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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.
The pathogenesis of ADPKD involves multiple factors, such as cystic epithelial cell proliferation and apoptosis, fibrosis, mitochondrial dysfunction, and cyst fluid accumulation. Sodium-glucose cotransporter 2 (SGLT2) inhibitors have been shown to improve renal outcomes in chronic kidney disease; however, their effects on ADPKD remain unclear. In this study, we investigated the effects of SGLT2 inhibitors on renal cyst progression and analyzed their underlying mechanisms using ADPKD model mice.
Pkd1 conditional knockout mice (Pkd1 flox/flox; Mx-1-Cre mice) were randomly assigned to the vehicle-treated group (CT group) and the dapagliflozin-treated group (DAPA group). Dapagliflozin was administered in drinking water at a concentration of 3.0 µg/mL from 28 days of age. All mice were sacrificed at 98 days of age. Cystic kidney phenotypes were assessed using kidney-to-body weight ratio (KW/BW), cystic index (CI), defined as the percentage of tissue area occupied by cysts, and biochemical data. Additionally, histological analysis and western blotting on whole kidneys were performed to evaluate cell proliferation, renal fibrosis, apoptosis and signaling pathways involved in cyst growth.
In the DAPA group, CI was significantly higher than in the CT group, while there was no significant difference in KW/BW between the two groups. Serum urea nitrogen and serum creatinine levels did not differ between the two groups. The glucose concentration in cyst fluid was significantly higher in the DAPA group compared to the CT group. Histological analysis showed that the percentage of fibrotic area in kidney tissue was significantly increased in the DAPA group, and immunofluorescence staining demonstrated that F4/80 in tubulointerstitial area was upregulated in the DAPA group. Aquaporin-2 on the apical side of the cyst wall was significantly upregulated in the DAPA group in immunostaining and western blotting. On the other hand, the DAPA group revealed a significant decrease in the ratio of Ki-67-positive cells and TUNEL-positive cells in cyst-lining cells compared to the CT group. In western blotting, the levels of phosphorylated-adenosine monophosphate activated protein kinase (p-AMPK) and peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α), promoters of mitochondrial biogenesis, were significantly increased in the DAPA group compared to CT group.
Dapagliflozin may exacerbate cyst fluid accumulation and fibrosis through aquaporin-2 activation and increased cystic glucose concentration, despite ameliorating pathogenic mechanisms by suppressing cell proliferation and apoptosis and restoring mitochondrial function.
