Pathogenesis of encapsulating peritoneal sclerosis in the role of complement regulatory proteins and glycation

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We explored the mechanisms of encapsulating peritoneal sclerosis (EPS)in the view point of advanced glycation end product (AGE) and complement activation. Peritoneal mesothelial cell and interstitium of peritoneum derived from the patients of peritoneal dialysis presented positive staining for AGE, C3, C4 and MAC. Especially in the specimens with the cases having peritonitis history, MAC staining were storong. In experimental model of mesothelial cell culture, deposition of factor H, C3 and MAC (properdin (P) was negative) were observed by adding normal human serum (NHS), however, the positive signal of C3 and MAC were enhanced by adding P before NHS. P might overwhelm H and leads complement alternative pathway activation on the surface of mesothelial cell. These results suggested that complement alternative pathway activation might involve the pathogenesis of EPS.