Abstract
Peritoneal fibrosis (PF) is a common morphological change in peritoneal dialysis (PD) patients. With the progression of PF, peritoneal membrane function is impaired, which leads to ultrafiltration failure. Furthermore, PF is an essential precursor condition for the development of encapsulating peritoneal sclerosis (EPS), which is the most serious complication of PD. Epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) plays a crucial role in PF. Transforming growth factor-?1 (TGF-?1) was thought to be the main regulator of EMT in PMCs. High glucose, hypertonicity, low pH, glucose degradation products and advanced glycation end-products in PD solution were suggested to induce TGF-?1 production. In addition, chronic inflammation mediated by infiltration of immune cells and peritoneal angiogenesis also play pivotal roles for the progression of PF.
Highlights
Peritoneal dialysis (PD) is a useful renal replacement therapy for end-stage renal disease (ESRD)
peritoneal fibrosis (PF) is a major risk factor for the development of encapsulating peritoneal sclerosis (EPS), which is the most serious complication of PD and considered to be one of the reasons why PD is avoided in ESRD patients [4,5]
Several clinical studies reported that peritoneal tissue samples obtained from PD patients showed the existence of elongated fibroblast-like cells expressing epithelial markers such as cytokeratin and intercellular adhesion molecule 1 (ICAM-1) in the fibrotic tissue of the submesothelial compact zone [9,13]
Summary
Peritoneal dialysis (PD) is a useful renal replacement therapy for end-stage renal disease (ESRD). Long-term PD leads to peritoneal damage and subsequently to peritoneal fibrosis (PF) [1,2,3]. PF is associated with ultrafiltration failure, which leads to discontinuation of the PD by the patient [1,2,3]. PF is a major risk factor for the development of encapsulating peritoneal sclerosis (EPS), which is the most serious complication of PD and considered to be one of the reasons why PD is avoided in ESRD patients [4,5]. The mechanisms of the initiation and progression of PF have been increasingly understood through numerous studies involving basic and clinical research
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