Pathophysiological changes to the peritoneal membrane during PD-related peritonitis: the role of mesothelial cells

Mediators Inflamm. 2012:2012:484167. doi: 10.1155/2012/484167. Epub 2012 Apr 10.

Abstract

The success of peritoneal dialysis (PD) is dependent on the structural and functional integrity of the peritoneal membrane. The mesothelium lines the peritoneal membrane and is the first line of defense against chemical and/or bacterial insult. Peritonitis remains a major complication of PD and is a predominant cause of technique failure, morbidity and mortality amongst PD patients. With appropriate antibiotic treatment, peritonitis resolves without further complications, but in some PD patients excessive peritoneal inflammatory responses lead to mesothelial cell exfoliation and thickening of the submesothelium, resulting in peritoneal fibrosis and sclerosis. The detrimental changes in the peritoneal membrane structure and function correlate with the number and severity of peritonitis episodes and the need for catheter removal. There is evidence that despite clinical resolution of peritonitis, increased levels of inflammatory and fibrotic mediators may persist in the peritoneal cavity, signifying persistent injury to the mesothelial cells. This review will describe the structural and functional changes that occur in the peritoneal membrane during peritonitis and how mesothelial cells contribute to these changes and respond to infection. The latter part of the review discusses the potential of mesothelial cell transplantation and genetic manipulation in the preservation of the peritoneal membrane.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Membrane / metabolism*
  • Defensins / metabolism
  • Epithelium / metabolism*
  • Fibrosis
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Inflammation
  • Nod Signaling Adaptor Proteins / metabolism
  • Peritoneal Dialysis / adverse effects*
  • Peritoneum / metabolism*
  • Peritonitis / etiology*
  • Peritonitis / physiopathology
  • Toll-Like Receptors / metabolism

Substances

  • Defensins
  • Nod Signaling Adaptor Proteins
  • Toll-Like Receptors