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综述

腹膜透析相关性腹膜纤维化机制的研究进展

  • 马龙飞 ,
  • 杜路 ,
  • 邓喜文 ,
  • 胡爽爽 ,
  • 郭明好
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  • 新乡医学院第一附属医院肾内科

收稿日期: 2022-01-20

  修回日期: 2022-04-02

  网络出版日期: 2022-06-12

Research progress on the mechanism of peritoneal fi-brosis associated with peritoneal dialysis

  • MA Long-Fei ,
  • DU Lu ,
  • DENG Xi-Wen ,
  • HU Shuang-Shuang ,
  • GUO Ming-Hao
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Received date: 2022-01-20

  Revised date: 2022-04-02

  Online published: 2022-06-12

摘要

腹膜透析(peritoneal dialysis,PD)是终末期肾病(end state renal disease,ESRD)重要的肾脏替代治疗方式之一,在提升患者生活质量的同时,也伴随着诸多并发症,其中腹膜纤维化(peritoneal fibrosis,PF)被认为是导致PD失败的最主要原因。为了促进PD技术的发展与应用,使其造福更多临床患者,众多学者对PF的发生机制展开了研究,现将近年来的发现作一综述。

本文引用格式

马龙飞 , 杜路 , 邓喜文 , 胡爽爽 , 郭明好 . 腹膜透析相关性腹膜纤维化机制的研究进展[J]. 中国血液净化, 2022 , 21(06) : 445 -448,460 . DOI: doi:10.3969/j.issn.1671-4091.2022.06.014

Abstract

Peritoneal dialysis (PD) is one of the important renal replacement treatments for end stage renal disease (ESRD). PD improves the patients’ quality of life but also has many complications, in which peritoneal fibrosis (PF) is considered to be the main cause of PD failure. In order to promote the development and application of PD technology and to benefit more ESRD patients, many scholars have conducted researches on the mechanism of PF. This paper reviews the recent achievements in this area.

参考文献

[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.
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