Key result
SGLT2 inhibitors linked to ~51% lower all-cause mortality in patients with HFpEF and ESRD.
Why the study?
Major trials established the cardiovascular benefits of SGLT2 inhibitors in HFpEF but excluded patients with very low eGFR or on dialysis, leaving data limited in patients with coexisting ESRD.
Do SGLT2 inhibitors reduce mortality, ADHF events, hospitalizations, and ED visits in patients with HFpEF and ESRD?
Cohort (n=7,238)
Yes
Do SGLT2 inhibitors reduce mortality, ADHF events, hospitalizations, and ED visits in patients with HFpEF and ESRD?
Hazard Ratio: 0.49 (95% CI 0.43–0.55)
Absolute Event Rate: 11.8% vs 24.4%
Absolute Risk Reduction: 12.6%
p-value: p=<0.001
SGLT2 inhibitor use in patients with HFpEF and ESRD is associated with significantly reduced risks of all-cause mortality, acute decompensated heart failure, and hospitalizations.
May support SGLT2i use in HFpEF-ESRD; extends trial data to dialysis patients but leaves randomized confirmation open.
Introduction: Heart failure with preserved ejection fraction (HFpEF) commonly coexists with end-stage renal disease (ESRD, together increasing cardiovascular risk [1,2,3,4,5]. While SGLT2 inhibitors (SGLT2i) reduce HF hospitalizations and cardiovascular death in trials like EMPEROR-Preserved and DELIVER, patients with very low eGFR or on dialysis were excluded [6,7]. While trials are ongoing, data on SGLT2i in this high-risk population remain limited. Hypothesis: SGLT2i is associated with improved cardiovascular outcomes in HFpEF patients with ESRD. Methods: We conducted a retrospective cohort analysis of deidentified, aggregate patient data from the TriNetX research network. Patients with HFpEF and ESRD between age 18-85 were included. Patients were stratified by SGLT2i use and propensity matched by demographics, baseline cardiac risk factors, DM medications, and etiology of HFpEF. Outcomes were evaluated within 18-months from the HFpEF + ESRD diagnosis. Primary endpoints included acute decompensated heart failure (ADHF) events, all-cause mortality, hospitalizations for any cause, and emergency department visits for any cause. Z-tests were used to calculate risk difference and Cox regression was used to compute hazard ratios over an 18-month period. Results: The study cohort included 7,238 patients (n = 3,619 per group; mean age 65.3 ± 11.0 years; 40.9% female; 47.3% White). In time-to-event analysis, the SGLT2i group had reduced risk of all-cause mortality (HR=0.49, 95%CI 0.43-0.55, p<0.001) and ADHF events (HR=0.72, 95%CI 0.67-0.77, p < 0.001). At 18 months SGLT2i group had lower rates of all-cause mortality (11.8% vs. 24.4%; RD -12.6%, p < 0.001), ADHF events (39.8% vs. 50.1%; RD -10.4%, p < 0.001) [Figure 1], hospitalizations (51.3% vs. 65.0%; RD -13.8%, p < 0.001) [Figure 1], and at least one ED visit (35.9% vs. 40.6%; RD -4.7%; p < 0.001). Conclusion: In this retrospective propensity-matched analysis, SGLT2i use in HFpEF with ESRD was associated with reduced mortality, ADHF, hospitalizations, and ED visits. Further investigation is needed to clarify mechanisms and guide clinical recommendations.
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Evenhuis et al. (2025) conducted a cohort in Heart failure with preserved ejection fraction (HFpEF) and end-stage renal disease (ESRD) (n=7,238). SGLT2 inhibitors vs. Non-use was evaluated on All-cause mortality (HR 0.49, 95% CI 0.43-0.55, p=<0.001). SGLT2 inhibitor use in patients with HFpEF and ESRD was associated with reduced all-cause mortality compared to non-use (11.8% vs 24.4%; HR 0.49; 95% CI 0.43-0.55; P<0.001).
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