ENDOTOXIN AND CHRONIC INFLAMMATION IN PATIENTS WITH CHRONIC KIDNEY DISEASE
Abstract
Endotoxin – obligatory component of gram-negative bacteria cell wall – one of the main etiological factors of chronic inflammation in patients with chronic kidney disease. Endotoxinemia severity increases with the progression of renal failure. The main sources of endotoxin are colon microbiome, as well as the biofilm formed by bacteria in the water treatment system, venous catheters, etc. Endotoxin causes persistent violations of homeostasis: cellular and humoral immunity, metabolic disorders, etc. The correction of these disorders is a complex problem. Endotoxinemia in patients with chronic kidney disease significantly affects the results of treatment and increases mortality.
About the Authors
A. V. Vatazin
Moscow regional research and clinical institute named after M.F. Vladimirsky
Russian Federation
Russian Federation
Andrey V. Vatazin, MD, PhD, Professor of medicine, DMedSci.
Head of the Department of Transplantation, Nephrology and Surgical hemocorrection.
129110, Moscow, Shchepkin Str., 61/2, building 6.
A. B. Zulkarnaev
Moscow regional research and clinical institute named after M.F. Vladimirsky
Russian Federation
Russian Federation
Alexey B. Zulkarnaev, MD, PhD, DMedSci.
Senior Researcher of transplantation and dialysis surgical department.
129110, Moscow, Shchepkin Str., 61/2, building 6.
References
1. Бикбов БТ, Томилина НА. Заместительная терапия терминальной хронической почечной недостаточности в Российской Федерации в 1998-2013 гг. Отчет по данным российского регистра заместительной почечной терапии. Часть первая. Нефрология и диализ 2015; 17(3, приложение): 5-111 [Bikbov BT, Tomilina NA. Zamestitel’naja terapija terminal’noj hronicheskoj pochechnoj nedostatochnosti v rossijskoj federacii v 1998-2013 gg. Otchet po dannym rossijskogo registra zamestitel’noj pochechnoj terapii. Chast’ pervaja. Nefrologija i dializ 2015; 17(3, prilozhenie): 5-111]
2. Terawaki H, Yokoyama, Yamada Y et al. Low-grade endotoxemia contributes to chronic inflammation in hemodialysis patients: examination with a novel lipopolysaccharide detection method. Ther Apher Dial 2010; 14(5):477-482. doi: 10.1111/j.17449987.2010.00815.x
3. McIntyre CW, Harrison LE, Eldehni MT et al. Circulating endotoxemia: a novel factor in systemic inflammation and cardiovascular disease in chronic kidney disease. Clin J Am Soc Nephrol 2011; 6(1):133-141. doi: 10.2215/CJN.04610510
4. Cardoso PG, Macedo GC, Azevedo V et al. Brucella spp noncanonical LPS: structure, biosynthesis, and interaction with host immune system. Microb Cell Fact 2006; 5:13
5. Villar J, Maca-Meyer N, Perez-Mendez L et al. Bench-tobedside review: understanding genetic predisposition to sepsis. Crit Care 2004; 8(3): 180-189
6. Gyorfy Z, Duda E, Vizler C. Interactions between LPS moieties and macrophage pattern recognition receptors. Vet Immunol Immunopathol 2013; 152(1-2):28-36. doi: 10.1016/j.vetimm.2012.09.020
7. Аниховская ИА, Опарина ОН, Яковлева ММ, Яковлев МЮ. Кишечный эндотоксин как универсальный фактор адаптации и патогенеза общего адаптационного синдрома. Физиология человека 2006; 32(2): 87-91
8. Ward PA. Role of C5 activation products in sepsis. ScientificWorldJournal 2010; 10:2395-2402. doi: 10.1100/tsw.2010.216
9. Kozarcanin H, Lood C, Munthe-Fog L et al. The lectin complement pathway serine proteases (MASPs) represent a possible crossroad between the coagulation and complement systems in thromboinflammation. J Thromb Haemost 2016; 14(3):531-545. doi: 10.1111/jth.13208
