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补体系统激活与腹膜结构改变:罪魁祸首还是无辜旁观者?

Complement system activation and peritoneal membrane alterations: Culprit or innocent bystander?

作者信息

Borceux Pauline, Morelle Johann, Goffin Eric

机构信息

Division of Nephrology, Cliniques universitaires St Luc, Brussels, Belgium.

Institut de Recherche Expérimentale et Clinique, UCLouvain, Brussels, Belgium.

出版信息

Perit Dial Int. 2020 Mar;40(2):115-123. doi: 10.1177/0896860819896242. Epub 2020 Jan 13.

DOI:10.1177/0896860819896242
PMID:32063185
Abstract

Peritoneal dialysis (PD) accounts for approximately 10% of the dialysis population worldwide. Major concern limiting long-term PD success is the loss of the peritoneal membrane function after prolonged exposure to dialysis solutions. The complement system is a major component of the innate immune system, which provides a first-line defense against pathogens. Uncontrolled activation of the complement system directly contributes to the pathophysiology of rare and common kidney diseases and to a growing number of nonrenal diseases. Here, we review currently available evidence of complement activation in patients treated with PD and its association with structural and functional alterations of the peritoneal membrane. Mainly, evidence point toward a local, intraperitoneal, production of complement molecules in response to PD exposure. Dialysis fluids, particularly glucose, play a role in complement activation and dysregulation leading to untoward PD-related pathophysiological processes such as peritoneal fibrosis, angiogenesis, and vasculopathy and, perhaps, encapsulating peritoneal fibrosis development. These findings could lead to further development and use of anticomplement therapeutics in PD patients to prevent membrane damage.

摘要

腹膜透析(PD)约占全球透析人群的10%。限制长期PD成功的主要问题是长期接触透析液后腹膜功能丧失。补体系统是固有免疫系统的主要组成部分,为抵御病原体提供一线防御。补体系统的失控激活直接导致罕见和常见肾脏疾病的病理生理学变化,并与越来越多的非肾脏疾病相关。在此,我们综述了目前关于接受PD治疗患者补体激活及其与腹膜结构和功能改变之间关联的现有证据。主要证据表明,腹膜局部会因接触PD而产生补体分子。透析液,尤其是葡萄糖,在补体激活和失调中起作用,导致与PD相关的不良病理生理过程,如腹膜纤维化、血管生成和血管病变,或许还会引发包裹性腹膜纤维化。这些发现可能会促使在PD患者中进一步研发和使用抗补体疗法以预防膜损伤。

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Molecular and Cellular Markers in Chlorhexidine-Induced Peritoneal Fibrosis in Mice.小鼠洗必泰诱导性腹膜纤维化中的分子和细胞标志物
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