*2.1. Renin and Aldosterone*

African Americans excrete a sodium load more slowly and less completely than whites [45]. This results in suppression of the renin-aldosterone-angiotensin system (RAAS) due to volume-loading that typically begins in childhood [46–49]. Ultimately, a low-renin state, which compensates for the relative tendency to retain sodium, ensues [50]. Low-renin hypertension is a frequent cause of hypertension, with a prevalence of 20%–30%, and higher in African Americans [51–53]. One study demonstrated lower levels of plasma renin activity and aldosterone in normotensive African Americans across all ages, with BP positively correlating with plasma aldosterone, an effect that increased as plasma renin activity decreased [48]. Thus, a typical biochemical profile in an African American person with hypertension is a low or high plasma aldosterone concentration, a low or suppressed plasma renin activity or direct renin concentration, and suppressed angiotensin I and II [36,50,54,55]. This results in a normal or elevated aldosterone-to-renin ratio, which can be categorized into two broad hypertension phenotypes: low or suppressed renin and elevated aldosterone (primary aldosteronism type, or hyporeninemic hyperaldosteronism) and low renin and low aldosterone (Liddle syndrome type, or hyporeninemic hypoaldosteronism) [56]. The threshold set to diagnose a low renin state is assay specific but generally defined as a plasma renin activity < 0.65 ng/mL/h or a direct renin concentration < 15μU/mL [52].
