Review Article: PDF OnlyPeritoneal Fibrosing Syndrome: Pathogenetic Mechanism and Current Therapeutic StrategiesHung, Kuan-Yua, b; Huang, Jenq-Wenb; Tsai, Tun-Junb, *; Hsieh, Bor-ShenbAuthor Information aDepartment of Internal Medicine, Far Eastern Memorial Hospital, National Taiwan University, Taipei, Taiwan, R.O.C. bDepartment of Internal Medicine, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C. *Correspondence to: Dr. Tun-Jun Tsai, Department of Internal Medicine, College of Medicine, National Taiwan University Hospital, 7, Chung-Shan South Road, Taipei 100, Taiwan, R.O.C. E-mail: [email protected] Received: December 2, 2004 • Accepted: July 4, 2005 Journal of the Chinese Medical Association: September 2005 - Volume 68 - Issue 9 - p 401-405 doi: 10.1016/S1726-4901(09)70154-6 Metrics Abstract Peritoneal dialysis (PD) has been established as a main renal replacement therapy for approximately 20 years. However, long-term peritoneal exposure to high glucose and other unphysiologic contents in the PD solution may potentiate the development of peritoneal fibrosing syndrome (PFS) in PD patients. PFS is composed of a wide spectrum of peritoneal alterations, which has been observed in PD patients. Molecular studies have shown that the fibrogenic effect of peritoneal mesothelial cells and the accompanying accumulation of extracellular matrix in the peritoneum are key events leading to PFS. In this review, we highlight the impact of PFS and its pathogenetic factors, including bioincompatible PD solution, multidisciplinary inflammatory mediators, and stimulatory cytokines in the peritoneal cavity. Current therapeutic strategies based on both clinical and basic evidence for the prevention or treatment of PFS are also reviewed. © 2005 by Lippincott Williams & Wilkins, Inc.