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Inflammation and Fibrosis |
Division of Nephrology, Department of Internal Medicine, Juntendo University School of Medicine, Tokyo, Japan
Correspondence to: Y. Tomino, 2-1-1 Hongo Bunkyo-ku, Tokyo 113-8421
Japan.
yasu{at}med.juntendo.ac.jp
Peritoneal fibrosis (PF) is invariably observed in patients undergoing
long-term peritoneal dialysis (PD). The condition is thought to occur in
response to a variety of insults, including bioincompatible dialysates (acidic
solution, high glucose, glucose degradation products, or a combination),
peritonitis, uremia, and chronic inflammation. Recently, the pathophysiologic
mechanisms that contribute to the fibrosing process have been intensively
studied. Transforming growth factor-β has been shown to be a key mediator
of PF. Loss of the mesothelial cell layer has been identified in several
studies and shown to correlate with submesothelial thickening and
vasculopathy. An association has also been identified between increased
submesothelial thickness in the peritoneal membrane and increased solute
transport, suggesting a relationship between PF and loss of ultrafiltration
capacity. Thus, to maintain long-term PD and improve quality of life for
patients, it is important to develop interventions for prevention and
treatment of PF.
Several strategies for peritoneal fibrosis intervention have been reported,
including developing biocompatible dialysate, targeting mediators responsible
for inflammation and fibrosis, and reconstituting the peritoneum using
mesothelial or bone marrow-derived cells. Recent experimental trials in animal
models and clinical studies are presented in this review.
KEY WORDS: KEY WORDS:; Peritoneal fibrosis; tranilast; intervention.
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