Characterization of Subclinical Primary Aldosteronism in Normotension

Presentation Number: SUN 525
Date of Presentation: April 2nd, 2017

Rene Baudrand*1, Francisco J Guarda1, Gregory Hundemer2, Jenifer Michelle Brown3, Gordon H Williams2 and Anand Vaidya2
1Pontificia Universidad Catolica de Chile, Santiago, Chile, 2Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 3Brigham and Women's Hospital, Harvard Medical School, MA


Context: Primary aldosteronism (PA) is classically a severe renin-independent aldosteronism that causes hypertension. Recent data suggest that milder forms of renin-independent aldosteronism may be common, even in normotension.

Methods: We investigated this hypothesis by identifying and characterizing PA among 210 normotensive participants in comparison to 387 untreated mild hypertensive participants. Participants completed an oral sodium suppression test, received an infusion of angiotensin II, and had measurements of blood pressure (BP) and renal blood flow (RBF). PA was defined by: urinary aldosterone excretion >12 mcg/24h in the setting of urinary sodium excretion >200 mmol/24h, plus a suppressed plasma renin activity (<1.0 ng/mL/h).

Results: The prevalence of PA was 14% (29/210) in normotension and 28% (107/387) in hypertension. Normotensives with PA, when compared to normotensives without PA, had higher 24h urinary aldosterone excretion (20.2±12.2 vs 6.2±2.9 mcg/24h, P<0.001), higher 24h urinary potassium excretion (P=0.039), and greater aldosterone stimulation with angiotensin II (+352% vs +206%; P<0.001); however, there were no differences in age, aldosterone-to-renin ratio (ARR), BP, or RBF. In contrast, participants with hypertensive PA, when compared to normotensive PA, were older (48.6±6.8 vs 42.4±9.9, P<0.001), had higher ARR (30.2±31.5 vs 14.9±15.2, P<0.01), higher systolic BP (149 ± 20 vs 111 ± 12 mmHg; P<0.001), and impaired renal blood flow (502 ± 95 vs 586 ± 92 mL/min/1.73m2P<0.001), despite having the same degree of urinary aldosterone excretion when sodium loaded (19.1 ± 8.1 vs. 20.2 ± 12.2 mcg/24h; P=0.57).

Conclusions: We detected a relatively high frequency of PA among normotensives who would typically never have been suspected to have PA. Normotensives with PA were younger and had an apparently normal vascular phenotype when compared to hypertensive PA. These findings suggest that PA may originate as a subclinical syndrome in normotension, and progress in severity to a clinical syndrome of hypertension and vascular dysfunction.


Nothing to Disclose: RB, FJG, GH, JMB, GHW, AV