SUN-228 Associations Between Aldosterone, Renin, and Arterial Stiffness in Indigenous and Non-Indigenous Australians

Disclosure: E. Ng: None. S.M. Gwini: None. B. Davison: None. P.J. Fuller: None. G. Singh: None. J. Yang: None. Background: Primary aldosteronism (PA), the most common endocrine cause of hypertension, is a modifiable risk factor for cardiovascular disease (CVD). Chronic aldosterone excess causes endothelial dysfunction and development of atherosclerosis and arterial stiffness. Indigenous Australians have a higher rate of hypertension and CVD, as well as higher rates of arterial stiffness, compared to the non-Indigenous population. However, the relationship between markers of PA and arterial stiffness has never been examined in Indigenous Australians. Aim: The aim of this study was to examine the relationship between markers of PA (aldosterone, renin and the aldosterone-to-renin ratio (ARR)) and arterial stiffness in participants of the Aboriginal Birth Cohort (ABC) (urban and remote) compared to age-matched non-Indigenous urban-residing participants of the Top End Cohort (TEC), at the age of 32-35 years. Methods: Arterial stiffness was measured non-invasively using a Cardio Wave Analyzer (SA-3000P) which provides information on several vascular parameters including arterial elasticity. Better vascular health is indicated by a higher value for arterial elasticity. Aldosterone and renin were measured by immunoassay. ARR > 50 or 70 pmol/L:mU/L (1.8 or 2.5 ng/dL:mU/L) were evaluated as thresholds for a positive screening test for PA. Results: There were 255 participants in the ABC (205 remote, 55 urban) and 76 in the TEC. Arterial elasticity was lower in the ABC compared to the TEC, with a median (P25, P75) value of -8 (-18, 6) in the urban ABC, -7 (-18, 8) in the remote ABC and 6 (-6, 16) in the TEC (p<0.001 for difference between groups). In the combined group, renin was inversely correlated with arterial elasticity, while ARR was positively associated with arterial elasticity, in both the unadjusted and adjusted analyses (accounting for BMI and eGFR). Evaluating the urban cohorts according to whether ARR was elevated or not did not identify significant differences in arterial elasticity. Discussion and Conclusion: Markers of PA did not correlate with a worse outcome in arterial elasticity. This may be a reflection of the young age of the cohort, given age is a major determinant of arterial stiffness. Even in the presence of aldosterone excess, chronicity is likely required before complications such as arterial stiffness occur. Follow-up of the vascular outcomes as the cohorts age may provide further insights into the relationship between markers of PA and vascular health, in both Indigenous and non-Indigenous Australians. Presentation: Sunday, July 13, 2025