[1]Hill N R, Fatoba S T, Oke J L, et al. Global Prevalence of Chronic Kidney Disease - A Systematic Review and Meta-Analysis[J]. PLoS One, 2016,11(7):e158765.
[2]Ricardo A C, Athavale A, Chen J, et al. Periodontal disease, chronic kidney disease and mortality: results from the third National Health and Nutrition Examination Survey[J]. BMC Nephrol, 2015,16:97.
[3]Zhang L, Wang F, Wang L, et al. Prevalence of chronic kidney disease in China: a cross-sectional survey[J]. Lancet, 2012,379(9818):815-822.
[4]Kaplan A A. Peritoneal Dialysis or Hemodialysis: Present and Future Trends in the United States[J]. Contrib Nephrol, 2017,189:61-64.
[5]Liyanage T, Ninomiya T, Jha V, et al. Worldwide access to treatment for end-stage kidney disease: a systematic review[J]. Lancet, 2015,385(9981):1975-1982.
[6]Briggs V, Davies S, Wilkie M. International Variations in Peritoneal Dialysis Utilization and Implications for Practice[J]. Am J Kidney Dis, 2019,74(1):101-110.
[7]Shrestha B M. Peritoneal Dialysis or Haemodialysis for Kidney Failure?[J]. JNMA J Nepal Med Assoc, 2018,56(210):556-557.
[8]van de Luijtgaarden M W, Jager K J, Segelmark M, et al. Trends in dialysis modality choice and related patient survival in the ERA-EDTA Registry over a 20-year period[J]. Nephrol Dial Transplant, 2016,31(1):120-128.
[9]Li P K, Chow K M, Van de Luijtgaarden M W, et al. Changes in the worldwide epidemiology of peritoneal dialysis[J]. Nat Rev Nephrol, 2017,13(2):90-103.
[10]Lee H B, Ha H. Mechanisms of Epithelial-Mesenchymal Transition of Peritoneal Mesothelial Cells During Peritoneal Dialysis[J]. Journal of Korean Medical Science, 2007,22(6):943.
[11]唐丽婷, 杨定平. 腹膜透析相关并发症及防治研究进展[J]. 疑难病杂志, 2021,20(12):1292-1296.
[12]Batra H, Antony V B. The pleural mesothelium in development and disease[J]. Front Physiol, 2014,5:284.
[13]Andrews P M, Porter K R. The ultrastructural morphology and possible functional significance of mesothelial microvilli[J]. Anat Rec, 1973,177(3):409-426.
[14]Bird S D. Mesothelial primary cilia of peritoneal and other serosal surfaces[J]. Cell Biol Int, 2004,28(2):151-159.
[15]Mutsaers S E. The mesothelial cell[J]. Int J Biochem Cell Biol, 2004,36(1):9-16.
[16]Moncrief J W. The Birth and Development of Continuous Ambulatory Peritoneal Dialysis[J]. Contrib Nephrol, 2017,189:85-90.
[17]Burmeister J E, Scapini A, Da R M D, et al. Glucose-added dialysis fluid prevents asymptomatic hypoglycaemia in regular haemodialysis[J]. Nephrol Dial Transplant, 2007,22(4):1184-1189.
[18]Perl J, Nessim S J, Bargman J M. The biocompatibility of neutral pH, low-GDP peritoneal dialysis solutions: benefit at bench, bedside, or both?[J]. Kidney Int, 2011,79(8):814-824.
[19]Jorres A, Topley N, Witowski J, et al. Impact of peritoneal dialysis solutions on peritoneal immune defense[J]. Perit Dial Int, 1993,13 Suppl 2:S291-S294.
[20]Haas S, Schmitt C P, Arbeiter K, et al. Improved acidosis correction and recovery of mesothelial cell mass with neutral-pH bicarbonate dialysis solution among children undergoing automated peritoneal dialysis[J]. J Am Soc Nephrol, 2003,14(10):2632-2638.
[21]Voyer L E, Alvarado C. [Maillard reaction. Pathogenic effects][J]. Medicina (B Aires), 2019,79(2):137-143.
[22]Nakamura S, Niwa T. Advanced glycation end-products and peritoneal sclerosis[J]. Semin Nephrol, 2004,24(5):502-505.
[23]Krediet R T, Ho-dac-Pannekeet M M, Imholz A L, et al. Icodextrin's effects on peritoneal transport[J]. Perit Dial Int, 1997,17(1):35-41.
[24]Lin A, Qian J, Li X, et al. Randomized controlled trial of icodextrin versus glucose containing peritoneal dialysis fluid[J]. Clin J Am Soc Nephrol, 2009,4(11):1799-1804.
