Cytokines and arterial stiffness at the early stage of chronic kidney disease: the relationship and prognostic role


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Abstract

Objective. To evaluate plasma cytokine levels (tumor necrosis factor а - TNF-а and interleukin-10 - IL-i0) and their relationship with arterial stiffness parameters in patients with renal dysfunction (RD) at an early stage of the disease. Material and methods. A total of 221 patients with RD aged from 19 to 88 years were examined. To assess the severity of RD, the glomerular filtration rate (GFR) using blood cystatin с level was measured. All examined patients underwent evaluation of the lipid spectrum and plasma uric acid levels. The TNF-а concentration (pg/mL) and IL-io concentration (pg/mL) in the blood plasma were evaluated by the reagent kits (ООО Vector-Best, Novosibirsk) using ELISA technique (stiffness index - SI, augmentation index - AIP, alternative stiffness index -aSI, vascular age - va, age index - agi, reflection index - ri, increase index at a pulse rate of 75 per minute - PR = 75 - AIP 75, and pulse wave amplitude - PWA) on the "AngioScan-01" device. Depending on the TNF-а concentration, all examined patients were randomly divided into two groups: the group 1 (n=166) included patients with TNF-а level <2.0 pg/mL and the group 2 (n=55) - patients with TNF-а level >2.01 pg/mL. results. Patients in the group 2 (TNF-а level >2.0i pg/mL) had higher AIP level - 13.3 (1.20-23.4) versus 9.35 (-3.7-21.5)% (р<0.05) and increase index with a pulse rate of 75 per minute (AIP 75) 16.1 (6.4-25.1) versus 10.5 (1.5-19.4)% (р<0.05) compared with the group 1 (TNF-a concentration <2.0 pg/mL). In the 2nd group, the statistically significant direct relationship between the TNF-a and blood plasma cystatin С concentrations (0.406; P=0.019), as well as the tendency of inverse correlation between TNF-a and the calculated GFR (-0.267; Р=0.051) were also revealed. Conclusion. At an early stage of RD, an increase in the TNF-a concentration is associated with an increase in AIP.

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About the authors

I. T Murkamilov

Kyrgyz State Medical Academy N.A. I.K. Akhunbaev; Kyrgyz-Russian Slavic University N.A. The First President of Russia B.N. Yeltsin

Email: murkamilov.i@mail.ru
PhD in Medical Sciences, Nephrologist of the 1st Qualification Category, Teaching Assistant at the Department of Faculty Therapy

K. A Aitbaev

Scientific Research Institute of Molecular Biology and Medicine at the National Center for Cardiology and Therapy of The Ministry of Health of the Kyrgyz Republic

Doctor of Medical Sciences, Professor, Head of the Laboratory of Pathological Physiology

V. V Fomin

FSBEI HE ”I.M. Sechenov First Moscow State Medical University”

Doctor of Medical Sciences, Professor, Head of the Department of Faculty Therapy № 1

Zh. A Murkamilova

Center for Family Medicine № 7, Bishkek

Nephrologist

I. S Sabirov

Kyrgyz-Russian Slavic University N.A. The First President of Russia B.N. Yeltsin

Doctor of Medical Sciences, Professor, Head of the Department of Therapy № 2 in the specialty "Medical Care"

