Is there an end in Sight for Encapsulating Peritoneal Sclerosis?

Paudel, Klara; Fan, Stanley

doi:10.3747/pdi.2014.00087

Cited by 3 publications

(1 citation statement)

References 18 publications

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“…We also did not find any difference in the risk of subsequently developing EPS. There were 14 patients in our cohort who subsequently developed EPS (6%), which is in keeping with other registry studies (16,17).…”

Section: Discussionsupporting

confidence: 91%

Comparison of Change in Peritoneal Function in Patients on Continuous Ambulatory PD vs Automated PD

Samad

Fan

2017

Perit Dial Int

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This is the largest study comparing the long-term effect of APD vs CAPD prescriptions. Despite more glucose being prescribed, there were no differences in the evolution of peritoneal membrane transport characteristics. The lower baseline Kt/V of APD patients might be explained by our aggressive use of incremental APD (tidal with dry day). Despite greater glucose prescriptions, initiating patients on APD based on patient preference appears to be safe for the long-term integrity of the peritoneal membrane.

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Section: Discussionsupporting

confidence: 91%

Comparison of Change in Peritoneal Function in Patients on Continuous Ambulatory PD vs Automated PD

Samad

Fan

2017

Perit Dial Int

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Encapsulating Peritoneal Sclerosis

Alston

Fan

Nakayama

2017

Seminars in Nephrology

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Hypoxia, cytokines and stromal recruitment: parallels between pathophysiology of encapsulating peritoneal sclerosis, endometriosis and peritoneal metastasis

Wilson

2018

Pleura and Peritoneum

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Peritoneal response to various kinds of injury involves loss of peritoneal mesothelial cells (PMC), danger signalling, epithelial-mesenchymal transition and mesothelial-mesenchymal transition (MMT). Encapsulating peritoneal sclerosis (EPS), endometriosis (EM) and peritoneal metastasis (PM) are all characterized by hypoxia and formation of a vascularized connective tissue stroma mediated by vascular endothelial growth factor (VEGF). Transforming growth factor-β1 (TGF-β1) is constitutively expressed by the PMC and plays a major role in the maintenance of a transformed, inflammatory micro-environment in PM, but also in EPS and EM. Persistently high levels of TGF-β1 or stimulation by inflammatory cytokines (interleukin-6 (IL-6)) induce peritoneal MMT, adhesion formation and fibrosis. TGF-β1 enhances hypoxia inducible factor-1α expression, which drives cell growth, extracellular matrix production and cell migration. Disruption of the peritoneal glycocalyx and exposure of the basement membrane release low molecular weight hyaluronan, which initiates a cascade of pro-inflammatory mediators, including peritoneal cytokines (TNF-α, IL-1, IL-6, prostaglandins), growth factors (TGF-α, TGF-β, platelet-derived growth factor, VEGF, epidermal growth factor) and the fibrin/coagulation cascade (thrombin, Tissue factor, plasminogen activator inhibitor [PAI]-1/2). Chronic inflammation and cellular transformation are mediated by damage-associated molecular patterns, pattern recognition receptors, AGE-RAGE, extracellular lactate, pro-inflammatory cytokines, reactive oxygen species, increased glycolysis, metabolomic reprogramming and cancer-associated fibroblasts. The pathogenesis of EPS, EM and PM shows similarities to the cellular transformation and stromal recruitment of wound healing.

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Is there an end in Sight for Encapsulating Peritoneal Sclerosis?

Cited by 3 publications

References 18 publications

Comparison of Change in Peritoneal Function in Patients on Continuous Ambulatory PD vs Automated PD

Comparison of Change in Peritoneal Function in Patients on Continuous Ambulatory PD vs Automated PD

Encapsulating Peritoneal Sclerosis

Hypoxia, cytokines and stromal recruitment: parallels between pathophysiology of encapsulating peritoneal sclerosis, endometriosis and peritoneal metastasis

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