The effect of fibrosis on peritoneal transport

Current sterile dialysis solutions cause inflammation in the sub-mesothelium that lead to fibrosis, angiogenesis, and eventual ultrafiltration failure. While the normal interstitium separates the peritoneal microvasculature from the dialysis fluid and makes trans-peritoneal transport less efficient, changes in the sub-mesothelial layer can result in progressive increases in solute transfer and ultrafiltration diminution. Years of exposure to dialysis solutions result in an epithelial-to-mesenchymal transition of mesothelial cells and the formation of an avascular layer of intersitial matrix and plasma proteins in the sub-mesothelial compact zone. The formation of this fibrotic layer separates the dialyzing solution from the exchange microvessels and markedly decreases the effective osmotic pressure near the exchange microvessels. Angiogenesis dissipates the osmotic driving force through increases the perfused vascular area and marked increases in solute permeability. These combined changes result in more rapid loss of the osmotic agent and diminished ultrafiltration.