title: Immunohistochemical detection of advanced glycosylation end-products in the peritoneum and its possible pathophysiological role in CAPD.
abstract: It has recently been suggested that advanced glycosylation end-products (AGEs) are formed in the peritoneum in patients on CAPD. However, the exact location of AGE accumulation, the relation with the duration of CAPD and its pathophysiological role in CAPD remain unclear. If the peritoneum is glycosylated, it could bring about altered peritoneal function. Therefore, the aim of this study is to clarify the localization of AGEs in the peritoneum in accordance with the duration of CAPD and to examine its relation to the peritoneal permeability. Fifteen non-diabetic patients were divided into three groups (each 5 patients) on the basis of the mean duration (D) of CAPD (Group 1, D = 0 month; Group II, D = 34 months; Group III, D = 84 months). The AGE staining by monoclonal anti-AGE antibody in the peritoneum and the four-hour peritoneal equilibration test (PET) were compared among these groups. AGE was absent or found only weakly in Group I. However, in groups II and III, AGE was moderately or strongly positive especially in the vascular walls and it was dominant in group III. PET revealed that peritoneal permeability for glucose, creatinine, beta2-microglobulin and albumin was increased in Group II as compared to Group I, and it was further increased in Group III. The results of this study indicate that AGEs become dominantly accumulated in the vascular wall in accordance with the prolongation of CAPD treatment, and this might play some roles for the increased permeability of the peritoneal membrane in CAPD.
authors.affiliation: Tokyo Jikei University School of Medicine, Department of Internal Medicine II, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Nakayama
authors.forename: Y
authors.initials: Y
authors.lastname: Kawaguchi
authors.forename: K
authors.initials: K
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Hasegawa
authors.forename: K
authors.initials: K
authors.lastname: Takazoe
authors.forename: N
authors.initials: N
authors.lastname: Katoh
authors.forename: H
authors.initials: H
authors.lastname: Hayakawa
authors.forename: N
authors.initials: N
authors.lastname: Osaka
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: A
authors.initials: A
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Kubo
authors.forename: T
authors.initials: T
authors.lastname: Shigematsu
authors.forename: O
authors.initials: O
authors.lastname: Sakai
authors.forename: S
authors.initials: S
authors.lastname: Horiuchi
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal; D001692:Biological Transport / Q000502:physiology; D005260:Female; D017127:Glycation End Products, Advanced / Q000032:analysis* / Q000276:immunology; D006801:Humans; D007150:Immunohistochemistry; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010531:Peritoneal Dialysis, Continuous Ambulatory; D010537:Peritoneum / Q000737:chemistry* / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D017127:Glycation End Products, Advanced