# Cardio-Vasculo-Renal Benefits of SGLT2 Inhibitors in Heart Failure: A Retrospective Study from a Lower-Resource Tertiary Center

**Authors:** Olivia-Maria Bodea, Gabriel Florin Răzvan Mogoș, Nilima Rajpal Kundnani, Abhinav Sharma, Ovidiu Adam, Daniel Marius Duda-Seiman, Dana Velimirovici, Marioara Nicula-Neagu, Ovidiu Horea Bedreag, Simona Dragan

PMC · DOI: 10.3390/medicina62020256 · 2026-01-26

## TL;DR

This study shows that SGLT2 inhibitors may reduce heart failure and kidney risks in patients with heart failure, even in lower-resource settings.

## Contribution

The study provides real-world evidence of SGLT2 inhibitors' benefits in a lower-resource setting with heart failure patients.

## Key findings

- SGLT2 inhibitors were linked to a 30% lower risk of cardio-vasculo-renal events.
- Patients on SGLT2 inhibitors had fewer heart failure hospitalizations.
- Kidney function declined more slowly in those treated with SGLT2 inhibitors.

## Abstract

Background and Objectives: Heart failure frequently coexists with CKD, compounding prognosis via cardio-renal interplay. Sodium glucose cotransporter 2 (SGLT2) inhibitors have demonstrated cardiovascular and renal benefits in randomized trials, but data remain limited in real-world lower-resource settings. Materials and Methods: We conducted a retrospective single-center cohort study at a tertiary university hospital in western Romania, including adults with chronic HF and LVEF ≤ 45%, monitored between 2021–2024. Patients were stratified based on receipt of SGLT2 inhibitors. The primary endpoint was a composite of cardiovascular death, HF hospitalization, or ≥40% sustained decline in eGFR/initiation of KRT. Annual eGFR slope was analyzed to assess renal trajectory. Results: Among 240 patients, treatment with SGLT2 inhibitors was associated with a lower risk of the composite cardio-vasculo-renal endpoint compared with no treatment (adjusted HR 0.70, 95% CI 0.50–0.98). The reduction was primarily driven by fewer heart failure hospitalizations. Decline in kidney function was slower among SGLT2 inhibitor-treated patients in longitudinal mixed-effects analyses. Conclusions: In this retrospective cohort, SGLT2 inhibitor use was associated with fewer cardio-renal events and a slower decline in kidney function. Given the observational design and residual confounding risk, these findings should be considered hypothesis-generating but provide implementation-relevant signals supporting further prospective evaluation.

## Linked entities

- **Diseases:** heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}
- **Diseases:** injury to (MESH:D014947), hepatic dysfunction (MESH:D008107), inflammation (MESH:D007249), volume overload (MESH:D019190), eGFR loss (MESH:D016388), fibrosis (MESH:D005355), kidney failure (MESH:D051437), eGFR decline (MESH:D060825), diabetes (MESH:D003920), endothelial dysfunction (MESH:D014652), ischemic (MESH:D002545), malignancy (MESH:D009369), CKD (MESH:D051436), azotemia (MESH:D053099), volume depletion (MESH:C536350), acute kidney injury (MESH:D058186), stroke (MESH:D020521), venous congestion (MESH:D006940), renal (MESH:D006030), arrhythmic (OMIM:212500), decline in kidney function (MESH:D007680), anemia (MESH:D000740), Cardio-Vasculo-Renal (MESH:D059347), albuminuria (MESH:D000419), hypertension (MESH:D006973), vascular stiffness (MESH:C566112), ventricular hypertrophy (MESH:D024741), atherosclerotic (MESH:D050197), Myocardial infarction (MESH:D009203), infection (MESH:D007239), CKD (MESH:D012080), Cardiovascular Diseases (MESH:D002318), output (MESH:D002303), atrial fibrillation (MESH:D001281), COVID-19 (MESH:D000086382), ischemic stroke (MESH:D002544), type 2 diabetes (MESH:D003924), HF (MESH:D006333), impaired kidney function (MESH:D007674), genitourinary infections (MESH:D014564), cardiac remodeling (MESH:D020257), type 1 diabetes mellitus (MESH:D003922), genital mycotic infections (MESH:D015821), DKA (MESH:D016883), myocardial dysfunction (MESH:D006331), systolic (MESH:D000092244), HFpEF (MESH:D054144)
- **Chemicals:** MRA (MESH:C502936), uric acid (MESH:D014527), aldosterone (MESH:D000450), canagliflozin (MESH:D000068896), peptide (MESH:D010455), empagliflozin (MESH:C570240), nitric oxide (MESH:D009569), EMPEROR (-), dapagliflozin (MESH:C529054), DAPA (MESH:C020269), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942245/full.md

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Source: https://tomesphere.com/paper/PMC12942245