Peritoneal ultrafiltration: physiology and failure

Abstract

Net ultrafiltration in peritoneal dialysis results from a complex set of forces within the tissue space surrounding the peritoneal cavity. Hydrostatic pressure due to the large volume of fluid drives water and solute into the surrounding tissue, and therefore a high osmotic pressure must be maintained in the cavity to draw fluid from blood capillaries distributed in the tissue adjacent to the peritoneum. The osmotic pressure in the interstitium decreases from that of the cavity to equilibration with the plasma in the first millimeter of tissue below the peritoneum. Osmotic pressure differences at the blood capillary produce a solute free ultrafiltrate via aquaporin 1 that is approximately 50% of the total filtration. The remainder of the fluid is filtered via interendothelial gaps lined with negatively charged glycocalyx, which alters the traditional Starling forces and is easily damaged by inflammation or ischemia. Ultrafiltration failure occurs when intraperitoneal pressure is too high, the inflamed peritoneum dissipates the osmotic agent rapidly because of hyperpermeable angiogenic vessels, or peritoneal scarring lowers the osmotic pressure near the blood supply and there is no force for fluid transport through the scar to the cavity. To remedy problems in net ultrafiltration, lowering the volume lowers the intraperitoneal pressure and often solves the problem of excessive pressure. Preventative measures to decrease inflammation and peritonitis are important for preservation of the barrier. Experimental measures such as peritoneal stem-cell transplants may someday permit reclamation of damaged barrier systems and allow patients to continue the dialytic technique.