Abstract
Peritoneal ultrafiltration capacity and small-solute transport characteristics seem to be relatively stable in most patients treated with PD for up to 3 years. However, in patients treated with PD for 4 years or more, there is a tendency towards increasing diffusive transport for small solutes as well as a tendency towards decreasing net UF, whereas the peritoneal protein clearances seem to be reduced or stable. Loss of UFC is a well-known complication during long-term PD treatment, and the risk for loss of UFC may be as high as 50% after 6 years on PD. Several different mechanisms of UFC loss have been reported. In particular, the most common mechanism for loss of UFC is increased diffusive transport resulting in rapid glucose absorption and thus rapid loss of the osmotic driving force. Also reported as causes of UFC loss have been: reduced efficiency of the osmotic agent (perhaps owing to decreased transcellular water transport); loss of peritoneal surface area with slow solute transport owing to fibrosis and the formation of adhesions (during the late stage of sclerosing peritonitis); and increased peritoneal fluid absorption. In individual patients, a combination of several mechanisms may be involved in the apparent UFC failure.
Published Version
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