Abstract: FR-PO0899
Topical Corticosteroid-Induced Syndrome of Apparent Mineralocorticoid Excess: A Reversible Cause of Resistant Hypertension and Hypokalemia
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Heady, Brittany, St Louis Kidney Consultants, Saint Louis, Missouri, United States
- Reisinger, Nathaniel, St Louis Kidney Consultants, Saint Louis, Missouri, United States
Introduction
Apparent mineralocorticoid excess (AME) is classically caused by genetic 11β-HSD2 deficiency or licorice ingestion. High-potency topical corticosteroids applied to large body surface area is an underrecognized exogenous cause. Sufficient systemic absorption can overwhelm 11β-HSD2 activity leading cortisol-induced activation of the mineralocorticoid receptor leading to a similar presentation to primary aldosteronism (PA).
Case Description
A 45-year-old woman with longstanding resistant hypertension and hypokalemia presented for nephrology evaluation. She was on a four-drug antihypertensive regimen including spironolactone with persistent hypokalemia despite supplementation (K 2.9-3.3), metabolic alkalosis (CO2 31), and a fully suppressed renin and aldosterone. A left adrenal nodule on prior CT had anchored evaluation toward a primary adrenal cause. Extensive history revealed years of daily high-potency topical triamcinolone applied to 40% body surface area (BSA) for psoriasis vulgaris. Spironolactone was stopped for ineffectiveness given the mineralocorticoid receptor is activated by cortisol rather than aldosterone. Amiloride was substituted for downstream ENaC blockade. Urgent dermatology referral was placed to pursue steroid-sparing therapy, and genetic testing was ordered to exclude Liddle syndrome and primary 11β-HSD2 deficiency.
Discussion
Combined suppression of both renin and aldosterone should prompt evaluation for exogenous glucocorticoid sources. Topical steroid burden is rarely quantified in hypertension workups but can be substantial with high-potency agents over large BSA. An incidental adrenal nodule led to early anchoring on PA, illustrating that imaging must be interpreted within the full biochemical context. AME from an exogenous source is better treated with ENaC blockade rather than reversible mineralocorticoid receptor antagonism and represents a potentially remediable etiology. Chronic high-potency topical corticosteroid use is important in the differential diagnosis for low-renin, low-aldosterone hypertension with hypokalemia. A thorough exposure history may reveal a treatable cause in otherwise refractory cases.