Endocrine Abstracts

A 58-year-old female presented with a 20-year history of resistant hypertension and hypokalaemia, with normal renal function. Investigations confirmed primary hyperaldosteronism that was not suppressed following a standard saline infusion test. CT scanning revealed a right-sided adrenal mass of 1.3 cm, with a signal intensity of −1 HU. The left adrenal was normal in appearance. A LDDST excluded ACTH-independent Cushing’s syndrome. Adrenal vein sampling confirmed right-sided unilateral hypersecretion of aldosterone; she underwent an uneventful right adrenalectomy in October 2011, following which her BP was controlled on atenolol alone.

In November 2011 she presented to other hospitals with acute kidney injury, postural hypotension and hyperkalaemia. In July 2012 she was admitted to our unit and was found to have a normal anion-gap metabolic acidosis, consistent with type IV renal tubular acidosis. A SST confirmed a normal adrenal–glucocorticoid axis (peak cortisol 630 nmol/l). Her aldosterone level was inappropriately low, given hypovolaemia and hyperkalaemia, suggesting hypoaldosteronism (plasma aldosterone 100 pmol/l; plasma renin activity 4.4 pmol/ml per h). In keeping with this, her biochemical abnormalities normalized following mineralocorticoid replacement. An attempt to reduce the dose of fludrocortisone resulted in a further reversible recurrence of both hyperkalaemia and acute kidney injury. She is now taking 100 μg fludrocortisone TDS, and remains well. Her atenolol has been changed to amlodipine, as ß-blockade may have prevented adequate recovery of her renin-aldosterone axis.

Post-operative hypoaldosteronism is well documented in cases of unilateral adrenalectomy for aldosterone-producing adenomas. This may relate to a decrease in adrenal mass, or a transient suppression of the contralateral gland (1). However, it is rare for this to be prolonged, or severe. This may occur in up to 5% of cases, and responds to mineralocorticoid treatment (2). Our case illustrates the importance of follow-up in the post-operative period.

References

1. Gadallah MF, Kayyas Y & Boules F. Reversible suppression of the renin-aldosterone axis after unilateral adrenalectomy for adrenal adenoma. Am J Kidney Dis 1998 32 (1) 160–163.

2. Fischer E, Hanslik G, Pallauf A, Degenhart C, Linsenmaier U, Beuschlein F, Bidlingmaier M, Mussack T, Ladurner R, Hallfeldt K, Quinkler M & Reincke M. Prolonged zona glomerulosa insufficiency causing hyperkalemia in primary aldosteronism after adrenalectomy. J Clin Endocrinol Metab 2012 97 (11) 3965–3973 (doi: 10.1210/jc.2012-2234).