References

  1. Мухин Н.А., Моисеев В.С., Кобалава Ж.Д. Поражение сердечно-сосудистой системы при заболеваниях почек. Кардиология: Новости. Мнения. Обучение 2015;2(5):63-6
  2. Lees J.S., Mark P.B., Jardine A.G. Cardiovascular complications of chronic kidney disease. Med. 2015;43:8:469-73. Doi:https://doi.org/10.1016/j. mpmed.2015.05.009.
  3. Сердечно-сосудистый риск и хроническая болезнь почек: стратегии кардио-нефропротекции. Национальные рекомендации. Рос. кардиологический журнал 2014;8(112):7-37.
  4. Bello A.K., Alrukhaimi M., Ashuntantang G.E., et al. Complications of chronic kidney disease: current state, knowledge gaps, and strategy for action. Kidney Int. 2017;7:2:122-129. Doi:https://doi.org/10.1016/j.kisu.2017.07.007.
  5. Encalada Landires M. Prevalencia del sindrome cardiorrenal en pacientes con enfermedad renal cronica en hemodiâlisis : дис. - Universidad de Guayaquil. Facultad de Ciencias Médicas. Escuela de Medicina, 2018. http://repositorio.ug.edu.ec/handle/redug/31015.
  6. Briet M., Boutouyrie P., Laurent S., London G.M. Arterial stiffness and pulse pressure in CKD and ESRD. Kidney Int. 2012;82:4:388-400. Doi:https:// doi.org/10.1038/ki.2012.131.
  7. Yong K., Ooi E. M., Dogra G., et al. Elevated interleukin-12 and interleukin-18 in chronic kidney disease are not associated with arterial stiffness. Cytokine. 2013;64:1:39-42. Doi:https://doi.org/10.1016/j.cyto.2013.05.023.
  8. Garnier A.-S., Briet M. Arterial Stiffness and Chronic Kidney Disease. Pulse. 2016;3(3-4):229-241. doi: 10.1159/000443616.
  9. London G.M. Arterial Stiffness in Chronic Kidney Disease and End-Stage Renal Disease. Blood purification. 2018;45(1-3):154-158. Doi:https://doi. org/10.1159/000485146.
  10. Aroor A.R., DeMarco V., Jia G., et al. The role of tissue renin-angiotensin-aldosterone system in the development of endothelial dysfunction and arterial stiffness. Front. Endocrinol. 2013;4:161. Doi:https://doi.org/10.3389/ fendo.2013.00161.
  11. Palit S., Kendrick J. Vascular calcification in chronic kidney disease: role of disordered mineral metabolism. Curr. Pharmacy. Desi. 2014;20(37): 5829-5833.
  12. Akchurin M., Kaskel F. Update on inflammation in chronic kidney disease. Blood Purificat. 2015;39(1-3):84-92. Doi:https://doi. org/10.1159/000368940.
  13. Yeo E.S., Hwang J.Y., Park J.E., et al. Tumor necrosis factor (TNF-a) and C-reactive protein (CRP) are positively associated with the risk of chronic kidney disease in patients with type 2 diabetes. Yonsei Med. J. 2010;51(4):519-525. Doi:https://doi.org/10.3349/ymj.2010.51.4.519.
  14. Levine B., Kalman J., Mayer L., et al. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N. Engl. J. Med. 1990;323(4):236-241. doi: 10.1056/NEJM199007263230405.
  15. Hoek F.J., Kemperman FA., Krediet R.T. A comparison between cystatin C., plasma creatinine and the Cockcroft and Gault formula for the estimation of glomerular fi ltration rate. Nephrol. Dial. Transpl. 2003;18(10):2024-31. doi: 10.1093/ndt/gfg349.
  16. Парфенов А.С. Ранняя диагностика сердечно-сосудистых заболеваний с использованием аппаратно-программного комплекса «Ангиоскан-01». Поликлиника 2012;2(1):70-74.
  17. Орлов А.И. Прикладная статистика. М., 2006. 671 с.
  18. Rao M., Wong C., Kanetsky P., et al. Cytokine gene polymorphism and progression of renal and cardiovascular diseases. Kidney Int. 2007;72(5):549-556. Doi:https://doi.org/10.1038/sj.ki.5002391.
  19. Eck M.J., Sprang S.R. The structure of tumor necrosis factor-alpha at 2.6 A resolution. Implications for receptor binding. J. Biol. Chem. 1989;264(29):17595-605.
  20. Wilson A.G., Symons J.A., McDowell T.L., et al. Effects of a polymorphism in the human tumor necrosisfactor a promoter on transcriptional activation. Proc. Nat. Acad. Sci. 1997;94(7):3195-3199.
  21. Maciejewski J., Selleri C., Anderson S., Young N.S. Fas antigen expression on CD34+ human marrow cells is induced by interferon gamma and tumor necrosis factor alpha and potentiates cytokine-mediated hematopoietic suppression in vitro. Blood. 1995;85(11):3183-3190.
  22. Bazzoni F., Beutler B. The tumor necrosis factor ligand and receptor families. New England J. Med. 1996;334(26):1717-1725. Doi:10.1056/ NEJM199606273342607.
