Preventing peritoneal membrane fibrosis in peritoneal dialysis patients.
Long-term peritoneal dialysis causes morphologic and functional changes in the peritoneal membrane. Although mesothelial-mesenchymal transition of peritoneal mesothelial cells is a key process leading to peritoneal fibrosis, and bioincompatible peritoneal dialysis solutions (glucose, glucose degradation products, and advanced glycation end products or a combination) are responsible for altering mesothelial cell function and proliferation, mechanisms underlying these processes remain largely unclear. Peritoneal fibrosis has 2 cooperative parts, the fibrosis process itself and the inflammation. The link between these 2 processes is frequently bidirectional, with each one inducing the other. This review outlines our current understanding about the definition and pathophysiology of peritoneal fibrosis, recent studies on key fibrogenic molecular machinery in peritoneal fibrosis, such as the role of transforming growth factor-β/Smads, transforming growth factor-β β/Smad independent pathways, and noncoding RNAs. The diagnosis of peritoneal fibrosis, including effluent biomarkers and the histopathology of a peritoneal biopsy, which is the gold standard for demonstrating peritoneal fibrosis, is introduced in detail. Several interventions for peritoneal fibrosis based on biomarkers, cytology, histology, functional studies, and antagonists are presented in this review. Recent experimental trials in animal models, including pharmacology and gene therapy, which could offer novel insights into the treatment of peritoneal fibrosis in the near future, are also discussed in depth.
Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. Electronic address: zhouqin001994@163.com.
Qin
Q
Zhou
Nephrology Service, Hospital Universitario La Paz, IdiPAZ, REDinREN, Fibroteam, IRSIN, Madrid, Spain.
M-Auxiliadora
MA
Bajo
Nephrology Service, Hospital Universitario La Paz, IdiPAZ, REDinREN, Fibroteam, IRSIN, Madrid, Spain.
Gloria
G
Del Peso
Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Xueqing
X
Yu
Nephrology Service, Hospital Universitario La Paz, IdiPAZ, REDinREN, Fibroteam, IRSIN, Madrid, Spain.
Rafael
R
Selgas
D000818:Animals; D015415:Biomarkers / Q000032:analysis; D001706:Biopsy; D015314:Dialysis Solutions / Q000009:adverse effects*; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000187:drug effects / Q000473:pathology; D005947:Glucose / Q000009:adverse effects*; D017127:Glycation End Products, Advanced / Q000009:adverse effects; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D010530:Peritoneal Dialysis / Q000009:adverse effects*; D056627:Peritoneal Fibrosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D010537:Peritoneum / Q000187:drug effects / Q000473:pathology; D062085:RNA, Long Noncoding / Q000378:metabolism; D058727:RNA, Small Untranslated / Q000378:metabolism; D015398:Signal Transduction; D051785:Smad Proteins / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000378:metabolism
D015415:Biomarkers; D015314:Dialysis Solutions; D017127:Glycation End Products, Advanced; D062085:RNA, Long Noncoding; D058727:RNA, Small Untranslated; D051785:Smad Proteins; D016212:Transforming Growth Factor beta; D005947:Glucose
biocompatibility; interventions; peritoneal fibrosis; peritoneal fluids; peritoneal inflammation