Chu Chenling, Huang Ying, Cao Luxi, Ji Shuiyu, Zhu Bin, Shen Quanquan
Department of Clinical Medicine, Hangzhou Normal University, Hangzhou, Zhejiang, China.
Urology & Nephrology Center, Department of Nephrology, Zhejiang Provincial People's Hospital (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, China.
Ren Fail. 2025 Dec;47(1):2474203. doi: 10.1080/0886022X.2025.2474203. Epub 2025 Mar 5.
Peritoneal dialysis (PD) can be used as renal replacement therapy when chronic kidney disease (CKD) progresses to end-stage renal disease. However, peritoneal fibrosis (PF) is a major cause of PD failure. Studies have demonstrated that PD fluid contains a significantly larger numbers of macrophages compared with the healthy individuals. During PD, macrophages can secrete cytokines to keep peritoneal tissue in sustained low-grade inflammation, and participate in the regulation of fibrosis-related signaling pathways, such as NF-κB, TGF-β/Smad, IL4/STAT6, and PI3K/AKT. A series of basic pathological changes occurs in peritoneal tissues, including epithelial mesenchymal transformation, overgeneration of neovasculature, and abnormal deposition of extracellular matrix. This review focuses on the role of macrophages in promoting PF during PD, summarizes the targets of macrophage-related inhibition of fibrosis, and provides new ideas for clinical research on delaying PF, maintaining the function and integrity of peritoneum, prolonging duration of PD as a renal replacement modality, and achieving longer survival in CKD patients.
当慢性肾脏病（CKD）进展至终末期肾病时，腹膜透析（PD）可作为肾脏替代疗法。然而，腹膜纤维化（PF）是PD失败的主要原因。研究表明，与健康个体相比，PD液中巨噬细胞数量显著增多。在PD过程中，巨噬细胞可分泌细胞因子，使腹膜组织持续处于低度炎症状态，并参与纤维化相关信号通路如NF-κB、TGF-β/Smad、IL4/STAT6和PI3K/AKT的调节。腹膜组织会发生一系列基本病理变化，包括上皮-间质转化、新生血管过度生成以及细胞外基质异常沉积。本综述重点关注巨噬细胞在PD过程中促进PF的作用，总结巨噬细胞相关抗纤维化的靶点，为延缓PF、维持腹膜功能和完整性、延长PD作为肾脏替代方式的时间以及提高CKD患者生存率的临床研究提供新思路。