[25]Dousdampanis P, Musso C G, Trigka K. Icodextrin and peritoneal dialysis: advantages and new applications[J]. Int Urol Nephrol, 2018,50(3):495-500.
[26]Misra P S, Nessim S J, Perl J. "Biocompatible" Neutral pH Low-GDP Peritoneal Dialysis Solutions: Much Ado About Nothing?[J]. Semin Dial, 2017,30(2):164-173.
[27]Htay H, Johnson D W, Wiggins K J, et al. Biocompatible dialysis fluids for peritoneal dialysis[J]. Cochrane Database Syst Rev, 2018,10:D7554.
[28]Fouque D, Kalantar-Zadeh K, Kopple J, et al. A proposed nomenclature and diagnostic criteria for protein-energy wasting in acute and chronic kidney disease[J]. Kidney Int, 2008,73(4):391-398.
[29]Chan W. Chronic Kidney Disease and Nutrition Support[J]. Nutr Clin Pract, 2021,36(2):312-330.
[30]Massague J. TGFbeta signalling in context[J]. Nat Rev Mol Cell Biol, 2012,13(10):616-630.
[31]Frangogiannis N. Transforming growth factor-beta in tissue fibrosis[J]. J Exp Med, 2020,217(3):e20190103.
[32]Si M, Wang Q, Li Y, et al. Inhibition of hyperglycolysis in mesothelial cells prevents peritoneal fibrosis[J]. Sci Transl Med, 2019,11(495).
[33]Lai K N, Lai K B, Szeto C C, et al. Growth factors in continuous ambulatory peritoneal dialysis effluent. Their relation with peritoneal transport of small solutes[J]. Am J Nephrol, 1999,19(3):416-422.
[34]Ebner R, Chen R H, Shum L, et al. Cloning of a type I TGF-beta receptor and its effect on TGF-beta binding to the type II receptor[J]. Science, 1993,260(5112):1344-1348.
[35]Blobe G C, Schiemann W P, Pepin M C, et al. Functional roles for the cytoplasmic domain of the type III transforming growth factor beta receptor in regulating transforming growth factor beta signaling[J]. J Biol Chem, 2001,276(27):24627-24637.
[36]Hill C S. The Smads[J]. Int J Biochem Cell Biol, 1999,31(11):1249-1254.
[37]Morrissey J, Hruska K, Guo G, et al. Bone morphogenetic protein-7 improves renal fibrosis and accelerates the return of renal function[J]. J Am Soc Nephrol, 2002,13 Suppl 1:S14-S21.
[38]Loureiro J, Schilte M, Aguilera A, et al. BMP-7 blocks mesenchymal conversion of mesothelial cells and prevents peritoneal damage induced by dialysis fluid exposure[J]. Nephrol Dial Transplant, 2010,25(4):1098-1108.
[39]Guo H, Leung J C, Lam M F, et al. Smad7 transgene attenuates peritoneal fibrosis in uremic rats treated with peritoneal dialysis[J]. J Am Soc Nephrol, 2007,18(10):2689-2703.
[40]Derynck R, Zhang Y E. Smad-dependent and Smad-independent pathways in TGF-beta family signalling[J]. Nature, 2003,425(6958):577-584.
[41]Tsauo J, Song H Y, Choi E Y, et al. EW-7197, an oral transforming growth factor beta type I receptor kinase inhibitor, for preventing peritoneal adhesion formation in a rat model[J]. Surgery, 2018,164(5):1100-1108.
[42]Zhang Y E. Non-Smad Signaling Pathways of the TGF-beta Family[J]. Cold Spring Harb Perspect Biol, 2017,9(2).
[43]Su J, Morgani S M, David C J, et al. TGF-beta orchestrates fibrogenic and developmental EMTs via the RAS effector RREB1[J]. Nature, 2020,577(7791):566-571.
[44]Xu Z G, Kim K S, Park H C, et al. High glucose activates the p38 MAPK pathway in cultured human peritoneal mesothelial cells[J]. Kidney Int, 2003,63(3):958-968.
[45]Liu Q, Zhang Y, Mao H, et al. A crosstalk between the Smad and JNK signaling in the TGF-beta-induced epithelial-mesenchymal transition in rat peritoneal mesothelial cells[J]. PLoS One, 2012,7(2):e32009.
[46]Poon P Y, Lan H Y, Kwan B C, et al. Peritoneal inflammation and fibrosis in C-reactive protein transgenic mice undergoing peritoneal dialysis solution treatment[J]. Nephrology (Carlton), 2017,22(2):125-132.
[47]Zhao Y, Zou W, Du J, et al. The origins and homeostasis of monocytes and tissue-resident macrophages in physiological situation[J]. J Cell Physiol, 2018,233(10):6425-6439.
