High Aldosterone Levels, Hypertension and Adrenal Adenoma in a 36 Year-Old Pregnant Patient: Is This Primary Hyperaldosteronism?

Presentation Number: SAT 377
Date of Presentation: April 1st, 2017

Amanda J Brahm*1, Stan Van Uum2, Deborah Penava3 and Dongmei Sun3
1Western University, London, ON, 2Division of Endocrinology and Metabolism, Department of Medicine, Western University, London, ON, Canada, 3Western University

Abstract

A 36-year-old woman with no personal or family history of hypertension presented at 16 weeks gestation with hypertensive urgency. Potassium was intermittently low (3.1mmol/L). Aldosterone was elevated (3000pmol/L (N <1118)), renin remained unsuppressed (40.7ng/L (N1.7-23.9)), with normal aldosterone to renin ratios. An adrenal MR detected a 1.8 x 1.4 cm left adrenal adenoma. 24-hour urine collection for metanephrines and catecholamines was normal. She was managed conservatively, with close maternal and fetal surveillance, and treatment with labetalol and nifedipine. She achieved reasonable blood pressure control, with no obstetric complications. Post-partum blood pressures remained elevated with normal aldosterone (539 pmol/L), unsuppressed renin (5.2 ng/L) and normal aldosterone-to-renin ratio (104 (N<144)). She had normal response to 1mg dexamethasone suppression test and normal suppression of aldosterone with saline infusion. These results suggest an alternative cause of her hypertesion with an incidental finding of an adrenal adenoma.

This case highlights the many difficulties associated with investigations and management of suspected primary hyperaldosteronism in pregnancy. Outside of pregnancy, the accepted screening test is the aldosterone to renin ratio, with confirmatory tests including a saline suppression test, captopril challenge or salt/fludrocortisone load. However, these tests lack validated pregnancy reference ranges or are contraindicated. Pregnancy has significant effects on the renin-angiotensin-aldosterone pathway leading to physiologic elevations in both aldosterone and renin: progesterone competitively binds to aldosterone receptors; ovaries and placental tissues secrete renin; estrogen stimulates angiotensinogen production. While primary hyperaldosteronism has been associated with poor pregnancy outcomes, optimal management in pregnancy is not clearly established. Conservative treatment with traditional antihypertensives, cautious use of mineralocorticoid receptor antagonists, or surgical adrenalectomy are all possible treatment options reported in the literature.

 

Nothing to Disclose: AJB, SV, DP, DS