Abstract: FR-PO0383
Uncommon Presentations of Primary Aldosteronism: Edema and Hormonal Cosecretion
Session Information
- Hypertension and CVD: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1602 Hypertension and CVD: Clinical
Authors
- Alam, Sreyoshi Fatima, Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Young, William F., Mayo Clinic Minnesota, Rochester, Minnesota, United States
- Garovic, Vesna D., Mayo Clinic Minnesota, Rochester, Minnesota, United States
Introduction
Primary aldosteronism (PA), classically defined by hypertension and hypokalemia, can present atypically with normotension, edema, or hormonal co-secretion. We present two such cases: one in a normotensive, lean woman with chronic edema, and the other in a hypertensive woman with cortisol co-secretion from a right adrenal aldosterone-producing adenoma (APA). These cases expand PA’s clinical spectrum and highlight the importance of individualized evaluation.
Case Description
Case 1: Normotensive PA with Chronic Edema
A 49-year-old woman (BMI 18.3) developed mild hypertension, treated with thiazide diuretics, resulting in hypokalemia. Her BP normalized, thiazide was stopped, but peripheral edema persisted. Labs showed PAC 29.6 ng/dL and PRA 0.5 ng/mL/hr. Imaging was initially read as negative, but re-review revealed left adrenal micronodularity. She chose medical therapy with eplerenone, titrated to achieve PRA >1 ng/mL/hr and normokalemia.
Case 2: Cortisol Co-Secreting Right Adrenal APA in Hypertensive Woman
A 41-year-old woman developed hypokalemia in the third trimester of pregnancy, later diagnosed with postpartum hypertension and persistent edema. Ongoing BP and potassium fluctuations prompted endocrine workup. Initial labs: PAC 21.8 ng/dL, PRA 0.5; repeat: PAC 20.6, PRA 0.9; 24-hour urine aldosterone: 25.8 mcg on high sodium diet (442 mEq). DHEA-S remained consistently low (15–16 mcg/dL), suggesting chronic corticotropin suppression and cortisol co-secretion. A 1-mg dexamethasone suppression test (DST) showed abnormal cortisol (2.7 mcg/dL); 8-mg DST confirmed subclinical hypercortisolism (17.9 mcg/dL). Adrenal vein sampling (AVS) showed marked cortisol and aldosterone lateralization to the right adrenal (cortisol: 1190 vs. 174 mcg/dL; aldosterone: 15,000 vs. 1872 ng/dL), consistent with a right adrenal APA with cortisol co-secretion. CT showed a 1.1 cm lipid-rich right adrenal nodule. She underwent laparoscopic right adrenalectomy.
Discussion
These cases illustrate atypical PA presentations. The first shows that PA can exist without hypertension, presenting as edema from aldosterone-driven volume expansion. The second underscores evaluating cortisol co-secretion in PA with adrenal adenomas, as it affects AVS interpretation and management. Both highlight the need for diagnostic approaches beyond the classical PA phenotype.