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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.
Peritoneal fibrosis (PF), a major cause of technique failure in peritoneal dialysis (PD) patients, is driven by the excessive deposition of extracellular matrix (ECM) proteins, primarily mediated by the activation of fibroblasts into myofibroblasts. This activation is associated with a metabolic reprogramming from oxidative phosphorylation (OXPHOS) to glycolysis, particularly under profibrotic stimuli such as TGF-β1. This study investigated the anti-fibrotic potential of sildenafil, a phosphodiesterase-5 inhibitor, in modulating metabolism and inflammation in human peritoneal fibroblasts (HPFBs).
HPFBs isolated from long-term PD patients (n = 8) and controls (n =8) were treated with TGF-β1 (10 ng/mL), alone or in combination with sildenafil (10 µM), 5HT2B receptor antagonist (1 µM), or both using pre- and post-treatment strategies. Metabolic analysis was performed using the SCENITH assay via flow cytometry. Gene expression was assessed by qPCR, and cytokines were quantified using ELISA. Renal fibroblast cell line was used for invitro experiments.
SCENITH analysis showed a non-significant increase in basal glycolytic dependency in patient-derived fibroblasts (32%) compared to controls (26%). However, TGF-β1 stimulation significantly enhanced glycolysis in patient fibroblasts (87%) versus controls (51%). This metabolic shift coincided with upregulation of glycolytic enzymes (GLUT1, LDHA, Hexokinase II) and profibrotic markers (α-SMA, fibronectin, collagen I). Sildenafil treatment effectively reduced glycolytic dependency (to 52.5% in patients and 39% in controls) while promoting OXPHOS (67%–73%). Furthermore, sildenafil significantly downregulated glycolytic and profibrotic gene expression (p < 0.001) and decreased pro-inflammatory cytokines, while upregulating IL-10, supporting an anti-inflammatory shift. To further evaluate this we treated the fibroblast cell line with serum samples of patients and control and observed that the conversion to myofibroblast was increased with the serum of patients as compared to control (p<0.001). Figure 1
Sildenafil attenuates peritoneal fibrosis by inhibiting fibroblast activation through metabolic reprogramming and immune modulation. These findings highlight the therapeutic potential of sildenafil in preventing PF and preserving peritoneal membrane function in PD patients.
