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


Citar

Texto integral

Acesso aberto Acesso aberto
Acesso é fechado Acesso está concedido
Acesso é fechado Acesso é pago ou somente para assinantes

Resumo

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.

Texto integral

Acesso é fechado

Sobre autores

Marina Kolomyitseva

Rostov State Medical University of the Ministry of Healthcare of Russia

Mitkhat Gasanov

Rostov State Medical University of the Ministry of Healthcare of Russia

Mikhail Batyushin

Rostov State Medical University of the Ministry of Healthcare of Russia

Bibliografia

  1. Батюшин М.М. Хроническая болезнь почек: современное состояние проблемы. Рациональная фармакотерапия в кардиологии. 2020; 6: 938-947. 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. 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. 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. 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. 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.

Arquivos suplementares

Arquivos suplementares
Ação
1. JATS XML

Declaração de direitos autorais © Bionika Media, 2021

Este site utiliza cookies

Ao continuar usando nosso site, você concorda com o procedimento de cookies que mantêm o site funcionando normalmente.

Informação sobre cookies