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甲基乙二醛在腹膜透析中导致的腹膜损伤

Peritoneal injury by methylglyoxal in peritoneal dialysis.

作者信息

Hirahara Ichiro, Kusano Eiji, Yanagiba Satoru, Miyata Yukio, Ando Yasuhiro, Muto Shigeaki, Asano Yasushi

机构信息

Department of Nephrology, Jichi Medical School, Kawachi-gun, Tochigi, Japan.

出版信息

Perit Dial Int. 2006 May-Jun;26(3):380-92.

PMID:16722033
Abstract

BACKGROUND

Peritonealdialysis (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.

摘要

背景

腹膜透析(PD)是肾功能减退或丧失患者的常见治疗方法。长期腹膜透析会导致腹膜损伤,出现结构改变和功能衰退,如超滤功能丧失。最严重的情况下,腹膜损伤会导致包裹性腹膜硬化,这是腹膜透析的一种严重并发症。腹膜透析液中含有的葡萄糖降解产物会导致传统腹膜透析液的生物不相容性。甲基乙二醛(MGO)是一种剧毒的葡萄糖降解产物。本研究检测了MGO在体内对腹膜的损伤作用。

方法

将雄性Sprague-Dawley大鼠(n = 6)每天给予含0、0.66、2、6.6或20 mmol/L MGO的腹膜透析液(pH 5.0),持续21天。在第22天,通过腹膜平衡试验评估腹膜功能。分析引流透析液中的IV型胶原-7S、基质金属蛋白酶(MMP)和血管内皮生长因子(VEGF)。同时进行组织学分析。

结果

在接受含超过0.66 mmol/L MGO腹膜透析液的大鼠中,腹膜功能显著下降,引流透析液中IV型胶原-7S和MMP-2水平显著升高。在接受20 mmol/L MGO治疗的大鼠中,出现体重减轻、VEGF表达、腹膜增厚和腹腔茧形成。MMP-2和VEGF由腹膜中的浸润细胞产生。IV型胶原在微血管基底膜中检测到。

结论

MGO在体内不仅诱导腹膜损伤,还诱导腹腔茧形成。腹膜功能下降可能是由于微血管基底膜重构或新生血管形成所致。

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