10. Esmon CT, Xu J, Lupu F. Innate immunity and coagulation. J Thromb Haemost 2011; 9 Suppl 1:182-188. doi: 10.1111/j.15387836.2011.04323.x
11. Lassenius MI, Pietilainen KH, Kaartinen K et al. Bacterial endotoxin activity in human serum is associated with dyslipidemia, insulin resistance, obesity, and chronic inflammation. Diabetes Care 2011; 34(8):1809-1815. doi: 10.2337/dc10-2197
12. Boutagy NE, McMillan RP, Frisard MI et al. Metabolic endotoxemia with obesity: Is it real and is it relevant? Biochimie 2016; 124:11-20. doi: 10.1016/j.biochi.2015.06.020
13. Белоглазов ВА, Климчук АВ, Гордиенко АИ и др. Динамика показателей гуморального антиэндотоксинового иммунитета и уровень С-реактивного белка у больных хронической болезнью почек, находящихся на программном гемодиализе, при четырехлетнем наблюдении. Нефрология и диализ 2013; 15(2): 140-143 [Beloglazov VA, Klimchuk AV, Gordienko AI i dr. Dinamika pokazatelej gumoral'nogo antijendotoksinovogo immuniteta i uroven' S-reaktivnogo belka u bol'nyh hronicheskoj bolezn'ju pochek, nahodjashhihsja na programmnom gemodialize, pri chetyrehletnem nabljudenii. Nefrologija i dializ 2013; 15(2): 140-143]
14. Feroze U, Kalantar-Zadeh K, Sterling KA et al. Examining associations of circulating endotoxin with nutritional status, inflammation, and mortality in hemodialysis patients. J Ren Nutr 2012; 22(3):317-326. doi: 10.1053/j.jrn.2011.05.004
15. Lau WL, Kalantar-Zadeh K, Vaziri ND. The Gut as a Source of Inflammation in Chronic Kidney Disease. Nephron 2015; 130(2):92-98. doi: 10.1159/000381990
16. Sabatino A, Regolisti G, Brusasco I et al. Alterations of intestinal barrier and microbiota in chronic kidney disease. Nephrol Dial Transplant 2015; 30(6):924-933. doi: 10.1093/ndt/gfu287
17. Shi K, Wang F, Jiang H et al. Gut bacterial translocation may aggravate microinflammation in hemodialysis patients. Dig Dis Sci 2014; 59(9):2109-2117. doi: 10.1007/s10620-014-3202-7
18. Hazzah WA, Hashish MH, El-Koraie AF et al. Circulating bacterial DNA fragments in chronic hemodialysis patients. Saudi J Kidney Dis Transpl 2015; 26(6):1300-1304. doi: 10.4103/13192442.168689
19. Marinho AC, Polay AR, Gomes BP. Accuracy of Turbidimetric Limulus Amebocyte Lysate Assay for the Recovery of Endotoxin Interacted with Commonly Used Antimicrobial Agents of Endodontic Therapy. J Endod 2015; 41(10):1653-1659. doi: 10.1016/j.joen.2015.05.020
20. Wong J, Vilar E, Farrington K. Endotoxemia in end-stage kidney disease. Semin Dial; 28(1):59-67. doi: 10.1111/sdi.12280
21. Shimizu T, Obata T, Sonoda H et al. Diagnostic potential of endotoxin scattering photometry for sepsis and septic shock. Shock 2013; 40(6):504-511. doi: 10.1097/SHK.0000000000000056
22. Ding JL, Ho B. Endotoxin detection-from limulus amebocyte lysate to recombinant factor C. Subcell Biochem 2010; 53:187-208. doi: 10.1007/978-90-481-9078-2_9
23. Yaguchi A, Yuzawa J, Klein DJ et al. Combining intermediate levels of the Endotoxin Activity Assay (EAA) with other biomarkers in the assessment of patients with sepsis: results of an observational study. Crit Care 2012; 16(3):R88. doi: 10.1186/cc11350
24. Poesen R, Ramezani A, Claes K et al. Associations of Soluble CD14 and Endotoxin with Mortality, Cardiovascular Disease, and Progression of Kidney Disease among Patients with CKD. Clin J Am Soc Nephrol 2015; 10(9):1525-1533. doi: 10.2215/CJN.03100315.
