Contribution of systemic inflammation to the development of vascular remodeling in patients with chronic kidney disease and sarcopenia


DOI: https://dx.doi.org/10.18565/therapy.2021.5.39-46

Kolomyitseva M.N., Gasanov M.Z., Batyushin M.M.

Rostov State Medical University of the Ministry of Healthcare of Russia, Rostov-on-Don
Abstract. The aim: to study the features of vascular blood flow, cardiohemodynamics and cardiovascular remodeling in patients with chronic kidney disease (CKD) stages 3A–5D, depending on the clinical parameters and the severity of CKD, as well as the identification of the relationship between the level of interleukin-6 (IL-6) in the blood serum with the discussed parameters.
Material and methods. The study included 80 patients (34 men and 46 women; average age 58,9±13,1 years) with CKD stages 3A–5D. The cohort of patients included in the study was divided into two groups: the first (pre-dialysis) group included 40 patients with CKD stages 3A–5, the second (dialysis) group included 40 patients with CKD 5D stages receiving treatment with programmed hemodialysis.
Results. In the general cohort of patients, the level of IL-6 was higher than normal values in 85% of cases (in group 1 – in 92,5% of patients, in group 2 – in 77,5% of patients). The increased level of IL-6 in the pre-dialysis group was more common and amounted to 13,1±0,9 vs 24,5±3,8 pg/ml in the 2nd group. The prevalence of sarcopenia in the 1st group was 12,5%, and in the 2nd group – 42,5%. It was found that renal blood flow in all vascular zones, from the orifices of the renal arteries to the interlobular zones, was significantly reduced in group 2 compared with group 1. At the same time, an increase in IL-6 was associated with an increase in blood flow velocity in interlobular arteries and with an increase in the thickness of the common carotid artery intima-media complex.
Conclusion. IL-6 makes a significant contribution to the progression of vascular remodeling, as well as the development of sarcopenia in patients with CKD stages 3A–5D.

Literature



  1. Батюшин М.М. Хроническая болезнь почек: современное состояние проблемы. Рациональная фармакотерапия в кардиологии. 2020; 6: 938–947. [Batyushin M.M. Chronic kidney disease: current state of the problem. Ratsional’naya farmakoterapiya v kardiologii = Rational Pharmacotherapy in Cardiology. 2020; 6: 938–947 (In Russ.)]. doi: https://dx.doi.org/10.20996/1819-6446-2020-11-06.

  2. Li P.K., Garcia-Garcia G., Lui S.F. et al.; for the World Kidney Day Steering Committee. Kidney health for everyone everywhere – from prevention to detection and equitable access to care. Kidney Int. 2020; 97(2): 226–32. doi: 10.1016/j.kint.2019.12.002.

  3. Foreman K.J., Marquez N., Dolgert A. et al. Forecasting life expectancy, years of life lost, and all-cause and cause-specific mortality for 250 causes of death: reference and alternative scenarios for 2016–40 for 195 countries and territories. Lancet. 2018; 392(10159): 2052–90. doi: 10.1016/S0140-6736(18)31694-5.

  4. Ronco C., Bellasi A., Di Lullo L. Cardiorenal syndrome: An overview. Adv Chronic Kidney Dis. 2018; 25(5): 382–90. doi: 10.1053/j.ackd.2018.08.004.

  5. Левицкая Е.С., Батюшин М.М., Пасечник Д.Г., Асрумян Э.Г. Ремоделирование почечных артерий – инициатор и мишень кардиоренального континуума. Кардиоваскулярная терапия и профилактика. 2015; 1: 90–96. [Levitskaya T.S., Batyushin M.M., Pasechnik D.G., Asrumian E.G. Renal arteries remodelling – the initiator and target of cardiorenal continuum. Kardiovaskulyarnaya terapiya i profilaktika = Cardiovascular Therapy and Prevention. 2015; 1: 90–96 (In Russ.)]. doi: http://dx.doi.org/10.15829/1728-8800-2015-1-90-96.

  6. Major R.W., Cheng M.R.I., Grant R.A. et al. Cardiovascular disease risk factors in chronic kidney disease: A systematic review and meta-analysis. PLoS One. 2018; 13(3): e0192895. doi: 10.1371/journal.pone.0192895.

