Peritoneal dialysis (PD) is a renal replacement therapy for patients with end-stage renal disease that is equivalent to hemodialysis with respect to adequacy, mortality, and other outcome parameters, yet providing superior quality-of-life measures and cost savings. However, long-term usage of the patient's peritoneal membrane as a dialyzer filter is unphysiological and leads to peritoneal fibrosis, which is a major factor of patient morbidity and PD technique failure, resulting in a transfer to hemodialysis or death. Peritoneal fibrosis pathophysiology involves chronic inflammation and the fibrotic process itself. Frequently, inflammation precedes membrane fibrosis development, although a bidirectional relationship of one inducing the other exists. This review aims at highlighting the histopathological definition of peritoneal fibrosis, outlining the interplay of fibrosis, angiogenesis and epithelial-to-mesenchymal transition (EMT), delineating important fibrogenic pathways involving Smad-dependent and Smad-independent transforming growth factor-β (TGF-β) as well as connective tissue growth factor (CTGF) signaling, and summarizing historic and recent studies of inflammatory pathways involving NOD-like receptor protein 3 (NLRP3)/interleukin (IL)-1β, IL-6, IL-17, and other cytokines.

腹膜透析 (PD) 是一种用于终末期肾病患者的肾脏替代疗法，在充分性、死亡率和其他结果参数方面与血液透析相当，但可提供卓越的生活质量措施和成本节约。然而，长期使用患者的腹膜作为透析器过滤器是不生理的，会导致腹膜纤维化，这是患者发病和 PD 技术失败的主要因素，导致转入血液透析或死亡。腹膜纤维化病理生理学涉及慢性炎症和纤维化过程本身。通常，炎症先于膜纤维化发展，尽管存在一种诱导另一种的双向关系。本综述旨在强调腹膜纤维化的组织病理学定义，