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Abstract: FR-OR016

Mortality Outcomes Related to Acute Declines in eGFR following RAAS Inhibition in Patients with Heart Failure

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention


  • McCallum, Wendy I., Tufts Medical Center, Boston, Massachusetts, United States
  • Tighiouart, Hocine, Tufts Medical Center, Boston, Massachusetts, United States
  • Ku, Elaine, University of California San Francisco Medical Center, San Francisco, California, United States
  • Salem, Deeb N., Tufts Medical Center, Boston, Massachusetts, United States
  • Sarnak, Mark J., Tufts Medical Center, Boston, Massachusetts, United States

Blockade of the renin-angiotensin-aldosterone system (RAAS) is beneficial for cardiovascular outcomes in heart failure with reduced ejection fraction (HFrEF). However, it is associated with acute declines in estimated glomerular filtration rate (eGFR). Whether the benefit of RAAS inhibition persists for all magnitudes and timing of acute declines remains unclear.


We performed a retrospective analysis of the Studies Of Left Ventricular Dysfunction (SOLVD) trial, in which patients with HFrEF were randomized to enalapril vs placebo. Multivariable Cox models were used to evaluate the association of % eGFR change from baseline to three follow-up time points (2 weeks, 6 weeks, 12 months) with mortality. We tested for an interaction between treatment group and % eGFR decline. In effort to separate eGFR decline secondary to RAAS inhibition from eGFR decline due to other causes, we also calculated the mortality hazard ratios for enalapril and placebo using the reference point of 0% eGFR decline on placebo.


Using the 2-week follow-up time point, 6,031 participants were included in the analysis (n=3,015 in the enalapril group, n=3,016 in placebo). Compared to placebo, enalapril was associated with a lower hazard of mortality at all levels of eGFR decline, with no significant interaction between treatment assignment and eGFR decline (Figure A). When compared to patients randomized to placebo with 0% eGFR decline, up to 20% decline in the enalapril group was still associated with a lower hazard of mortality (Figure B). Declines of >20% in placebo had higher hazard of mortality compared to placebo with 0% decline, but similar declines in the enalapril group were not. Results were consistent using the time points of 6 weeks and 12 months.


Enalapril decreases mortality at all levels of eGFR decline when compared to placebo. In patients with HFrEF, ACE inhibitors should be continued even if there is an acute decline in GFR up to 20%.


  • Other NIH Support