Key result
Higher baseline renin is linked to ~47% increased death or HF hospitalization.
Why the study?
Data are limited on the associations of renin and aldosterone levels with clinical profiles, treatment response, and outcomes in patients with heart failure.
Does elevated baseline renin and aldosterone increase the risk of all-cause mortality or heart failure hospitalization in patients with symptomatic heart failure?
Cohort (n=2,039)
Yes
Does elevated baseline renin and aldosterone increase the risk of all-cause mortality or heart failure hospitalization in patients with symptomatic heart failure?
Hazard Ratio: 1.47 (95% CI 1.16–1.86)
p-value: p=0.002
Circulating levels of renin and aldosterone in heart failure reflect disease severity and MRA use, but do not provide additive prognostic value over established clinical risk models.
Elevated renin signals higher HF event risk but adds no prognostic value; leaves open any therapeutic role beyond reflecting disease severity.
Aims Activation of the renin–angiotensin–aldosterone system plays an important role in the pathophysiology of heart failure (HF) and has been associated with poor prognosis. There are limited data on the associations of renin and aldosterone levels with clinical profiles, treatment response, and study outcomes in patients with HF. Methods and results We analysed 2,039 patients with available baseline renin and aldosterone levels in BIOSTAT-CHF (a systems BIOlogy study to Tailored Treatment in Chronic Heart Failure). The primary outcome was the composite of all-cause mortality or HF hospitalization. We also investigated changes in renin and aldosterone levels after administration of mineralocorticoid receptor antagonists (MRAs) in a subset of the EPHESUS trial and in an acute HF cohort (PORTO). In BIOSTAT-CHF study, median renin and aldosterone levels were 85.3 (percentile25–75 = 28–247) μIU/mL and 9.4 (percentile25–75 = 4.4–19.8) ng/dL, respectively. Prior HF admission, lower blood pressure, sodium, poorer renal function, and MRA treatment were associated with higher renin and aldosterone. Higher renin was associated with an increased rate of the primary outcome [highest vs. lowest renin tertile: adjusted-HR (95% CI) = 1.47 (1.16–1.86), P = 0.002], whereas higher aldosterone was not [highest vs. lowest aldosterone tertile: adjusted-HR (95% CI) = 1.16 (0.93–1.44), P = 0.19]. Renin and/or aldosterone did not improve the BIOSTAT-CHF prognostic models. The rise in aldosterone with the use of MRAs was observed in EPHESUS and PORTO studies. Conclusions Circulating levels of renin and aldosterone were associated with both the disease severity and use of MRAs. By reflecting both the disease and its treatments, the prognostic discrimination of these biomarkers was poor. Our data suggest that the “point” measurement of renin and aldosterone in HF is of limited clinical utility.
No takes yet. Share an insight, caveat, or question.
Kobayashi et al. (2020) conducted a cohort in Symptomatic Heart Failure (n=2,039). Higher baseline renin levels (highest tertile) vs. Lowest renin tertile was evaluated on Composite of all-cause mortality or heart failure hospitalization (adjusted-HR 1.47, 95% CI 1.16-1.86, p=0.002). Higher baseline renin levels were associated with a 47% increased risk of all-cause mortality or heart failure hospitalization compared to the lowest tertile (adjusted HR 1.47), but did not improve prognostic risk stratification.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: