Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Diabetic kidney disease (DKD) is a severe complication of diabetes that significantly contributes to morbidity and mortality. Sodium-glucose cotransporter 2 (SGLT2) inhibitors have shown promise in improving kidney survival in DKD. However, the underlying mechanisms for the protective effect of SGLT2 inhibitors remain unclear. This study aimed to examine the effect of inhibition of SGLT2 on the oxidative and inflammatory stress of diabetic kidney disease, and its impact on glomerular function.
A three-month experimental study was performed using Wistar rats (n = 10), randomly assigned to five groups: a naïve control group, a diabetic control group (induced with streptozotocin [STZ]), and three ERTU-treated groups. ERTU was administered orally at 2 mg/kg from diabetes onset (E-ERU 2 mg/kg), at 2 mg/kg beginning seven weeks post-induction (L-ERU 2 mg/kg), and at 5 mg/kg beginning seven weeks post-induction (L-ERU 5 mg/kg). At the end of the 12 weeks, glomerular function and biological and immunological studies were performed. Tissue homogenates were used to determine oxidative stress markers (total nitric oxide, thiobarbituric acid reactive substances, glutathione, and superoxide dismutase) and kidney injury/inflammatory biomarkers (Kidney Injury Molecule 1, cystatin C, adiponectin, IL-1b, and IL-18). Immunohistochemistry staining was used for the measurement of the expression of NLRP3 inflammasome complex (Apoptosis-associated speck-like protein containing a CARD, Pro-caspase-1, and NLRP3 inflammasome) and its downstream product IL-18. The statistical difference was measured by using the Kruskal-Wallis test and one-way ANOVA test, where (p̂<0.05) was considered statistically significant.
ERTU treatment significantly reduced kidney injury, oxidative stress, and activation of NLRP3 Inflammasome complex (p̂<0.05).
In conclusion, the SGLT2 inhibitor exhibited dose-dependent and time-dependent antioxidant and anti-inflammatory effects that may have contributed to the stabilization of kidney function. Study of the NLRP3 inflammasome pathway may reveal additional insights into the direct impact of ERTU’s renal protection.
