继发性腹膜透析腹膜超滤衰竭发病机制的研究进展

Advances on pathogenesis of acquired peritoneal ultrafiltration failure in peritoneal dialysis

腹膜超滤衰竭是腹膜透析(peritoneal dialysis,PD)患者PD技术失败和心血管疾病死亡的常见原因。基于三孔模型的血管内皮细胞间小孔和跨内皮细胞超小孔(水孔蛋白1)是腹膜水转运的主要通道。随着PD的进行,小孔和超小孔依赖水(自由水)转运均降低,其中以自由水转运下降更为显著,导致腹膜超滤衰竭。自由水转运下降与腹膜溶质快速转运、间质葡萄糖吸收增加导致的晶体渗透压下降及水孔蛋白1功能异常和腹膜间质纤维化导致的葡萄糖渗透传导率下降等因素相关。而小孔依赖水转运降低受PD液晶体渗透压的快速丢失、腹膜毛细血管病变介导的静水压下降和小孔数量减少等因素影响。本文主要综述长期PD中继发性腹膜超滤衰竭发生机制的研究进展。

Peritoneal ultrafiltration failure is a common reason for peritoneal dialysis(PD)withdrawal as well as mortality in PD patients.Based on the three-pore system,inter-cellular small pores and trans-cellular ultra-small pores(aquaporin-1)are mainly responsible for water transfer across the peritoneum.Both small and ultra-small pores-dependent water(free water)transport decline accompanied with time on PD,with more significant decrease in free water,resulting in peritoneal ultrafiltration failure.The reduction of free water transport is associated with fast peritoneal solute transfer,reduced crystalloid osmotic gradient due to increased interstitial glucose absorption,and declined osmotic conductance to glucose resulted from impaired aquaporin-1 function and peritoneal interstitial fibrosis.The decline of small pore-based water is mainly because of fast loss of crystalloid osmotic gradient,decrease of hydrostatic pressure mediated by peritoneal vasculopathy,as well as reduced absolute number of small pores.The current review discusses the advance on pathogenesis of acquired peritoneal ultrafiltration failure in long-term PD.