  23. Walczak H., Miller R.E., Ariail K., et al. Tumoricidal activity of tumor necrosis factor-related apoptosis-inducing ligand in vivo. Nat. Med. 1999;5(2):157.
  24. Sampaio E.P., Sarno E.N., Galilly R., et al. Thalidomide selectively inhibits tumor necrosis factor alpha production by stimulated human monocytes. J. Exp. Med. 1991;173(3):699-703. doi: 10.1084/jem.173.3.699.
  25. Sutton T.A., Fisher C.J., Molitoris B.A. Microvascular endothelial injury and dysfunction during ischemic acute renal failure.Kidney international 2002;62(5): 1539-1549. Doi:https://doi.org/10.1046//. 1523-1755.2002.00631.x.
  26. Howard M., O’Garra A., Ishida H., et al. Biological properties of interleukin 10. J. Clin. Immunol. 1992;12(4):239-247
  27. Chernoff A.E., Granowitz E.V., Shapiro L., et al. A randomized, controlled trial of IL-10 in humans. J. Immunol. 1995;154(10):5492-5499.
  28. Moore K.W., de Waal Malefyt R., Coffman R.L., O’Garra A. Interleukin-10 and the interleukin-10 receptor. Ann. Rev. Immunol. 2001;19(1):683-765. Doi:https://doi.org/10.1146/annurev.immunol.19.1.683.
  29. Bruunsgaard H., Skinhoj P., Pedersen A.N., et al.Ageing, tumour necrosisfactor-alpha (TNF-a) and atherosclerosis. Clin. Exp. Immunol. 2000;121(2):255-260. Doi:https://doi.org/10.1046/j.1365-2249.2000.01281.x.
  30. Dinarello C.A. Interleukin-1ß, Interleukin-18, and the Interleukin-1ß converting enzyme. Ann. N. Y. Acad. Sci. 1998;856(1):1-11. Doi:https://doi. org/10.1111/j.1749-6632.1998.tb08307.x.
  31. Wanidvoranun C., Strober W. Predominant role of tumor necrosis factor-a in human monocyte IL-10 synthesis. J. Immuno. 1993;151:6853-6861.
  32. Yssel H., de Waal Malefyt R., Roncarolo M.G., et al. IL-10 is produced by subsets of human CD4+T-cell clones and peripheral blood T-cell. J. Immunol. 1992;149:2378-2384.
  33. Вашурина Т.В., Сергеева Т.В. Гломерулярное воспаление и интерлейкин-10. Нефрология и диализ. 2000;3(2):146-144.
  34. Zhou T., Edwards C.3., Yang P., et al. Greatly accelerated lymphadenopathy and autoimmune disease in lpr mice lacking tumor necrosis factor receptor I. J. Immunol. 1996;156(8):2661-2665.
  35. Муркамилов И.Т., Фомин В.В., Айтбаев К.А. и др. Цитокиновая модель развития сердечно-сосудистых осложнений при хронической болезни почек. Клиническая нефрология. 2017;2:71-75.
  36. Eardley K.S., Cockwell P. Macrophages and progressive tubulointerstitial disease. Kidney Int. 2005;68(2):437-455. Doi:https://doi.org/10.1111/ j.1523-1755.2005.00422.x.
  37. Rodriguez-Iturbe B., Pons H., Herrera-Acosta J., Johnson R.J. Role of immunocompetent cells in nonimmune renal diseases. Kidney Int. 2001;59(5): 1626-1640. Doi:https://doi.org/10.1046/j. 1523-1755.2001. 0590051626.x.
  38. Brady H.R. Leukocyte adhesion molecules and kidney diseases Kidney Int. 1994;45(5):1285-1300. Doi:https://doi.org/10.1038/ki.1994.169.
  39. Murphy P.M., Baggiolini M., Charo I.F., et al. International union of pharmacology. XXII. Nomenclature for chemokine receptors. Pharmacol. Rev. 2000;52(1):145-176.
  40. Kluth D.C., Rees A.J. New approaches to modify glomerular inflammation. J. Nephrol. 1999;12:2:66-75.
  41. Honkanen E., von Willebrand E., Teppo A.M., et al. Adhesion molecules and urinary tumor necrosisfactor-a in idiopathic membranous glomerulonephritis. Kidney Int. 1998;53(4):909-917. Doi:https://doi.org/10.1111/J.1523-1755.1998.00833.X.
  42. Mitchell D. Rodgers K., Hanly J., et al. Lipoxins inhibit Akt/PKB activation and cell cycle progression in human mesangial cells. Am. J. Pathol. 2004; 164(3):937-946. Doi:https://doi.org/10.1016/S0002-9440(10)63181-1.
  43. Клебанова Е.М. Окислительный стресс, функциональная активность бета-клеток и содержание фактора некроза опухолей альфа у больных сахарным диабетом 2-го типа. Клиническая медицина. 2006;8:40-43.
  44. Schram M.T., Chaturvedi N., Schalkwijk C.G., et al. Markers of inflammation are cross-sectionally associated with microvascular complications and cardiovascular disease in type 1 diabetes - the EURODIAB Prospective Complications Study. Diabetol. 2005;48(2):370-378.
  45. Min D., Lyons J.G., Bonner J., et al. Mesangial cell-derived factors alter monocyte activation and function through inflammatory pathways: possible pathogenic role in diabetic nephropathy. Am. J. Physiol Renal. Physiol. 2009;297(5):1229-123 7. Doi:https://doi.org/10.1152/ ajprenal.00074.2009.
