Gender features of cardiorenal relationships and cytokine status in patients with chronic kidney disease


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Objective. Evaluation of cardiovascular disorders and cytokine status, and their relationship with the glomerular filtration rate in men and women at the predialysis stage of chronic kidney disease (CKD). Material and methods. 170 patients aged 19 to 86 years who had CKD with high and very high (additional) cardiovascular risk were examined. The mean age of the examined patients was 56.2±13.9 years. CKD was diagnosed in accordance with the recommendations of the Russian Scientific Society of Nephrology. The serium interleukin-6 (IL-6), iL-10 levels were evaluated. Glomerular filtration rate (GFR) was calculated by the method of F.J. Hoek et al., proposed in 2003 (80.35/CystatinS-4.32=GFR). All patients underwent ultrasound examination of the heart and blood vessels, and central arterial pressure was measured. The patients were randomized into two age-, anthropometric- and hemodynamic parameter-matched groups: 1st (n=77) female, and 2nd (n=93) male. Results. A decrease in GFR less than 60 ml/min/1.73 m2 was detected in 49.4% of the examined patients. In the male group, C4-stage CKD was significantly more frequently recorded. The diameter of the left ventricular outflow tract (3.31±0.35 versus 3.11±0.40 cm; p<0.05), the carotid intima-media thickness (carotid IMT) (1.12 against 0.97 mm; p<0.05), left atrial size (3.98±0.57 versus 3.75±0.59 cm; p<0.05), left ventricle (LV) enddiastolic diameter (5.24±0, 66 vs 4.97±0.43 cm; p<0.05), the interventricular septum thickness (0.983±0.179 vs 0.925±0.180 cm; P<0.05), and LV mass (200.51±70.50 g versus 171.18±57.87 g; p <0.05) were significantly higher, and the LV ejection fraction (52.47±12.36 versus 58.28±5.79%; p<0.05), on the contrary, significantly lower in male group compared with female group. Concentric hypertrophy was significantly more common in men compared with women [16 (48.5%) versus 10 (33.3%); p<0.05], as well as concentric LV remodeling [12 (12.9%) versus 4 (5.1%); p<0.05]. At the same time, the number of patients with eccentric LV hypertrophy was significantly higher in women than in men [20 (66.7%) versus 17 (51.5%); p<0.05]. The values of the median and interquartile range of IL-10 [6,122 (2,381-7,204) versus 4,167 (1,761-7,500) pg/ml; p<0.05], the blood cystatin C and creatinine levels were significantly higher, and the GFR was lower in men compared with women. In men, a close relationship between the GFR and the central arterial pressure (r=-0.364; p=0.001) and the carotid IMT (r=-0.342; p=0.001) was also observed. At the same time, significant correlation between GFR and the serum IL-10 level was noted in the female group (r=-0.243; p=0.023).

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Sobre autores

I. Murkamilov

Kyrgyz State Medical Academy n.a. I.K. Akhunbaev; Kyrgyz-Russian Slavic University n.a. the First President of the Russian Federation B.N. Yeltsin

Email: murkamilov.i@mail.ru
PhD in Medical Sciences, Nephrologist, Deputy Associate Professor at the Department of Faculty Therapy

K. Aitbaev

Scientific Research Institute of Molecular Biology and Medicine

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

V. Fomin

FSBEI he "I.M. Sechenov First Moscow State Medical University''

Doctor of Medical Sciences, Professor, Corresponding Member of the Russian Academy of Sciences, Vice-Rector for Clinical Work and Postgraduate Professional Education, Director of the V.N. Vinogradov Faculty Therapy Clinic, Head of the Faculty Therapy Department № 1

