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Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Endothelial dysfunction is a major contributor to cardiovascular morbidity in patients with chronic kidney disease (CKD). Sodium-glucose co-transporter-2 (SGLT-2) inhibitors, such as dapagliflozin and empagliflozin, provide cardiovascular and renal protection beyond their glucose-lowering effects, partly by improving endothelial function. Variations in the endothelial nitric oxide synthase (eNOS) gene, particularly the T(-786)C polymorphism, may alter nitric oxide (NO) bioavailability and influence vascular responses to these agents. This study aimed to compare the effects of dapagliflozin and empagliflozin on endothelial function in CKD patients and to determine whether the eNOS T(-786)C polymorphism modulates this response.
A 12-week, prospective, controlled study was conducted in 180 CKD patients (eGFR 25–75 mL/min/1.73 m²). Participants were randomized to receive dapagliflozin (10 mg/day, n=90) or empagliflozin (10 mg/day, n=90). Endothelial function was assessed by brachial artery flow-mediated dilation (FMD) at baseline and after 12 weeks using high-resolution ultrasound (10 MHz linear transducer). Measurements were obtained in the morning, after an overnight fast and 10 minutes of rest, in a temperature-controlled room. FMD was expressed as the percentage change in arterial diameter from baseline to post-occlusion hyperemia.
Genotyping for the eNOS T(-786)C polymorphism was performed by PCR, and patients were stratified into TT, TC, and CC genotype subgroups (Table 1)
Table 1. Frequency of eNOS 786T>C (rs2070744) Genotypes and Alleles
eNOS 786T>C Genotype
Group I (n = 90)
Group II (n = 90)
p
TT
27 (30.0%)
29 (32.2%)
0.747
TC
28 (31.1%)
0.871
CC
35 (38.9%)
34 (37.8%)
0.878
Allele
T
82 (45.6%)
85 (47.2%)
0.833
C
98 (54.4%)
95 (52.8%)
0.864
After randomization, a total of 180 patients with chronic kidney disease were assigned to two treatment groups: Group I, which received dapagliflozin 10 mg daily (n = 90), and Group II, which received empagliflozin 10 mg daily (n = 90). At baseline, there were no significant differences between the two groups in demographic or clinical variables, including age, BMI, disease duration, blood pressure, glycemic status, lipid parameters, and serum creatinine ( p > 0.05). After 2 monthes of SGLT-2 inhibitor treatment, a marked and statistically significant improvement in endothelial function was observed in patients carrying the TT and TC genotypes of the eNOS T(−786)C polymorphism. In Group I, mean FMD increased from 6.2 ± 0.4 % to 7.7 ± 0.5 % in TT carriers and from 6.1 ± 0.5 % to 7.4 ± 0.4 % in TC carriers (both p < 0.001). A similar pattern was observed in Group II, where FMD rose from 6.2 ± 0.4 % to 7.9 ± 0.5 % in TT carriers and from 6.1 ± 0.5 % to 7.6 ± 0.4 % in TC carriers (both p < 0.001). In contrast, patients with the CC genotype showed only a minimal, non-significant improvement (dapagliflozin: 6.0 ± 0.4 → 6.3 ± 0.5 %; empagliflozin: 6.0 ± 0.4 → 6.2 ± 0.5 %; p > 0.05). Two-way ANOVA confirmed a significant genotype-related influence on FMD change (p < 0.001) but revealed no difference in treatment effect between the two SGLT-2 inhibitors (p > 0.05). Taken together, these results indicate that both dapagliflozin and empagliflozin significantly improve endothelial function in patients with CKD, particularly among TT and TC carriers of the eNOS T(−786)C polymorphism, while the CC genotype is associated with a reduced vascular response. The findings suggest that the improvement in endothelial function reflects a class effect of SGLT-2 inhibitors, likely mediated through nitric-oxide–dependent mechanisms.
Both dapagliflozin and empagliflozin significantly improved endothelial function in patients with chronic kidney disease, with the most pronounced effect observed among those carrying the TT and TC genotypes of the eNOS T(−786)C polymorphism. In contrast, no meaningful improvement was detected in individuals with the CC genotype, suggesting that the endothelial response to SGLT-2 inhibitors may be influenced by genetic variations affecting nitric oxide synthesis. These results point to a possible genotype-dependent modulation of vascular benefit and underscore the importance of considering eNOS polymorphisms when evaluating individual responsiveness to SGLT-2 inhibitor therapy. Nevertheless, the findings should be interpreted cautiously. Larger, multicenter studies and mechanistic investigations are warranted to confirm these associations and to better understand how genetic background may influence the endothelial and cardiovascular effects of SGLT-2 inhibitors in patients with chronic kidney disease.