25. Raj DS, Shah VO, Rambod M et al. Association of soluble endotoxin receptor CD14 and mortality among patients undergoing hemodialysis. Am J Kidney Dis 2009; 54(6):1062-1071. doi: 10.1053/j.ajkd.2009.06.028
26. Cobo G, Qureshi AR, Lindholm B, Stenvinkel P. C-reactive Protein: Repeated Measurements will Improve Dialysis Patient Care. Semin Dial 2016; 29(1):7-14. doi: 10.1111/sdi.12440
27. Cross AS. Development of an anti-endotoxin vaccine for sepsis. Subcell Biochem 2010; 53: 285-302
28. Muller-Loennies S, Brade L, Brade H. Neutralizing and cross-reactive antibodies against enterobacterial lipopolysaccharide. Int J Med Microbiol 2007; 297(5): 321-340
29. Santos MF, New RR, Andrade GR et al. Lipopolysaccharide as an antigen target for the formulation of a universal vaccine against Escherichia coli O111 strains. Clin Vaccine Immunol 2010; 17(11): 1772-1780
30. Harkin DW, Arnold R, Hoper M. Anti-endotoxin hyperimmune globulin attenuates portal cytokinaemia, phagocytic cell priming, and acute lung injury after lower limb ischaemiareperfusion injury. Eur J Vasc Endovasc Surg 2007; 33(3): 330-339
31. Pini A, Falciani C, Mantengoli E et al. A novel tetrabranched antimicrobial peptide that neutralizes bacterial lipopolysaccharide and prevents septic shock in vivo. FASEB J 2010; 24(4): 1015-1022
32. Li J, Shang G, You M et al. Endotoxin removing method based on lipopolysaccharide binding protein and polyhydroxyalkanoate binding protein PhaP. Biomacromolecules 2011; 12(3): 602-608
33. Liu D, Lu F, Qin G et al. C1 inhibitor-mediated protection from sepsis. J Immunol 2007; 179(6): 3966-3972
34. Kaconis Y, Kowalski I, Howe J et al. Biophysical mechanisms of endotoxin neutralization by cationic amphiphilic peptides. Biophys J 2011; 100(11): 2652-6261
35. Peri F, Piazza M. Therapeutic targeting of innate immunity with Toll-like receptor 4 (TLR4) antagonists. Biotechnol Adv 2012; 30(1): 251-260
36. Fujita T. Molecular mechanism of endotoxin tolerance. Hepatology 2009; 50(4): 1322
37. Brandenburg K, Heinbockel L, Correa W et al. Peptides with dual mode of action: Killing bacteria and preventing endotoxininduced sepsis. Biochim Biophys Acta 2016; 1858(5):971-979. doi: 10.1016/j.bbamem.2016.01.011
38. Sun Y, Shang D. Inhibitory Effects of Antimicrobial Peptides on Lipopolysaccharide-Induced Inflammation. Mediators Inflamm 2015; 2015:167572. doi: 10.1155/2015/167572
39. Moraes C, Fouque D, Amaral AC et al. Trimethylamine N-Oxide From Gut Microbiota in Chronic Kidney Disease Patients: Focus on Diet. J Ren Nutr 2015; 25(6):459-465. doi: 10.1053/j.jrn.2015.06.004
40. Machowska A, Carrero JJ, Lindholm B et al. Therapeutics targeting persistent inflammation in chronic kidney disease. Transl Res 2016; 167(1):204-213. doi: 10.1016/j.trsl.2015.06.012
41. Tzanno-Martins C, Biavo BM, Ferreira-Filho O et al. Clinical efficacy, safety and anti-inflammatory activity of two sevelamer tablet forms in patients on low-flux hemodialysis. Int J Immunopathol Pharmacol 2014; 27(1):25-35
42. Rossi M, Johnson DW, Campbell KL. The Kidney-Gut Axis: Implications for Nutrition Care. J Ren Nutr 2015; 25(5):399-403. doi: 10.1053/j.jrn.2015.01.017
43. Sun PP, Perianayagam MC, Jaber BL. Endotoxinbinding affinity of sevelamer: a potential novel anti-inflammatory mechanism. Kidney Int Suppl 2009; (114):S20-5. doi: 10.1038/ki.2009.403
44. Rodriguez-Osorio L, Zambrano DP, Gracia-Iguacel C et al. Use of sevelamer in chronic kidney disease: beyond phosphorus control. Nefrologia 2015; 35(2):207-217. doi: 10.1016/j.nefro.2015.05.022
45. Mafra D, Fouque D. Gut microbiota and inflammation in chronic kidney disease patients. Clin Kidney J 2015; 8(3):332-334. doi: 10.1093/ckj/sfv026
