed hyporeninaemic hypoaldosteronism (renin activity serum 0.41 pmol/ml per l (1.15–4.37), aldosterone <58 pmol/l (135–400)), presumed secondary to long-term type 2 diabetes mellitus. He was commenced on fludrocortisone replacement which was titrated up to 100 mcg bd. His blood pressure and potassium are now well controlled on this dose with additional beta and calcium channel blockade. The case describes the rare occurrence of hyporenininaemic hypoaldosteronism in a patient with surgically cured Conn’s syndrome secondary to an aldosterone producing adenoma. The autonomous aldosterone excess ‘masked’ the diabetes-associated underlying renin insufficiency which was exposed following the adrenalectomy. It highlights the issues of managing both primary aldosteronism and non-aldosterone mediated hypertension in complex patients with comorbidities and also the management of hypertension in aldosterone deficiency.

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