Plasma renin activity and risk of cardiovascular and mortality outcomes among individuals with elevated and nonelevated blood pressure

Abstract

BackgroundWe sought to evaluate plasma renin activity (PRA) levels and risk of mortality and cardiovascular events among individuals with elevated blood pressure [systolic blood pressure (SBP) ≥ 140 mmHg] and those with controlled blood pressure (SBP < 140 mmHg) in a large diverse population.MethodsA retrospective cohort study between January 1, 2007, and December 31, 2013, among adults (≥ 18 years) within an integrated health system was conducted. Subjects were categorized by SBP into 2 groups: SBP < 140 mmHg and SBP ≥ 140 mmHg and then further categorized into population-based PRA tertiles within each SBP group. Cox proportional hazard modeling was used to estimate hazard ratios for cardiovascular and mortality outcomes among tertiles of PRA levels.ResultsAmong 6,331 subjects, 32.6% had SBP ≥ 140 mmHg. Multivariable hazard ratios and 95% confidence interval for PRA tertiles T2 and T3 compared to T1 in subjects with SBP ≥ 140 mmHg were 1.42 (0.99–2.03) and 1.61 (1.12–2.33) for ischemic heart events; 1.40 (0.93–2.10) and 2.23 (1.53–3.27) for congestive heart failure; 1.10 (0.73–1.68) and 1.06 (0.68–1.66) for cerebrovascular accident; 1.23 (0.94–1.59) and 1.43 (1.10–1.86) for combined cardiovascular events; and 1.39 (0.97–1.99) and 1.35 (0.92–1.97) for all-cause mortality, respectively. Among the SBP < 140 mmHg group, there was no relationship between PRA levels and outcomes.ConclusionHigher PRA levels demonstrated increased risk for ischemic heart events and congestive heart failure and a trend toward higher mortality among individuals with SBP ≥ 140 mmHg but not among those with SBP < 140 mmHg.

Treatment combining aliskiren with paricalcitol is effective against progressive renal tubulointerstitial fibrosis via dual blockade of intrarenal renin

“…Angiotensin-converting enzyme (ACE) then converts angiotensin I to angiotensin II, and it also degrades bradykinins to inactive fragments, reducing the serum levels of endogenous vasodilators [ 4 ]. Thus, renin is positioned at the top of the renin-angiotensin system (RAS) that preserves end-organ perfusion by regulating extracellular fluid, sodium and water balance, and cardiovascular activity [ 4 – 5 ]. In various renal injury models, the activation of the RAS increases transforming growth factor-beta (TGF-β), plasminogen activator inhibitor (PAI)-1 and α-smooth muscle actin (α-SMA) expressions in the kidneys [ 1 , 6 ], contributing to the progression of renal interstitial fibrosis.…”

Renin Feedback Is an Independent Predictor of Outcome in HFpEF

“…PRA correlates with blood pressure and pre-treatment plasma renin levels were able to predict the response to blood pressure medication [ 12 , 13 ]. Present data also suggest that patients with higher levels of plasma renin have an increased risk for ischemic events and congestive HF, even irrespective of blood pressure [ 14 ]. Pavo et al have recently described low- and high-renin HFrEF phenotypes, indicating that patients react to RAAS inhibitors with a different extent of renin up-regulation [ 15 ].…”

Renin Activity in Heart Failure with Reduced Systolic Function—New Insights

“…Higher PRA levels were associated with a greater likelihood for prevalence of congestive HF in a large diverse cross sectional study on hypertensive individuals [168]. Elevated PRA levels demonstrated increased risk for congestive HF and a trend toward higher mortality among patients with systolic blood pressure (SBP) ≥ 140 mmHg, but this was not true for individuals with SBP < 140 mmHg [169]. PRA was significantly elevated in ambulatory chronic HFrEF patients and in acute HFrEF patients [170].…”