46. Wing MR, Patel SS, Ramezani A et al. Gut microbiome in chronic kidney disease. Exp Physiol 2016; 101(4):471-477. doi: 10.1113/EP085283
47. Coulliette AD, Arduino MJ. Hemodialysis and water quality. Semin Dial 2013; 26(4):427-438. doi: 10.1111/sdi.12113
48. Schiffl H. High-flux dialyzers, backfiltration, and dialysis fluid quality. Semin Dial 2011; 24(1):1-4. doi: 10.1111/j.1525139X.2010.00786.x
49. Glorieux G, Hulko M, Speidel R et al. Looking beyond endotoxin: a comparative study of pyrogen retention by ultrafilters used for the preparation of sterile dialyis fluid. Sci Rep 2014; 4:6390. doi: 10.1038/srep06390
50. Kashiwagi T, Sato K, Kawakami S et al. The performance evaluation of endotoxin retentive filters in haemodialysis. J Nippon Med Sch 2011; 78(4):214-223
51. Glorieux G, Neirynck N, Veys N, Vanholder R. Dialysis water and fluid purity: more than endotoxin. Nephrol Dial Transplant 2012; 27(11):4010-4021. doi: 10.1093/ndt/gfs306
52. Bowry SK, Gatti E, Vienken J. Contribution of polysulfone membranes to the success of convective dialysis therapies. Contrib Nephrol 2011; 173:110-118. doi: 10.1159/000328960
53. Thomas M, Moriyama K, Ledebo I. AN69: Evolution of the world’s first high permeability membrane. Contrib Nephrol 2011; 173:119-129. doi: 10.1159/000328961
54. Perego AF. Adsorption techniques: dialysis sorbents and membranes. Blood Purif 2013; 35 Suppl 2:48-51. doi: 10.1159/000350848
55. Aucella F, Gesuete A, Vigilante M et al. Adsorption dialysis: from physical principles to clinical applications. Blood Purif 2013; 35 Suppl 2:42-47. doi: 10.1159/000350847
56. Tijink MS, Wester M, Sun J et al. A novel approach for blood purification: mixed-matrix membranes combining diffusion and adsorption in one step. Acta Biomater 2012; 8(6):2279-2287. doi: 10.1016/j.actbio.2012.03.008
57. Tijink MS, Kooman J, Wester M et al. Mixed matrix membranes: a new asset for blood purification therapies. Blood Purif 2014; 37(1):1-3. doi: 10.1159/000356226
58. Li L, Ling Y, Huang M et al. Heparin inhibits the inflammatory response induced by LPS and HMGB1 by blocking the binding of HMGB1 to the surface of macrophages. Cytokine 2015; 72(1):3642. doi: 10.1016/j.cyto.2014.12.010
59. Li X, Liu Y, Wang L et al. Unfractionated heparin attenuates LPS-induced IL-8 secretion via PI3K/Akt/NF-κB signaling pathway in human endothelial cells. Immunobiology 2015; 220(3):399-405. doi: 10.1016/j.imbio.2014.10.008
60. Li X, Li X, Zheng Z et al. Unfractionated heparin suppresses lipopolysaccharide-induced monocyte chemoattractant protein-1 expression in human microvascular endothelial cells by blocking Kruppel-like factor 5 and nuclear factor-κB pathway. Immunobiology 2014; 219(10):778-785. doi: 10.1016/j.imbio.2014.06.005
61. Li X, Zheng Z, Li X, Ma X. Unfractionated heparin inhibits lipopolysaccharide-induced inflammatory response through blocking p38 MAPK and NF-κB activation on endothelial cell. Cytokine 2012; 60(1):114-121. doi: 10.1016/j.cyto.2012.06.008
62. Li X, Zheng Z, Mao Y, Ma X. Unfractionated heparin promotes LPS-induced endothelial barrier dysfunction: a preliminary study on the roles of angiopoietin/Tie2 axis. Thromb Res 2012; 129(5):e223-228. doi: 10.1016/j.thromres.2012.03.003
63. Luan ZG, Naranpurev M, Ma XC. Treatment of low molecular weight heparin inhibits systemic inflammation and prevents endotoxin-induced acute lung injury in rats. Inflammation 2014; 37(3):924-932. doi: 10.1007/s10753-014-9812-6
Review
For citations:
Vatazin A.V., Zulkarnaev A.B. ENDOTOXIN AND CHRONIC INFLAMMATION IN PATIENTS WITH CHRONIC KIDNEY DISEASE. Nephrology (Saint-Petersburg). 2016;20(6):26-32. (In Russ.)
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