Kidney Week

Abstract: FR-OR016

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

Session Information

• AKI: Can We Improve Outcomes?
  October 26, 2018 | Location: 6A, San Diego Convention Center
  Abstract Time: 05:30 PM - 05:42 PM

Category: Acute Kidney Injury

• 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

• McCallum, Wendy I., Tufts Medical Center, Boston, Massachusetts, United States

Wendy I. McCallum, MD



Wendy McCallum is a Nephrology Fellow at Tufts Medical Center in Boston, MA. She completed medical school at Umass Medical School and completed her internal medicine residency at Tufts Medical Center.

• Tighiouart, Hocine, Tufts Medical Center, Boston, Massachusetts, United States

Hocine Tighiouart,

• Ku, Elaine, University of California San Francisco Medical Center, San Francisco, California, United States

Elaine Ku,

• Salem, Deeb N., Tufts Medical Center, Boston, Massachusetts, United States

Deeb N. Salem,

• Sarnak, Mark J., Tufts Medical Center, Boston, Massachusetts, United States

Mark J. Sarnak,

Background

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.

Methods

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.

Results

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.

Conclusion

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%.

Funding

• Other NIH Support