Pathophysiological description of the ultrastructural changes of the peritoneal membrane during long-term continuous ambulatory peritoneal dialysis.

Some of the patients on continuous ambulatory peritoneal dialysis (CAPD) develop with time on treatment an increased transperitoneal transport of small solutes, implying that glucose is more rapidly absorbed from the dialysate. Hence, the dialysate/serum crystalloid osmotic gradient dissipates at a faster rate, so that ultrafiltration failure may result. The pathophysiological correlates to these changes are not well understood. However, it seems that with time on CAPD, there are changes in the submesothelial interstitium, affecting both the ground substance and spacing and orientation of collagen fibers. There may also be mesothelial alterations with patchy shedding of the cells. The present article discusses these changes in terms of a modified three-pore model of peritoneal permeability. In this model, the capillary walls act as a major barrier for solutes ranging in size from inulin (molecular radius 14 A) to macromolecules (molecular radius > 30 A). However, for solutes smaller than inulin both capillary wall and insterstitium contribute to the blood-peritoneum transport impedance. The increased small-solute exchange sometimes occurring in long-term CAPD can be explained either by recruitment of vascular surface area, due, e.g., to an increased capillarization of the peritoneal membrane with time, or, more likely, a drop in the interstitial transport resistance to small solutes. The latter possibility is supported by the often more pronounced increase in the transperitoneal transfer of small solutes than that of macromolecules over time in CAPD.