Abstract
Long-term peritoneal dialysis (PD) is associated with peritoneal membrane remodeling. This includes changes in peritoneal vasculature, which may ultimately lead to inadequate solute and water removal and treatment failure. The potential cause of such alterations is chronic inflammation induced by repeated episodes of infectious peritonitis and/or exposure to bioincompatible PD fluids. While these factors may jeopardize the peritoneal membrane integrity, it is not clear why adverse peritoneal remodeling develops only in some PD patients. Increasing evidence points to the differences that occur between patients in response to the same invading microorganism and/or the differences in the course of inflammatory reaction triggered by different species. Such differences may be related to the involvement of different inflammatory mediators. Here, we discuss the potential role of IL-17 in these processes with emphasis on its impact on peritoneal mesothelial cells and peritoneal vascularity.
Highlights
The potential cause of such alterations is chronic inflammation induced by repeated episodes of infectious peritonitis and/or exposure to bioincompatible peritoneal dialysis (PD) fluids
Studies of peritoneal structure and function indicate that two major processes occur during long-term PD treatment: (i) changes in the peritoneal vasculature resulting in increased transport of small solutes, (ii) changes in the peritoneal interstitium leading to reduced osmotic conductance of the membrane
Fibrotic thickening of the peritoneum will increase resistance to fluid flux and will decrease water flow through the interstitium. It appears that the gradual loss of peritoneal ultrafiltration with time is initially related to increased solute transport leading to proportional dissipation of the osmotic gradient
Summary
Peritoneal dialysis (PD) is a well-established treatment modality and the most commonly practiced form of home dialysis, its penetration is well below the utilization rate of 25–30% considered as optimal (Lameire and Van Biesen, 2010). Studies of peritoneal structure and function indicate that two major processes occur during long-term PD treatment: (i) changes in the peritoneal vasculature resulting in increased transport of small solutes, (ii) changes in the peritoneal interstitium leading to reduced osmotic conductance of the membrane. By applying an extended 3-pore model of the peritoneum (Davies et al, 2011), it is possible to explain how the peritoneal membrane displays increased transport rates for small solutes and, at same time, becomes more restrictive to water flow. Fibrotic thickening of the peritoneum will increase resistance to fluid flux and will decrease water flow through the interstitium It appears that the gradual loss of peritoneal ultrafiltration with time is initially related to increased solute transport leading to proportional dissipation of the osmotic gradient. These studies demonstrate that a decline in ultrafiltration can be partially prevented by anti-angiogenic therapy (Margetts et al, 2002)
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