Heimbürger O, Wang T, Lindholm B
Department of Clinical Science, Karolinska Institutet, Huddinge Hospital, Stockholm, Sweden.
Perit Dial Int. 1999;19 Suppl 2:S83-90.
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.
在大多数接受腹膜透析(PD)治疗长达3年的患者中,腹膜超滤能力和小分子溶质转运特性似乎相对稳定。然而,在接受PD治疗4年或更长时间的患者中,小分子溶质的扩散转运有增加的趋势,同时净超滤有减少的趋势,而腹膜蛋白清除率似乎降低或保持稳定。超滤能力丧失是长期PD治疗期间众所周知的并发症,在接受PD治疗6年后,超滤能力丧失的风险可能高达50%。已经报道了几种不同的超滤能力丧失机制。特别是,超滤能力丧失最常见的机制是扩散转运增加,导致葡萄糖快速吸收,从而使渗透驱动力迅速丧失。也有报道称超滤能力丧失的原因包括:渗透剂效率降低(可能由于跨细胞水转运减少);由于纤维化和粘连形成(在硬化性腹膜炎后期)导致腹膜表面积丧失和溶质转运缓慢;以及腹膜液吸收增加。在个别患者中,几种机制的组合可能参与了明显的超滤能力衰竭。