From hypokalemia to hyponatremia: Sequential recognition of primary aldosteronism and central adrenal insufficiency after tuberculum sellae meningioma surgery

Abstract

Background: Coexisting primary aldosteronism (PA) and adrenal insufficiency is rare and diagnostically challenging because mineralocorticoid excess and cortisol deficiency may produce overlapping or opposing abnormalities. We report PA with newly recognized central adrenal insufficiency following surgery for tuberculum sellae meningioma.

Case summary: A 40-year-old woman with 5 years of hypertension presented with recurrent sudden-onset limb weakness for 4 years that improved with potassium supplementation. She underwent craniotomy for tuberculum sellae meningioma in January 2025 and received high-dose glucocorticoids postoperatively. During steroid tapering, her weakness worsened with severe hypokalemia. Preoperative assessment had shown preserved cortisol reserve. Laboratory evaluation showed potassium 2.91 mmol/L, suppressed renin (0.631 mIU/L), elevated aldosterone (257.9 pmol/L), and an aldosterone-to-renin ratio of 408.8 pmol/mIU, supporting PA. CT revealed a left adrenal adenoma, presumed to be the source of autonomous aldosterone secretion. Persistent hyponatremia (nadir 128 mmol/L) despite correction of hypokalemia prompted reassessment of the HPA axis. Morning cortisol was 294 nmol/L and ACTH 36.1 pg/mL; a short Synacthen test showed an inadequate peak cortisol 308 nmol/L, supporting adrenal insufficiency. Considering the previously normal cortisol reserve, recent tuberculum sellae surgery, and glucocorticoid exposure, the insufficiency was considered central, with postoperative hypothalamic-pituitary dysfunction and steroid-induced HPA suppression as plausible mechanisms. She received potassium and sodium supplementation, a mineralocorticoid receptor antagonist, and glucocorticoid replacement, followed by left adrenalectomy in September 2025. Adrenal venous sampling was unavailable, so lateralization was based on biochemical findings and CT. By January 2026, weakness had resolved, potassium was 4.2 mmol/L, and blood pressure was controlled without antihypertensives. Morning cortisol was 324 nmol/L and aldosterone decreased to 3.2 ng/dL.

Conclusions: This case emphasizes that persistent or discordant electrolyte abnormalities after neurosurgery may reflect coexisting endocrine disorders. Concurrent evaluation of the renin-aldosterone system and HPA axis can facilitate accurate diagnosis and appropriate treatment. Lack of adrenal venous sampling remains an important limitation.

[J Assoc Clin Endocrinol Diabetol Bangladesh, 2026;5(Suppl 1): S65]