  46. Duran-Salgado M.B., Rubio-Guerra A.F. Diabetic nephropathy and inflammation. World J. Diabet. 2014;5(3):393.
  47. Kalantarinia K., Awad A.S., Siragy H.M. Urinary and renal interstitial concentrations of TNF-alpha increase prior to the rise in albuminuria in diabetic rats. Kidney Int. 2003;64(4):1208-1213.
  48. Navarro J.F., Milena F.J., Mora C., et al. Renal pro-inflammatory cytokine gene expression in diabetic nephropathy: effect of angiotensin-converting enzyme inhibition and pentoxifylline administration. Am. J. Nephrol. 2006;26(6):562-70.
  49. Amann B., Tinzmann R., Angelkort B. ACE inhibitors improve diabetic nephropathy through suppression of renal MCP-1. Diabetes Care. 2003;26(8):2421-2425.
  50. Chow F.Y., Nikolic-Paterson D.J., Ozols E., et al. Monocyte chemoattractant protein-1 promotes the development of diabetic renal injury in streptozotocintreated mice. Kidney Int. 2006;69(1):73-80.
  51. Семешина О.В., Лучанинова В.Н., Маркелова Е.В. и др. Особенности экскреции цитокинов с мочой при хронической болезни почек у детей. Клиническая нефрология 2017;3:46-53
  52. Семешина О.В., Лучанинова В.Н., Ни А. и др. Диагностическая значимость цитокинового профиля сыворотки крови при хронической болезни почек у детей. Нефрология. 2018;22(4):81-89. Doi:https:// doi.org/10.24884/1561-6274-2018-22-4-81-89.
  53. Михайлова Н.А., Тимонова А.Н., Князева Л.А., Безгин А.В. Провоспалительная цитокинемия и жесткость артериальной стенки у больных ревматоидным артритом с артериальной гипертензией. Int. J. Immunorehabilit. 2010;2(12):141а.
  54. Miles E.A., Rees D., Banerjee T., et al. Age-related increases in circulating inflammatory markers in men are independent of BMI, blood pressure and blood lipid concentrations. Atherosclerosis. 2008;196(1):298-305. Doi:https://doi.org/10.1016/j.atherosclerosis.2006.11.002.
  55. Садикова Р.И., Сахаутдинова Г.М., Федотов А.Л. Состояние сосудистой стенки и уровень цитокинов как маркеры сердечно-сосудистых осложнений у больных острым инфарктом миокарда. Медицинский вестник Башкортостана. 2016;4:11(64):63- 67.
  56. Лондон Ж.М. Перевод Захаровой Е.В. Ремоделирование артерий и артериальное давление у больных с уремией. Нефрология и диализ. 2000;2(3): 124-30.
  57. Ao D.H., Zhai F.F., Han F., et al. Large vessel disease modifies the relationship between kidney injury and cerebral small vessel disease. Front. Neurol. 2018;9:498. Doi:https://doi.org/10.3389/fneur.2018.00498.
  58. Lee W-H., Hsu P-C., Chu C-Y., et al. Association of renal systolic time intervals with brachial-ankle pulse wave velocity. Int. J. Med. Sci. 2018;15(11):1235-1240. doi: 10.7150/ijms.24451.
  59. Jankowski P. Value of arterial stiffness in predicting cardiovascular events and mortality. Medicographia. 2015;37:399-403.
  60. Joo H.J., Cho S.A., Cho J.Y., et al. The Relationship between Pulse Wave Velocity and Coronary Artery Stenosis and Percutaneous Coronary Intervention: a retrospective observational study. BMC. Cardiovasc. Dis. 2017;17:1-45. Doi:https://doi.org/10.1186/s12872-017-0476-7.
  61. Zieman S.J., Melenovsky V., Kass D.A. Mechanisms, pathophysiology, and therapy of arterial stiffness.Arterioscler. Thromb. Vasc. Biol. 2005;25(5):932-943. Doi:https://doi.org/10.1161/01.ATV.0000160548.78317.29.
  62. Barbaro N.R., de Araujo T.M., Tanus-Santos J.E., et al. Vascular damage in resistant hypertension: TNF-alpha inhibition effects on endothelial cells. BioMed. Res. Int. 2015;2015. Doi:http://dx.doi.org/10.1155/2015/631594.
  63. Angel K., Provan S.A., Gulseth H.L., et al. Tumor necrosis factor-a antagonists improve aortic stiffness in patients with inflammatory arthropathies: a controlled study. Hypertension. 2010;55(2):333-338. doi: 10.1161/HYPERTENSION AHA.109.143982.
  64. Dulai R., Perry M., Twycross-Lewis R., et al. The effect of tumor necrosis factor-a antagonists on arterial stiffness in rheumatoid arthritis: a literature review. Seminars in arthritis and rheumatism. WB Saunders. 2012;42(1):1-8. Doi:https://doi.org/10.1016/j.semarthrit.2012.02.002.
  65. Муркамилов И.Т., Фомин В.В., Айтбаев К.А. и др. Хроническая болезнь почек и цереброваскулярные расстройства: роль цистатина С. Клиническая нефрология 2017;3:60-67.

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