title: Effects of low glucose degradation products peritoneal dialysis fluid on the peritoneal fibrosis and vascularization in a chronic rat model.
abstract: In the present study, we examined the effects of a new peritoneal dialysis fluid (PDF) with a low level of low glucose degradation products (GDP) on the functional and structural stability of the peritoneal membrane (PM). Male Sprague-Dawley rats were divided into three groups: group C (n = 8), without dialysate infusion; group P (n = 12), infused with low-level GDP solution (4.25% Physioneal, pH 7.0-7.4); and group D (n = 12), infused with conventional solution (4.25% Dianeal, pH 5.2, adjusted to pH 7.0). In groups D and P, animals were infused through a permanent catheter with 25 mL of PDF, twice daily for 8 weeks. Lipopolysaccharide was added into the PDF immediately before infusion on days 8, 9 and 10 in the two dialysis groups. When compared with group P, group D showed a higher glucose mass transfer at weeks 6 and 8, D/P urea at week 8, TGF-beta1 at weeks 4 and 8, and VEGF level at week 8. The submesothelial matrix layer of the parietal peritoneum was significantly thickened in group D and the lectin-stained blood vessels in this layer were well-visualized in group D compared with group P. There were significantly more peritoneal blood vessels in group D than group P. The transforming growth factor-beta induced gene-h3 (betaig-h3) and TGF-beta1 levels in the peritoneal effluent correlated with the submesothelial thickness, which correlated with the dialysate-to-plasma ratio (D/P) of protein and, inversely, with the rate of glucose transport (D/D(0) glucose, where D is glucose concentration in the dialysate and D(0) is glucose concentration in the dialysis solution before it is infused into the peritoneal cavity). The present study showed that low-GDP PDF effectively attenuated the peritoneal vascularization and fibrosis related to conventional solution.
authors.affiliation: Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu, Korea.
authors.forename: Chan-Duck
authors.initials: CD
authors.lastname: Kim
authors.forename: Hyeog-Man
authors.initials: HM
authors.lastname: Kwon
authors.forename: Sun-Hee
authors.initials: SH
authors.lastname: Park
authors.forename: Eun-Joo
authors.initials: EJ
authors.lastname: Oh
authors.forename: Mi-Hyung
authors.initials: MH
authors.lastname: Kim
authors.forename: Soon-Youn
authors.initials: SY
authors.lastname: Choi
authors.forename: Min-Jeong
authors.initials: MJ
authors.lastname: Choi
authors.forename: In-San
authors.initials: IS
authors.lastname: Kim
authors.forename: Min-Sun
authors.initials: MS
authors.lastname: Park
authors.forename: Yong-Jin
authors.initials: YJ
authors.lastname: Kim
authors.forename: Yong-Lim
authors.initials: YL
authors.lastname: Kim
mesh_terms: D000818:Animals; D015153:Blotting, Western; D015314:Dialysis Solutions / Q000494:pharmacology*; D016326:Extracellular Matrix Proteins / Q000378:metabolism; D005355:Fibrosis; D005947:Glucose / Q000494:pharmacology*; D007150:Immunohistochemistry; D008297:Male; D010530:Peritoneal Dialysis; D010537:Peritoneum / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016212:Transforming Growth Factor beta / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D000099222:betaIG-H3 Protein
chemical_list: D015314:Dialysis Solutions; D016326:Extracellular Matrix Proteins; D005947:Glucose; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D000099222:betaIG-H3 Protein