Los estudios realizados en biopsias peritoneales de pacientes con fallo renal que son tratados mediante diálisis peritoneal (DP) han demostrado que esta terapia provoca daños en la membrana peritoneal, caracterizados por fibrosis y angiogénesis, y que culminan en la pérdida de la capacidad de ultrafiltración de la membrana peritoneal. Estos estudios son descriptivos y apenas han contribuido al conocimiento de los mecanismos implicados en el proceso patológico inducido por la exposición de la membrana peritoneal a los líquidos de diálisis. Así, es necesario el desarrollo de modelos experimentales en animales para suplir las deficiencias presentadas por los estudios en pacientes. Aquí tratamos las ventajas y dificultades de la utilización de modelos experimentales de diálisis peritoneal y las expectativas para el futuro.

neal dialysis-patients have demonstrated that exposure to peritoneal dialysis fluid induce peritoneal deterioration. The main alterations of peritoneal membrane are fibrosis and angiogenesis that ends with the failure of the ultrafiltration capacity of the peritoneal membrane. These studies are descriptivist and scarcely help to investigate the mechanisms and stages involved on the process. Therefore, it is necessary to supply the deficiencies presented by the studies with patients. The experimental models have strongly contributed to the knowledge of the pathologic process that is induced by the continuous exposition of the peritoneal membrane to the dialysis fluids. Most of the peritoneal dialysis studies use the rat as the experimental animal. Due to the difficulty of working with small animals, few studies have been done in mice. However, models in mice offers great advantages, as long as they allow us to employ different strains and genetically modified animals. We have recently developed an experimental model in mouse of exposure of the peritoneal membrane to dialysis fluids, which resembles the process of peritoneal damage that take place during peritoneal dialysis treatment in human patients.