BACKGROUND: Sclerosing encapsulating peritonitis (SEP) is a life-threatening complication of continuous ambulatory peritoneal dialysis. To elucidate the mechanism and develop treatments for this condition, an experimental SEP model in mice was constructed. METHODS: C57BL/6 mice were administered 0.3 ml of 0.1% chlorhexidine gluconate and 15% ethanol dissolved in saline, intraperitoneally, on a daily basis for 56 days (group 1, n=15). A control group of C57BL/6 mice were administered 0.3 ml of phosphate-buffered saline only in the same manner (group 2, n=15). The mice were sacrificed on days 3, 7, 21, 56 and were prepared for histological analysis. RESULTS: In group 1, all mice had developed macroscopic evidence of SEP 56 days after the injection. Microscopically we observed peritoneal fibrosis and an increase in infiltrates of mononuclear cells over time. The peritoneal fibrosis reached the chronic inflammatory stage by 56 days after the injection. CONCLUSION: We have developed a convenient experimental model of SEP in mice, which may be useful in elucidating the pathogenesis of SEP and in establishing possible treatments.
BACKGROUND: Sclerosing encapsulating peritonitis (SEP) is a life-threatening complication of continuous ambulatory peritoneal dialysis. To elucidate the mechanism and develop treatments for this condition, an experimental SEP model in mice was constructed. METHODS: C57BL/6 mice were administered 0.3 ml of 0.1% chlorhexidine gluconate and 15% ethanol dissolved in saline, intraperitoneally, on a daily basis for 56 days (group 1, n=15). A control group of C57BL/6 mice were administered 0.3 ml of phosphate-buffered saline only in the same manner (group 2, n=15). The mice were sacrificed on days 3, 7, 21, 56 and were prepared for histological analysis. RESULTS: In group 1, all mice had developed macroscopic evidence of SEP 56 days after the injection. Microscopically we observed peritoneal fibrosis and an increase in infiltrates of mononuclear cells over time. The peritoneal fibrosis reached the chronic inflammatory stage by 56 days after the injection. CONCLUSION: We have developed a convenient experimental model of SEP in mice, which may be useful in elucidating the pathogenesis of SEP and in establishing possible treatments.