Renin Angiotensin Inhibition and Lower Risk of Kidney Failure in Patients with Heart Failure: Subtitle: RAS inhibition and kidney failure in heart failure

Authors

Samir S. Patel, Veterans Affairs Medical Center, Washington, DC; George Washington University, Washington, DC.
Venkatesh K. Raman, Veterans Affairs Medical Center, Washington, DC; Georgetown University, Washington, DC.
Sijian Zhang, Veterans Affairs Medical Center, Washington, DC.
Helen M. Sheriff, Veterans Affairs Medical Center, Washington, DC; George Washington University, Washington, DC.
Gregg C. Fonarow, University of California, Los Angeles, CA.
Paul A. Heidenreich, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA; Stanford University School of Medicine, Stanford, CA.
Charles Faselis, Veterans Affairs Medical Center, Washington, DC; George Washington University, Washington, DC; Uniformed Services University, Washington, DC.
Phillip H. Lam, Georgetown University, Washington, DC; MedStar Washington Hospital Center, Washington, DC.
Charity J. Morgan, Veterans Affairs Medical Center, Washington, DC; University of Alabama at Birmingham, Birmingham, AL.
Hans Moore, Veterans Affairs Medical Center, Washington, DC; George Washington University, Washington, DC; Georgetown University, Washington, DC; Uniformed Services University, Washington, DC.
David Atkins, Veterans Affairs Medical Center, Washington, DC.
Yan Cheng, Veterans Affairs Medical Center, Washington, DC; George Washington University, Washington, DC.
Yijun Shao, Veterans Affairs Medical Center, Washington, DC; George Washington University, Washington, DC.
Prakash Deedwania, Veterans Affairs Medical Center, Washington, DC; University of California, San Francisco, CA.
Carlos E. Palant, George Washington University, Washington, DC.
Brian C. Sauer, Veterans Affairs Medical Center, Salt Lake City, Utah; University of Utah, Salt Lake City, Utah.
Ravindra L. Mehta, University of California San Diego, La Jolla, CA.
Thomas E. Love, Case Western Reserve University, Cleveland, OH.
Richard M. Allman, George Washington University, Washington, DC; MedStar Washington Hospital Center, Washington, DC; Wake Forest University, Winston-Salem, NC.
Michael S. Heimall, Veterans Affairs Medical Center, Washington, DC; HealthWell Foundation, Germantown, MD.
Wen-Chih Wu, Veterans Affairs Medical Center, Providence, RI; Brown University, Providence, RI.
Qing Zeng-Treitler, Veterans Affairs Medical Center, Washington, DC; George Washington University, Washington, DC.
Ali Ahmed, Veterans Affairs Medical Center, Washington, DC; George Washington University, Washington, DC; Georgetown University, Washington, DC. Electronic address: ali.ahmed@va.gov.

Document Type

Journal Article

Publication Date

5-7-2025

Journal

The American journal of medicine

DOI

10.1016/j.amjmed.2025.04.038

Keywords

RAS inhibitors; heart failure; kidney failure

Abstract

BACKGROUND: Renin-angiotensin system (RAS) inhibitors reduce risk of kidney failure in patients with chronic kidney disease, but worsen kidney function in heart failure patients, especially in those with chronic kidney disease. Less is known about risk of kidney failure in heart failure patients receiving RAS inhibitors. METHODS: We used propensity score matching for outcome-blinded assembly of 168,860 Veterans with heart failure phenotyped by artificial intelligence who were balanced on 77 baseline characteristics and initiated on RAS inhibitors. Hazard ratio (95% CI) for 5-year kidney failure in high-dose (versus low-dose) RAS inhibitor group was estimated, accounting for competing risk of death. Kidney failure was defined as kidney replacement therapy or estimated glomerular filtration rate (eGFR) <15 mL/min/1.73m. RESULTS: New-onset kidney failure occurred in 4.1% (3455/84,430) and 3.5% (2966/84,430) of patients in low-dose and high-dose RAS inhibitor groups, respectively (HR, 0.85; 95%CI, 0.81-0.89). Respective HRs (95%CIs) in eGFR subgroups ≥60, 45-59 and 15-44 mL/min/1.73m were 1.21 (1.08-1.36), 0.93 (0.82-1.05) and 0.82 (0.77-0.87). The association was similar across ejection fraction subgroups. There was a lower risk of death in the subgroup with ejection fraction ≤40%. CONCLUSIONS: Patients with heart failure receiving high-dose (versus low-dose) RAS inhibitors had a lower associated risk of kidney failure, which was driven by the subgroup with chronic kidney disease. This new information may help to inform future guideline recommendations and clinical practice regarding RAS inhibitor use in these patients. Future studies need to examine this association in those with normal kidney function.

Department

Medicine

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