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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.
Sodium-glucose cotransporter 2 (SGLT2) inhibitors have demonstrated significant protective effects in patients with chronic kidney disease (CKD), extending beyond glucose-lowering properties. Emerging evidence also indicates benefits in acute kidney injury (AKI). However, the mechanisms underlying these protective actions–particularly at the tubular epithelial level–remain poorly defined. We hypothesized that SGLT2 inhibitors exert direct cytoprotective effects on renal tubular epithelial cells independent of systemic hemodynamic influences. To test this, we examined the effects of dapagliflozin on primary human renal proximal tubular epithelial cells (hRPTECs) exposed to cisplatin-induced injury.
Primary hRPTECs were isolated from non-tumor renal cortex obtained from nephrectomy specimens of patients with malignancies, following written informed consent and approval by the Medical Research Ethics Committee of the Institute of Science Tokyo (M2022-005). Renal cortex samples were diced, enzymatically digested, and cultured to establish primary hRPTECs. Cells were treated with cisplatin (10 μM) in the presence or absence of dapagliflozin (1 μM). Cell viability and the expression of Kidney Injury Molecule-1 (KIM-1), SGLT2, and programmed death-ligand 1 (PD-L1) were assessed using quantitative PCR, western blotting, and immunostaining. To evaluate paracrine pro-fibrotic effects, conditioned media (free of residual cisplatin) were applied to mouse renal cortical fibroblasts, and myofibroblast activation was quantified via α-smooth muscle actin (α-SMA) expression. Colocalization of KIM-1 and PD-L1 was analyzed in renal biopsy samples from CKD patients.
Primary hRPTECs exhibited robust SGLT2 expression, in contrast to immortalized RPTEC/TERT1 cells. Cisplatin markedly reduced cell viability and strongly upregulated KIM-1 and PD-L1, consistent with tubular injury and activation of immune tolerance pathways. Co-treatment with dapagliflozin significantly improved cell viability and suppressed the induction of KIM-1 and PD-L1 expression. Conditioned media from cisplatin-injured hRPTECs promoted myofibroblast activation in renal fibroblasts, indicating the release of pro-fibrotic paracrine mediators. This effect was markedly attenuated when dapagliflozin was co-administered with cisplatin. Immunostaining of CKD kidney tissues demonstrated colocalization of KIM-1 and PD-L1, underscoring the clinical relevance of these findings.
Dapagliflozin directly protects primary human renal proximal tubular epithelial cells from cisplatin-induced injury by downregulating KIM-1 and PD-L1 expression and mitigating paracrine pro-fibrotic signaling. These effects suppress myofibroblast activation and may prevent the maladaptive transition from AKI to CKD. Our findings reveal a direct tubular mechanism contributing SGLT2 inhibitor-mediated renoprotection, independent of glomerular hemodynamic effects.
