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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 membrane dysfunction is a major cause of withdrawal from peritoneal dialysis (PD). The characteristic pathological features of peritoneal dysfunction are recognized mainly to be increases in vascular density and peritoneal membrane fibrosis. Carbon monoxide (CO) exhibits potent anti-inflammatory and cytoprotective properties, however, its safe and sustained delivery remains challenging. Ultrafine bubbles (UFB), defined as gas bubbles with a particle size of 1 µm or less, are remarkably stable in liquids and have recently attracted attention as novel platforms for therapeutic gas delivery. This study investigated whether intraperitoneal administration of CO ultrafine bubbles (CO-UFB) could improve peritoneal membrane dysfunction by inhibiting inflammation and fibrosis in a mouse model of peritoneal fibrosis.
Male C57BL/6 mice were randomly assigned to four groups: Control, and chlorhexidine gluconate (CG)-induced peritoneal fibrosis treated with Saline, CO-Dissolved, or CO-UFB solutions. Peritoneal fibrosis was induced by intraperitoneal injection of CG every other day for two weeks. Saline, CO-Dissolved, or CO-UFB solutions were administered intraperitoneally one hour after each CG injection. Peritoneal membrane function was evaluated using the peritoneal equilibration test (n = 6 per group). Histological, immunohistochemical, and quantitative RT-PCR analyses were performed to evaluate inflammation, fibrosis, angiogenesis, and lymphangiogenesis in the peritoneum and diaphragm (n = 6 per group).
CO-UFB treatment significantly preserved peritoneal membrane function compared with saline-treated mice, as evidenced by higher drained volume (Saline: 1.06 ± 0.11 mL; CO-UFB: 1.49 ± 0.24 mL, p < 0.05) and lower glucose absorption (Saline: 338 ± 75.8 mg/d; CO-UFB: 516 ± 68.8 mg/dL, p < 0.01). CO-UFB markedly attenuated peritoneal thickening (Saline: 144 ± 51.5 µm; CO-UFB: 73.8 ± 12.7 µm, p < 0.01). In the peritoneum, CO-UFB markedly suppressed mRNA expression of profibrotic (Tgfb1, Col1a2) and angiogenic (Pecam1) protein and mRNA, whereas CO-Dissolved treatment suppressed these to a less extent. Additionally, CO-UFB suppressed mRNA expression of inflammatory (Il6) and lymphagiogenic (Vegfc, Lyve1) protein and mRNA in the diaphragm.
Intraperitoneal delivery of CO-UFB effectively inhibits peritoneal inflammation, fibrosis, angiogenesis, and lymphangiogenesis, thereby preserving peritoneal membrane function in a mouse model of peritoneal fibrosis. CO-UFB represents a promising therapeutic strategy for maintaining peritoneal integrity and prolonging the viability of PD, providing a safe and sustained approach for CO delivery.
