Key result
Finerenone, SGLT2 inhibitors, and GLP-1 receptor agonists significantly reduced the risk of major adverse cardiovascular events compared to placebo (RR 0.88, 0.84, and 0.88, respectively) in patients with T2DM and CKD.
Why the study?
To evaluate the comparative cardiovascular and renal benefits of finerenone, SGLT2 inhibitors, and GLP-1 receptor agonists in patients with type 2 diabetes mellitus and chronic kidney disease.
Do finerenone, SGLT2 inhibitors, or GLP-1 receptor agonists reduce cardiovascular and renal events in patients with T2DM and CKD?
Meta-Analysis (n=51,496)
Yes
Do finerenone, SGLT2 inhibitors, or GLP-1 receptor agonists reduce cardiovascular and renal events in patients with T2DM and CKD?
Relative Risk: 0.88 (95% CI 0.8–0.97)
In patients with T2DM and CKD, SGLT2 inhibitors, finerenone, and GLP-1 receptor agonists offer distinct cardiorenal benefits, with SGLT2i showing the most robust reductions in renal events and heart failure hospitalizations.
SGLT2i may be prioritized for renal and HHF risk reduction in T2DM-CKD; extends comparative RCT evidence among these therapies.
Objective: To evaluate the cardiovascular and renal benefits of finerenone, sodium-glucose cotransporter-2 inhibitors (SGLT2i) and glucagonlike peptide-1 receptor agonists (GLP-1 RA) in patients with Type 2 Diabetes Mellitus (T2DM) and chronic kidney disease (CKD) with network meta-analysis.Methods: Systematic literature searches were conducted of PubMed, Cochrane Library, Web of Science, Medline and Embase covering January 1, 2000 to December 30, 2021. Randomized control trials (RCTs) comparing finerenone, SGLT-2i and GLP-1 RA in diabetics with CKD were selected. We performed a network meta-analysis to compare the three drugs indirectly. Results were reported as risk ratio (RR) with corresponding 95% confidence interval (CI).Results: In all, 17 RCTs were selected, including 51,496 patients. Finerenone reduced the risk of renal events and hospitalization for heart failure (HHF) (RR [95%CI]; 0.86 [0.79–0.93], 0.79 [0.67,0.92], respectively). SGLT-2i were associated with reduced risks of major adverse cardiovascular events (MACE) (RR [95%CI]; 0.84 [0.78–0.90]), renal events (RR [95%CI]; 0.67 [0.60–0.74], HHF (RR [95%CI]; 0.60 [0.53–0.68]), all-cause death (ACD) (RR [95%CI]; 0.89 [0.81–0.91]) and cardiovascular death (CVD) (RR [95%CI]; 0.86 [0.77–0.96]) compared to placebo. GLP-1 RA were associated with a lower risk of MACE (RR [95%CI]; 0.88 [0.80–0.97]). As for renal outcomes and HHF, SGLT2i had significant effect in comparison to finerenone (RR [95%CI]; 1.29 [1.13–1.47], 1.31 [1.07–1.61], respectively) and GLP-1 RA (RR [95%CI]; 1.36 [1.16–1.59], 1.49 [1.18–1.89], respectively). Compared with placebo, there was a trend toward reduction in ACD with finerenone (RR [95%CI]; 0.90 [0.80–1.00]). GLP-1 RA did not reduce the risk of renal events, HHF, CVD and ACD, but the analysis based on chemical structure showed that a GLP-1 analogues, liraglutide (RR [95%CI]; 0.79 [0.67–0.92], 0.69 [0.52–0.90], 0.76 [0.62–0.93], respectively) showed significant effect in HHF, CVD and ACD, while an exendin-4 analogues, exenatide (RR [95%CI]; 1.10 [0.83–1.46], 1.19 [0.84–1.69], 1.10 [0.87–1.39], respectively), did not.Conclusions: In patients with T2DM and CKD, finerenone led to a risk reduction in renal events and HHF, SGLT2i were associated with a decreased risk of cardiovascular and renal events. GLP-1 RA were associated with a decreased risk of MACE. Among GLP-1 RA, GLP-1 analogues showed significantly reduced cardiovascular events compared with exendin-4 analogues.
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Zhang et al. (2022) conducted a meta-analysis in Type 2 Diabetes Mellitus and Chronic Kidney Disease (n=51,496). Finerenone, SGLT2 inhibitors, and GLP-1 receptor agonists vs. Placebo was evaluated on Major adverse cardiovascular events (MACE) (RR 0.88, 95% CI 0.80-0.97). Finerenone, SGLT2 inhibitors, and GLP-1 receptor agonists significantly reduced the risk of major adverse cardiovascular events compared to placebo (RR 0.88, 0.84, and 0.88, respectively) in patients with T2DM and CKD.
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