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Department of Nephrology, Jichi Medical School, Kawachi-gun, Tochigi, Japan
Correspondence to: I. Hirahara, Department of Nephrology, Jichi Medical School, 3311-1 Yakushiji, Minamikawachi-machi, Kawachi-gun, Tochigi, 329-0498, Japan.hirahara{at}rpf.jp
Background: Peritoneal dialysis (PD) is a common treatment
for patients with reduced or absent renal function. Long-term PD leads to
peritoneal injury with structural changes and functional decline, such as
ultrafiltration loss. At worst, peritoneal injury leads to encapsulating
peritoneal sclerosis, a serious complication of PD. Glucose degradation
products contained in PD fluids contribute to the bioincompatibility of
conventional PD fluids. Methylglyoxal (MGO) is an extremely toxic glucose
degradation product. The present study examined the injurious effect of MGO on
peritoneum in vivo. Methods: Male Sprague-Dawley rats (n = 6) were
administered PD fluids (pH 5.0) containing 0, 0.66, 2, 6.6, or 20 mmol/L MGO
every day for 21 days. On day 22, peritoneal function was estimated by the
peritoneal equilibration test. Drained dialysate was analyzed for type IV
collagen-7S, matrix metalloproteinase (MMP), and vascular endothelial growth
factor (VEGF). Histological analysis was also performed. Results: In rats receiving PD fluids containing more than
0.66 mmol/L MGO, peritoneal function decreased significantly and levels of
type IV collagen-7S and MMP-2 in drained dialysate increased significantly. In
the 20-mmol/L MGO-treated rats, loss of body weight, expression of VEGF,
thickening of the peritoneum, and formation of abdominal cocoon were induced.
MMP-2 and VEGF were produced by infiltrating cells in the peritoneum. Type IV
collagen was detected in basement membrane of microvessels. Conclusion: MGO induced not only peritoneal injury but
also abdominal cocoon formation in vivo. The decline of peritoneal function
may result from reconstitution of microvessel basement membrane or
neovascularization.
KEY WORDS: Abdominal cocoon; encapsulating peritoneal sclerosis; glucose degradation products; matrix metalloproteinase-2; methylglyoxal; peritoneal injury; type IV collagen.
Received 4 February 2005; accepted 13 September 2005.
This article has been cited by other articles:
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  I. Hirahara, Y. Ishibashi, S. Kaname, E. Kusano, and T. Fujita Methylglyoxal induces peritoneal thickening by mesenchymal-like mesothelial cells in rats Nephrol. Dial. Transplant., September 12, 2008; (2008) gfn495v1. [Abstract] [Full Text] [PDF]
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I. Hirahara, M. Inoue, K. Okuda, Y. Ando, S. Muto, and E. Kusano The potential of matrix metalloproteinase-2 as a marker of peritoneal injury, increased solute transport, or progression to encapsulating peritoneal sclerosis during peritoneal dialysis--a multicentre study in Japan Nephrol. Dial. Transplant., February 1, 2007; 22(2): 560 - 567. [Abstract] [Full Text] [PDF]
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