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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
SGLT2 inhibitors improve renal outcomes in patients with CKD when used in combination with RAS inhibitors. SGLT2 inhibitors exert an antihypertensive effect through inhibition of sodium reabsorption without activation of the RAS, and this blood pressure (BP)-lowering effect is thought to contribute to their cardio-renal protective properties. Excessive salt intake attenuates the renoprotective effect of RAS inhibitors, while mineralocorticoid receptor (MR) antagonists suppress this attenuation (Nishimoto et al., Hypertension Research 2019). However, although SGLT2 inhibitors, similar to MR antagonists, exert an additional effect on RAS inhibitors, the influence of salt intake on their BP-lowering and renoprotective effects has not been clarified.
A retrospective observational study was conducted. Among patients who visited our department and were treated with dapagliflozin for more than three months, 45 patients (age 74 ± 12 years) with proteinuria before treatment and for whom pre- and post-treatment data were available were included. Based on the median of estimated daily salt intake at baseline (eUNa), patients were divided into low-salt and high-salt groups. Systolic BP (SBP) after treatment, changes in the urinary protein-to-creatinine ratio (UPCR), and the rate of change in eGFR before and after treatment were compared between the two groups.
At baseline, SBP was 136.1 ± 17.4mmHg, , median eGFR was 43.5 mL/min/1.73 m² (interquartile range [IQR] 27.4–52.9), UPCR was 0.75 g/gCr (0.32–1.76), and eUNa was 7.9 g (6.6–9.8). After treatment, SBP was 124.1 ± 18.2 mmHg, and the change in UPCR was 0.60 (0.29–0.81); both changes were statistically significant. The decrease in SBP was greater in the high-salt group (–15.1 ± 16.9 mmHg) than in the low-salt group (–3.3 ± 15.5 mmHg, p = 0.04), and this difference remained significant even after adjusting for the presence or absence of hypertension (p < 0.05, two-way ANOVA). In contrast, there were no significant differences in the UPCR change rate (log UPCR change rate: –0.60 ± 0.43 vs. –0.53 ± 0.75, p = 0.79), or eGFR change rate before and after treatment (–1.2 ± 15.0 mL/min/1.73 m²/year vs. –2.1 ± 14.9, p = 0.86). A similar analysis was performed using the urinary sodium/potassium ratio (uNa/K), but no significant difference in BP reduction was observed.
The BP-lowering effect of dapagliflozin depended on salt intake and was not correlated with uNa/K, suggesting that the antihypertensive mechanism is attributable to direct inhibition of tubular sodium reabsorption rather than indirect effects through RAS modulation. On the other hand, the reduction in urinary protein excretion appears to be largely attributable to the reduction of intraglomerular pressure rather than systemic BP lowering. These findings also suggest that dapagliflozin has a relatively weak effect in ameliorating residual renal risk after RAS inhibitor.
In patients with high salt intake, the BP-lowering effect of dapagliflozin was greater, but this effect was not associated with enhanced renal protection.
