title: Pathogenesis of peritoneal sclerosis.
abstract: Peritoneal sclerosis is an almost invariable consequence of peritoneal dialysis. In most circumstances it is "simple" sclerosis, manifesting clinically with an increasing peritoneal transport rate and loss of ultrafiltration capacity. In contrast, encapsulating peritoneal sclerosis is a life threatening and usually irreversible condition, associated with bowel obstruction, malnutrition and death. It is unknown whether common etiological factors underlie the development of these 2 clinically and pathologically distinct forms of peritoneal sclerosis. The majority of studies to date have investigated factors that contribute to "simple" sclerosis, although it remains possible that similar mechanisms are amplified in patients who develop encapsulated peritoneal sclerosis. The cellular elements that promote peritoneal sclerosis include the mesothelial cells, peritoneal fibroblasts and inflammatory cells. Factors that stimulate these cells to promote peritoneal fibrosis and neoangiogenesis, both inherent in the development of peritoneal sclerosis, include cytokines that are induced by exposure of the peritoneal membrane to high concentrations of glucose, advanced glycation of the peritoneal membrane and oxidative stress. The cumulative exposure to bioincompatible dialysate is likely to have an etiological role as the duration of dialysis correlates with the likelihood of developing peritoneal sclerosis. Indeed peritoneal dialysis using more biocompatible fluids has been shown to reduce the development of peritoneal sclerosis. The individual contribution of the factors implicated in the development of peritoneal sclerosis will only be determined by large scale peritoneal biopsy registries, which will be able to prospectively incorporate clinical and histological data and support clinical decision making.
authors.affiliation: Royal North Shore Hospital, University of Sydney, St Leonards, NSW 2065 Australia. carpol@med.usyd.edu.au
authors.forename: C
authors.initials: C
authors.lastname: Pollock
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D015314:Dialysis Solutions / Q000009:adverse effects / Q000494:pharmacology; D005355:Fibrosis; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D009389:Neovascularization, Pathologic; D018384:Oxidative Stress; D010537:Peritoneum / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D010538:Peritonitis / Q000473:pathology; D012598:Sclerosis
chemical_list: D016207:Cytokines; D015314:Dialysis Solutions; D017127:Glycation End Products, Advanced