title: Glucocorticoid protects against the development of encapsulating peritoneal sclerosis on peritoneal dialysis.
abstract: Encapsulating peritoneal sclerosis (EPS) is an important complication of peritoneal dialysis in which all or part of the intestine is enveloped in a fibrous ball resulting in a cocoon. Previously, we reported that acid dialysis solution (DS) induces peritoneal fibrosis. In the present study, we examined the effect of treatment with glucocorticoid (GC) in a model of EPS in rats. We divided 20 male Wistar-Kyoto rats into four groups and dialyzed them with various solutions for 40 days as follows: (1) pH 3.5 DS, 10 mL (pH 3.5, containing 1.35% glucose, n = 5); (2) pH 3.5 DS, 10 mL + GC (0.1 mg dexamethasone daily, n = 5); (3) pH 7.0 DS, 10 mL (n = 5); and (4) pH 7.0 DS, 10 mL + GC (n = 5). At the end of 40 days, all rats were humanely killed by decapitation. Expression of mRNA of aquaporins (AQPs) and glucose transporters (GLUTs) were studied by reverse-transcriptase polymerase chain reaction. In rats treated with pH 3.5 DS, necropsy findings showed evidence of EPS. The typical appearance was multiple surfaces covered with granulation tissue or fibrotic tissue or both. Multiple adhesions were present. Microscopic findings revealed that low-pH DS induced peritoneal fibrosis and loss of mesothelium. In the dialyzed rats, mRNA of AQP-1, AQP-4, GLUT-1, GLUT-4, and GLUT-5 was expressed in peritoneum. In rats treated with pH 3.5 DS, expression of AQPs was significantly suppressed and expression of GLUTs was significantly enhanced. However, glucocorticoid treatment prevented the progression of peritoneal fibrosis and adhesion of peritoneum. In rats treated with pH 7.0 DS, no signs of EPS were seen. Our study suggests that low-pH DS induced the development of EPS. Glucocorticoid protects against the development of EPS on peritoneal dialysis.
authors.affiliation: Department of Nephrology, Saitama Medical School, Saitama, Japan.
authors.forename: Hiroe
authors.initials: H
authors.lastname: Imai
authors.forename: Hidetomo
authors.initials: H
authors.lastname: Nakamoto
authors.forename: Rie
authors.initials: R
authors.lastname: Fucshima
authors.forename: Yasuhito
authors.initials: Y
authors.lastname: Yamanouchi
authors.forename: Yuji
authors.initials: Y
authors.lastname: Ishida
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D020346:Aquaporins / Q000378:metabolism; D003907:Dexamethasone / Q000008:administration & dosage*; D015314:Dialysis Solutions / Q000737:chemistry; D005938:Glucocorticoids / Q000008:administration & dosage*; D006863:Hydrogen-Ion Concentration; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000378:metabolism; D010530:Peritoneal Dialysis / Q000009:adverse effects*; D010537:Peritoneum / Q000378:metabolism / Q000473:pathology*; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D011921:Rats, Inbred WKY; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012598:Sclerosis; D016212:Transforming Growth Factor beta / Q000378:metabolism
chemical_list: D020346:Aquaporins; D015314:Dialysis Solutions; D005938:Glucocorticoids; D009004:Monosaccharide Transport Proteins; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D003907:Dexamethasone