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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.
Salt-loaded Spontaneously Diabetic Torii (SDT) fatty rats develop hypertension and diabetic nephropathy. These rats exhibited low renin levels, resulting in a limited response to first-line ACE inhibitors. Although plasma aldosterone concentrations in SDT rats are comparable to those in Sprague-Dawley rats, mineralocorticoid receptor (MR) activation can also occur through aldosterone-independent mechanisms triggered by obesity, hyperglycemia, and excessive salt intake. Therefore, SDT fatty rats were considered at risk for MR-mediated disease progression. In this study, we evaluated the effect of MR antagonist finerenone (FIN), as a first-line agent on salt-loaded SDT fatty rats.
Male SDT fatty rats (n = 15) were used for the experiment. Body weight (BW) was measured weekly from 8 to 17 weeks of age (w). Salt loading (0.3% NaCl solution) and drug administration (FIN; 10 mg/kg/day) began at 10 w. Systolic (SBP) and diastolic blood pressure (DBP) were measured at 8 w (baseline) and 12, 14, and 16 w. Urine albumin-to-creatinine ratio (ACR), serum total cholesterol (T-CHO), triglyceride (TG), and potassium concentration (K+) were analyzed at 13 and 17 w. Fasting blood glucose level (FGBL) was measured at 16 w. Kidney tissues were collected at 17 w for histological analyses (HE, PAS, and Sirius Red staining) and gene expression analyses (Havcr1 and Lcn2) by qRT-PCR.
Salt loading significantly increased SBP, DBP, ACR, T-CHO and TG levels, all of which were significantly suppressed by FIN treatment, reaching values comparable to those in the untreated group. The tubulointerstitial injury score, glomerular damage, and renal expression of Havcr1 and Lcn2 were elevated by salt loading, and these changes were attenuated by FIN treatment. These findings suggest that FIN ameliorated hypertension, dyslipidemia and renal dysfunction in diabetic nephropathy associated with hyporeninemic hypertension. No significant differences were observed in BW, FGBL and serum K+ levels among groups.
Finerenone, a nonsteroidal MR antagonist, may be a promising first-line treatment option for diabetic nephropathy with hyporeninemic hypertension.
