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International Journal of Nephrology
Volume 2013, Article ID 263285, 7 pages
Review Article

Are the Mesothelial-to-Mesenchymal Transition, Sclerotic Peritonitis Syndromes, and Encapsulating Peritoneal Sclerosis Part of the Same Process?

1Centro de Biología Molecular Severo Ochoa, CSIC-UAM, Campus de Cantoblanco, Calle de Nicolás Cabrera 1, 28049 Madrid, Spain
2Servicio de Nefrología, Hospital Universitario La Paz, Instituto de Investigación Sanitaria La Paz (IdiPAZ), Paseo de la Castellana, 261, 28046 Madrid, Spain
3Servicio de Anatomía Patológica, Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Princesa (IP), Calle de Diego de León 62, 28006 Madrid, Spain
4Unidad de Biología Molecular and Servicio de Nefrología, Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Princesa (IP), Calle de Diego de León 62, 28006 Madrid, Spain

Received 13 August 2012; Revised 13 November 2012; Accepted 31 December 2012

Academic Editor: Peter J. Margetts

Copyright © 2013 Jesús Loureiro et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mesothelial-to-mesenchymal transition (MMT) is an autoregulated physiological process of tissue repair that in uncontrolled conditions, such as peritoneal dialysis (PD), can lead to peritoneal fibrosis. The maximum expression of sclerotic peritoneal syndromes (SPS) is the encapsulating peritoneal sclerosis (EPS) for which no specific treatment exists. The SPS includes a wide range of peritoneal fibrosis that appears progressively and is considered as a reversible process, while EPS does not. EPS is a serious complication of PD characterized by a progressive intra-abdominal inflammatory process that results in bridles and severe fibrous tissue formation which cover and constrict the viscera. Recent studies show that transdifferentiated mesothelial cells isolated from the PD effluent correlate very well with the clinical events such as the number of hemoperitoneum and peritonitis, as well as with PD function (lower ultrafiltration and high Cr-MTC). In addition, in peritoneal biopsies from PD patients, the MMT correlates very well with anatomical changes (fibrosis and angiogenesis). However, the pathway to reach EPS from SPS has not been fully and completely established. Herein, we present important evidence pointing to the MMT that is present in the initial peritoneal fibrosis stages and it is perpetual over time, with at least theoretical possibility that MMT initiated the fibrosing process to reach EPS.