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Nephrology Dialysis Transplantation 2006 21(Supplement 2):ii2-ii7; doi:10.1093/ndt/gfl183
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Epithelial-to-mesenchymal transition of the mesothelial cell—its role in the response of the peritoneum to dialysis

Rafael Selgas1, Auxiliadora Bajo1, José A. Jiménez-Heffernan2, Jose A. Sánchez-Tomero3, Gloria del Peso1, Abelardo Aguilera3 and Manuel López-Cabrera3

1 Servicio de Nefrología, Hospital Universitario La Paz, Madrid, 2 Departamento de Patología, Hospital Universitario de Guadalajara, Guadalajara and 3 Servicio de Nefrología y Unidad de Biología Molecular, Hospital Universitario de la Princesa, Instituto Reina Sof ía de Investigaciones Nefrológicas, Madrid, Spain

Correspondence and offprint requests to: Dr Rafael Selgas, Servicio de Nefrología, Hospital Universitario La Paz, Castellana, 261, Madrid 28046, Spain. Email: rselgas.hlpr{at}salud.madrid.org

Peritoneal membrane fibrosis, ranging from mild inflammation to severe sclerosing peritonitis, is one of the complications of peritoneal dialysis (PD). In parallel with fibrosis, the peritoneum shows a progressive increase of capillaries and vasculopathy, involved in increased small solute transport across the membrane and ultrafiltration failure. Glucose and glucose degradation products from PD solutions are responsible of stimulating transforming growth factor-ß (TGF-ß) and vascular endothelial growth factor (VEGF) production by mesothelial cells (MCs). TGF-ß is a potent pro-fibrotic factor and inducer of epithelial-to-mesenchymal transition (EMT) of the MC. Local production of VEGF by transitional MC appears to play a central role in the processes leading to peritoneal angiogenesis.

This review addresses the mechanism involved in peritoneal structural alteration by dialysis and points to the EMT of MC as the initiating mechanism of peritoneal injury. Information from multiple origins about TGF-ß and VEGF is integrated into EMT process in a comprehensive manner. Regulation and new targets for inhibition of EMT or its deleterious effects are discussed.

Keywords: angiogenesis; epithelial-to-mesenchymal transition; mesothelial cells; peritoneal dialysis; transforming growth factor; vascular endothelial growth factor


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