[48]Shapouri-Moghaddam A, Mohammadian S, Vazini H, et al. Macrophage plasticity, polarization, and function in health and disease[J]. J Cell Physiol, 2018,233(9):6425-6440.
[49]Sutherland T E, Shaw T N, Lennon R, et al. Ongoing Exposure to Peritoneal Dialysis Fluid Alters Resident Peritoneal Macrophage Phenotype and Activation Propensity[J]. Front Immunol, 2021,12:715209.
[50]Duni A, Liakopoulos V, Roumeliotis S, et al. Oxidative Stress in the Pathogenesis and Evolution of Chronic Kidney Disease: Untangling Ariadne's Thread[J]. Int J Mol Sci, 2019,20(15).
[51]Chugh S, Chaudhry S, Ryan T, et al. Peritoneal Membrane Injury and Peritoneal Dialysis[J]. Advances in Nephrology, 2014,2014:1-10.
[52]Kuo H T, Chen H W, Hsiao H H, et al. Heat shock response protects human peritoneal mesothelial cells from dialysate-induced oxidative stress and mitochondrial injury[J]. Nephrol Dial Transplant, 2009,24(6):1799-1809.
[53]Gotloib L. Mechanisms of cell death during peritoneal dialysis. A role for osmotic and oxidative stress[J]. Contrib Nephrol, 2009,163:35-44.
[54]Hung K Y, Liu S Y, Yang T C, et al. High-dialysate-glucose-induced oxidative stress and mitochondrial-mediated apoptosis in human peritoneal mesothelial cells[J]. Oxid Med Cell Longev, 2014,2014:642793.
[55]Scarcello E, Herpain A, Tomatis M, et al. Hydroxyl radicals and oxidative stress: the dark side of Fe corrosion[J]. Colloids Surf B Biointerfaces, 2020,185:110542.
[56]Kuo H T, Chen H W, Hsiao H H, et al. Heat shock response protects human peritoneal mesothelial cells from dialysate-induced oxidative stress and mitochondrial injury[J]. Nephrol Dial Transplant, 2009,24(6):1799-1809.
[57]Bartel D P. MicroRNAs: genomics, biogenesis, mechanism, and function[J]. Cell, 2004,116(2):281-297.
[58]Wei X, Bao Y, Zhan X, et al. MiR-200a ameliorates peritoneal fibrosis and functional deterioration in a rat model of peritoneal dialysis[J]. Int Urol Nephrol, 2019,51(5):889-896.
[59]Guo R, Hao G, Bao Y, et al. MiR-200a negatively regulates TGF-beta1-induced epithelial-mesenchymal transition of peritoneal mesothelial cells by targeting ZEB1/2 expression[J]. Am J Physiol Renal Physiol, 2018,314(6):F1087-F1095.
[60]Shang J, He Q, Chen Y, et al. miR-15a-5p suppresses inflammation and fibrosis of peritoneal mesothelial cells induced by peritoneal dialysis via targeting VEGFA[J]. J Cell Physiol, 2019,234(6):9746-9755.
[61]He Q, Wen L, Wang L, et al. miR-15a-5p suppresses peritoneal fibrosis induced by peritoneal dialysis via targeting VEGF in rats[J]. Ren Fail, 2020,42(1):932-943.
[62]Fountain J H, Lappin S L. Physiology, Renin Angiotensin System[J]. 2022.
[63]Zhou G, Wu J, Gu C, et al. Prorenin independently causes hypertension and renal and cardiac fibrosis in cyp1a1-prorenin transgenic rats[J]. Clin Sci (Lond), 2018,132(12):1345-1363.
[64]Wong C, Falkenham A, Myers T, et al. Connective tissue growth factor expression after angiotensin II exposure is dependent on transforming growth factor-beta signaling via the canonical Smad-dependent pathway in hypertensive induced myocardial fibrosis[J]. J Renin Angiotensin Aldosterone Syst, 2018,19(1):1605484098.
[65]Kyuden Y, Ito T, Masaki T, et al. Tgf-beta1 induced by high glucose is controlled by angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker on cultured human peritoneal mesothelial cells[J]. Perit Dial Int, 2005,25(5):483-491.
[66]Kocak G, Azak A, Astarci H M, et al. Effects of renin-angiotensin-aldosterone system blockade on chlorhexidine gluconate-induced sclerosing encapsulated peritonitis in rats[J]. Ther Apher Dial, 2012,16(1):75-80.
[67]Jing S, Kezhou Y, Hong Z, et al. Effect of renin-angiotensin system inhibitors on prevention of peritoneal fibrosis in peritoneal dialysis patients[J]. Nephrology (Carlton), 2010,15(1):27-32.