Bibliografia

  1. Naghavi M, Abajobir A.A., Abbafati C., et al. Global, regional, and national age-sex specific mortality for 264 causes of death, 1980-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet. 2017;390:10100:1151-210. Doi:https://doi.org/10.1016/S0140-6736(17)32152-9.
  2. Thomas B., Matsushita K., Abate K.H., et al. Global cardiovascular and renal outcomes of reduced GFR. J. Am. Soc. Nephrol. 2017;28:7:2167-2179. Doi: https://doi.org/10.1681/ASN.2016050562.
  3. Quiroga B., Verdalles U, Reque J., et al. Cardiovascular events and mortality in chronic kidney disease (stages I-IV). Nefrologia (English Edition). 2013;33:4:539-545. doi: 10.3265/Nefrologia.pre2013.Dec.12385.
  4. Alani H., Tamimi A., Tamimi N. Cardiovascular co-morbidity in chronic kidney disease: Current knowledge and future research needs. World J. Nephrol. 2014;3:4:156. doi: 10.5527/wjn.v3.i4.156.
  5. Cozzolino M., Mangano M., Stucchi A., et al. Cardiovascular disease in dialysis patients. Nephrol. Dial. Transplant. 2018;33(3):28-34. doi: 10.1093/ndt/gfy174.
  6. Моисеев В.С., Мухин Н.А., Смирнов А.В. и др. Сердечно-сосудистый риск и хроническая болезнь почек: стратегии кардио-нефропротекции. Рос. кардиологический журнал. 2014;(8):7-37. Doi:https:// doi.org/10.15829/1560-4071-2014-8-7-37. [Moiseev V.C., Mukhin N.A., Smirnov A.K, et al. Cardiovascular risk and chronic kidney disease: cardio-nephroprotection strategies. Rus. J. Cardiol. 2014;(8):7-37. Doi: https://doi.org/10.15829/1560-4071-2014-8-7-37. (In Russ.)].
  7. HoekF.J., Kemperman F.A., KredietR.T. A comparison between cystatin C, plasma creatinine and the Cockcroft and Gault formula for the estimation of glomerular fi ltration rate. Nephrol. Dial. Transplant. 2003;18(10):2024-31. Doi:10.1093/ ndt/gfg349.
  8. Lang R.M., Lang R.M., Bierig M., et al. Recommendations for chamber quantification. Eur. J. Echocardiography. 2006;7:2:79-108. Doi:https://doi. org/10.1016/j.euje.2005.12.014.
  9. Lang R.M., Lang R.M., Badano L.P., et al. Recommendationsfor cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur. Heart J. Cardiovasc. Imaging. 2015;16:3:233-271. Doi:https://doi. org/10.1093/ehjci/jev014.
  10. Devereux R.B., Alonso D.R., Lutas E.M., et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am. J. Cardiol. 1986;57:6:450-8. Doi:https://doi.org/10.1016/0002-9149(86)90771-X
  11. Williams B., Mancia G., Spiering W., et al. 2018 ESC/ESH Guidelines for the management of arterial hypertension. Eur. Heart J. 2018;39:33:3021-104. Doi:https://doi.org/10.1093/eurheartj/ehy339.
  12. Mancia G., Fagard R., Narkiewicz K., et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Blood Pressure. 2013;22:4:193-278. Doi:https://doi. org/10.3109/08037051.2013.812549
  13. Мухин Н.А., Фомин В.В., Лебедева М.В. Гиперурикемия как компонент кардиоренального синдрома. Тер. архив. 2011;83(6):5-13.
  14. Кобалава Ж.Д., Виллевальде С.В., Ефремовцева М.А., Моисеев В.С. Кардиоренальные взаимоотношения: современные представления. Кардиоваскулярная терапия и профилактика. 2010;9(4):4-11.
  15. Moulin B. Cardiorenal syndromes: definition and classification. Rev. Prat. 2016;66(6):608-10. PMID: 27538311.
  16. Резник Е.В., Никитин И.Г. Кардиоренальный синдром у больных с сердечной недостаточностью как этап кардиоренального континуума (часть I): определение, классификация, патогенез, диагностика, эпидемиология (обзор литературы). Архивъ внутренней медицины. 2019;9(1):5-22. Doi:https://doi.org/10.20514/2226-6704-2019-9-1-5-22 Doi:https://doi. org/10.20514/2226-6704-2019-9-1-5-22
  17. Takahama H., Kitakaze M. Pathophysiology of cardiorenal syndrome in patients with heart failure: potential therapeutic targets. Am. J. Physiol. Heart Circul. Physiol. 2017;313(4):715-21. Doi:https://doi.org/10.1152/qjpheart.00215.2017
  18. Di Lullo L., Bellasi A., Barbera V., et al. Pathophysiology of the cardio-renal syndromes types 1-5: An uptodate. Ind. Heart J. 2017;69:2:255-265. Doi:https:// doi.org/10.1016/j.ihj.2017.01.005