  7. Roumeliotis S., Mallamaci F., Zoccali C. Endothelial dysfunction in chronic kidney disease, from biology to clinical outcomes: A 2020 update. J Clin Med. 2020; 9(8): 2359. doi: 10.3390/jcm9082359.

  8. Муркамилов И.Т., Айтбаев К.А., Фомин В.В. с соавт. Провоспалительные цитокины у больных с хронической болезнью почек: в фокусе интерлейкин-6. Архивъ внутренней медицины. 2019; 6: 428–433. [Murkamilov I.T., Aitbaev K.A., Fomin V.V. et al. Pro-inflammatory cytokines in patients with chronic kidney disease: interleukin-6 in focus. Arkhiv vnutrenney meditsiny = Archive of Internal Medicine. 2019; 6: 428–433 (In Russ.)]. doi: https://doi.org/10.20514/2226-6704-2019-9-6-428-433.

  9. Muzasti R.A., Hariman H., Daulay E.R. Interleukin 6 concentration elevation as a risk of carotid intima-media thickness in chronic kidney disease patients with dialysis. Med Glas (Zenica). 2020; 17(2): 346–51. doi: 10.17392/1172-20.

  10. Гасанов М.З. Саркопения у пациентов с хронической болезнью почек: распространенность, особенности патогенеза и клиническое значение. Нефрология. 2021; 1: 47–58. [Gasanov M.Z. Sarcopenia in patients with chronic kidney disease: prevalence, pathogenesis and clinical significance. Nefrologiya = Nephrology. 2021; 1: 47–58 (In Russ.)]. doi: https://doi.org/10.36485/1561-6274-2021-25-1-47-58.

  11. Gupta J., Mitra N., Kanetsky P.A. et al. Association between albuminuria, kidney function, and inflammatory biomarker profile. Clin J Am Soc Nephrol. 2012; 7(12): 1938–46. doi: 10.2215/CJN.03500412.

  12. Su H., Lei C.T., Zhang C. Interleukin-6 signaling pathway and its role in kidney disease: An update. Front Immunol. 2017; 8: 405. doi: 10.3389/fimmu.2017.00405.

  13. Chen W., Yuan H., Cao W. et al. Blocking interleukin-6 trans-signaling protects against renal fibrosis by suppressing STAT3 activation. Theranostics. 2019; 9(14): 3980–91. doi: 10.7150/thno.32352.

  14. Шутов А.М., Ефремова Е.В., Мензоров М.В. с соавт. Современная концепция – почечный континуум (острое повреждение почек, острая болезнь почек, хроническая болезнь почек). Архивъ внутренней медицины. 2021; 2: 94–97. [Shutov A.M., Efremova E.V., Menzorov M.V. et al. Modern concept – renal continuum (acute kidney injury, acute kidney disease, chronic kidney disease). Arkhiv vnutrenney meditsiny = Archive of Internal Medicine. 2021; 2: 94–97 (In Russ.)]. doi: https://doi.org/10.20514/2226-6704-2021-11-2-94-97.

  15. Durlacher-Betzer K., Hassan A., Levi R. et al. Interleukin-6 contributes to the increase in fibroblast growth factor 23 expression in acute and chronic kidney disease. Kidney Int. 2018; 94(2): 315–25. doi: 10.1016/j.kint.2018.02.026.


About the Autors


Marina N. Kolomyitseva, postgraduate of the Department of internal diseases No. 2 of Rostov State Medical University of the Ministry of Healthcare of Russia. Address: 344022, Rostov-on-Don, 29 Nakhichevansky Lane. Tel.: +7 (928) 122-61-18. E-mail: marina_matlaeva@mail.ru. ORCID: 0000-0001-6905-6115
Mitkhat Z. Gasanov, PhD, associate professor of the Department of internal diseases No.1 of Rostov State Medical University of the Ministry of Healthcare of Russia. Address: 344022, Rostov-on-Don, 29 Ln, Nakhichevansky. Tel.: +7 (988) 947-37-50. E-mail: mitkhat@mail.ru. ORCID: 0000-0001-5856-0404
Mikhail M. Batyushin, MD, professor, professor of the Department of internal diseases No.2, head of the nephrology Department, the Clinic of Rostov State Medical University of the Ministry of Healthcare of Russia. Address: 344022, Rostov-on-Don, 29 Ln, Nakhichevansky. Tel.: +7 (918) 501-88-01. E-mail: batjushin-m@rambler.ru. ORCID: 0000-0002-2733-4524


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