P1-10: Renin-aldosterone axis deficiency without frank hyperkalemia following unilateral adrenalectomy for primary aldosteronism (PA) : about 4 cases

Abstract

Background Aldosterone-producing adenoma is classically treated by unilateral adrenalectomy. Severe hyperkalemia, related to adrenal insufficiency, have been already reported after surgery. We describe here 4 male patients who, despite subnormal kalemia, developed a failure of the renin-aldosterone (RA) axis, resulting in a decrease in extracellular fluid volume (ECFV) following surgery Methods PA diagnosis was established according to French recommendations. Unilateral adrenalectomy was performed in all. Postoperative explorations included ECFV measurement using inulin, and RA axis functionally test by orthostatic and ACTH stimulation. Abstract P1-10 – Table Patient 1 2 3 4 ECFV (mL/kg) N:180-210 108 165 166 167 Plasma potassium (mmol/L) 4.9 4.6 4.5 4.2 Plasma renin (mUI/L) N:2.8-39.9 5.5 3.1 19.4 10.5 Plasma aldosterone (ng/L): Supine N:10-105 15 10 21 16 1-hour orthostatism N:34-273 14 31 14 Post ACTH 41 35 48 12 A decrease in ECFV with low renin level, and insufficient orthostatism-induced aldosterone production were depicted. The ACTH test demonstrated no glucocorticoid deficiency, along with responsive aldosterone secretion. The discrepancy in aldosterone response in orthostatic position versus ACTH stimulation test suggested that hypoaldosteronism primarily results from the lack of angiotensin 2 stimulation as a result of hyporeninism. Conclusions Following unilateral adrenalectomy for PA, the occurrence of normal-to-high kalemia prompted an evaluation of the RA system using ortho-static stimulation test rather than simply measuring baseline values and evaluating the glucocorticoid axis. When confirmed, RA axis depression causes latent hypovolemia, meaning that all treatment likely to further decrease plasma volume should be avoided, while this may at times require mineralo-corticoid substitution.