  19. Kingma J., Simard D., Rouleau J., et al. The Physiopathology of Cardiorenal Syndrome: A Review of the Potential Contributions of Inflammation. J. Cardiovasc. Devel. Dis. 2017;4(4):21-23. Doi:https://doi.org/10.3390/jcdd4040021.
  20. Yan L., Bowman M.A. Chronic sustained inflammation links to left ventricular hypertrophy and aortic valve sclerosis: a new link between S100/RAGE and FGF23. Inflamm. Cell. Signal. 2014;1(5):e279. doi: 10.14800/ics.279.
  21. Li Z.C., Yu H.Y., Wang X.X., et al. Olmesartan medoxomil reverses left ventricle hypertrophy and reduces inflammatory cytokine IL-6 in the renovascular hypertensive rats. Eur. Rev. Med. Pharmacol. Sci. 2013;17(24):3318-3322.
  22. Yin J.C., Yin J.C., Platt M.J., et al. Cellular interplay via cytokine hierarchy causes pathological cardiac hypertrophy in RAF1-mutant Noonan syndrome. Nat. Communicat. 2017;8:15518:1-1511. doi: 10.1038/ncomms15518.
  23. Zafar U., Khaliq S., Ahmad H.U., Lone K.P. Serum profile of cytokines and their genetic variants in metabolic syndrome and healthy subjects: a comparative study. Biosci. Rep. 2019;39(2)BSR20181202. doi: 10.1042/BSR20181202.
  24. Trifunovic J., Miller L., Debeljak Z., & Horvat V. Pathologic patterns of interleukin 10 expression-a review. Biochem. Med. 2015;25:1:36-48. Doi:https:// doi.org/10.11613/BM.2015.004.
  25. Конради А.О. Лечение артериальной гипертензии в особых группах больных. Типертрофия левого желудочка. Артериальная гипертензия. 2005;11(2):105- 110.
  26. Konradi AO. Treatment of hypertension in special groups of patients. Left ventricular hypertrophy. Arterial. Hypertension. 2005;11(2):105-110. (In Russ.)].
  27. Вебер В.Р., Рубанова М.П., Жмайлова С.В. и др. Ремоделирование левого и правого желудочка сердца при артериальной гипертензии и возможности медикаментозной коррекции. РМЖ. 2009;2:5-9.
  28. Кобалава Ж.Д., Котовская Ю.В., Сафарова А.Ф. и др. Эхокардиографическая оценка фиброза миокарда у молодых мужчин с артериальной гипертонией и разными типами ремоделирования левого желудочка. Кардиология. 2011;51(2):34-9.
  29. Душина А.Т., Лопина Е.А., Либис Р.А. Особенности хронической сердечной недостаточности в зависимости от фракции выброса левого желудочка. Рос. кардиол. журнал. 2019;(2):7-11. Doi:https://doi.org/10.15829/1560-4071-2019-2-7-11. Doi:https://doi.org/10.15829/1560-4071-2019-2- 7-11.
  30. Муркамилов И.Т., Айтбаев К.А., Фомин В.В. Половые особенности сердечнососудистых осложнений у больных хроническим гломерулонефритом на преддиализной стадии заболевания. Тер. архив (архив до 2018 г.). 2017;89:6:56-61. doi: 10.17116/terarkh201789656-61. doi: 10.17116/terarkh201789656-61.
  31. Муркамилов И.Т., Сабиров И.С., Айтбаев К.А. и др. Почечная дисфункция и показатели артериальной жесткости у лиц пожилого и старческого возраста. Успехи геронтологии. 2018;31:4:549-555.
  32. Dijk J.M., van der Graat G., Bots M.L., et al. Carotid intima-media thickness and the risk of new vascular events in patients with manifest atherosclerotic disease: the SMART study. Eur. Heart J. 2006; 24:1971-1978. Doi:https://doi.org/10.1093/ eurheartj/ehl136.
  33. Bots M.L., Hoes A.W., Koudstaal P.J., et al. Common carotid intima-media thickness and risk of stroke and myocardial infarction. The Rotterdam Study. Circulation.1997;96:1432-1437.
  34. Doi:https://doi.org/10.1161/01.CIR.96.5.1432
  35. Kablak A., Kablak A., Przewlocki T., et al. Relationship between carotid intima-media thickness, cytokines, atherosclerosis extent and a two-year cardiovascular risk in patients with arteriosclerosis. Kardiol. Polska. (Polish Heart Journal). 2011;69:10:1024-1031.
  36. Momeni A., Taheri A., Mansuri M., et al. Association of carotid intima-media thickness with exercise tolerance test in type 2 diabetic patients. Int. J. Cardiol. Heart. Vasc. 2018;21:74-77. doi: 10.1016/j.ijcha.2018.10.002.

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