Сывороточный тропонин-I как маркер кардиотоксического действия фактора роста фибробластов-23 (FGF-23) у больных хронической болезнью почек - Журнал Терапевтический архив №6 Вопросы нефрологии 2019
Сывороточный тропонин-I как маркер кардиотоксического действия фактора роста фибробластов-23 (FGF-23) у больных хронической болезнью почек
Таранова М.В., Милованова Л.Ю., Козловская (Лысенко) Л.В. и др. Сывороточный тропонин-I как маркер кардиотоксического действия фактора роста фибробластов-23 (FGF-23) у больных хронической болезнью почек. Терапевтический архив. 2019; 91 (6): 85–92. DOI: 10.26442/00403660.2019.06.000253
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Аннотация
Установлено, что повышение уровня фактора роста фибробластов (FGF-23) в сыворотке крови больных хронической болезнью почек (ХБП) вносит существенный вклад в ремоделирование сердца и сосудов. Точные механизмы влияния избыточного уровня FGF-23 на миокард в настоящее время активно изучаются. В то же время полагают, что эффекты FGF-23 на сердце могут быть обусловлены нарастающим дефицитом белка Klotho по мере прогрессирования ХБП. Параллельно этим изменениям ряд работ указывает на персистирование умеренно повышенных уровней тропонинов в сыворотке крови больных ХБП даже при отсутствии у них клинических проявлений кардиоваскулярных заболеваний (КВЗ).
Цель исследования. Установить/опровергнуть наличие причинно-следственной связи между повышенным уровнем FGF-23, сниженным уровнем Klotho и повышенным уровнем тропонина-I (Tr-I) как наиболее специфического тропонина при ХБП.
Материалы и методы. В исследование включено 130 пациентов с ХБП стадий 1–5D без клинически выраженных симптомов КВЗ (ИБС II–IV ФК, ХСН II–IV класса по NYHA, миокардит, перикардит, аритмии), а также тяжелой артериальной гипертензии (АГ; артериальное давление >160/90 мм рт. ст.) по данным лабораторных и инструментальных методов обследования. У отобранной группы больных изучены: сывороточные уровни FGF-23 (Human FGF-23 ELISA kit with antibodies to native FGF-23 molecule), Klotho (Human soluble Klotho with antiKlotho monoclonal antibodies), Tr-I (high-sensitive assay), а также данные инструментальных методов обследования: электрокардиографии, эхокардиографии [индекс массы миокарда левого желудочка (ИММЛЖ), степень кальцификации структур сердца (СКС) – с помощью полуколичественной балльной шкалы], сфигмографии [индексы аугментации (жесткости) сосудов, скорость пульсовой волны (СПВ), центральное (аортальное) давление (ЦАД), кровоснабжение субэндокарда (КСЭ) – с помощью прибора Shygmacor (Австралия)].
Результаты и обсуждение. Изменение сывороточных уровней FGF-23, Klotho и Tr-I зависит от стадии ХБП. Выявлены следующие корреляции: FGF-23 – с Tr-I (r=0,601; p<0,01), ИММЛЖ (r=0,628; p<0,01), эксцентрическим типом ремоделирования миокарда (РМ; r=0,509; p<0,01), диастолической дисфункцией левого желудочка сердца (ДД; r=0,458; p<0,05), КСЭ (r=-0,499; p<0,05), СПВ (r=0,514; p<0,01). У пациентов, имеющих повышенный уровень ЦАД (>120/80 мм рт. ст.), и у пациентов с нормальным уровнем ЦАД (90–120/60-79 мм рт. ст.) средние уровни FGF-23 в сыворотке крови статистически значимо не различались (р=0,071). В то же время сывороточный уровень Tr-I коррелировал с ИММЛЖ (r=0,567; p<0,05), эксцентрическим типом РМ (r=0,461; p<0,01), ДД (r=0,473; p<0,05), длительностью ХБП (r=0,512; p<0,05), КСЭ (r=-0,497; p<0,01), ЦАД (r=0,534; p<0,01). Между сывороточными уровнями Klotho и Tr-I (r=-0,537; p<0,01), СПВ (r=-0,647; p<0,01), СКС (r=-0,612; p<0,01), ИММЛЖ (r=-0,539; p<0,01), концентрическим типом РМ (r=-0,528; p<0,01) мы выявили отрицательную взаимосвязь. По данным многофакторного анализа (логистическая регрессия), отмечено наличие достоверной ассоциации только между повышенным уровнем FGF-23 и повышенным уровнем Tr-I у больных ХБП, включенных в исследование.
Заключение. Умеренно повышенный уровень Tr-I в сыворотке крови у больных ХБП без клинических признаков КВЗ и тяжелой АГ ассоциирован, главным образом, с повышенным сывороточным уровнем FGF-23.
Ключевые слова: хроническая болезнь почек, FGF-23, Klotho, тропонин-I.
Materials and methods. The study included 130 CKD stages 1–5D patients without clinically pronounced symptoms of СVD (Coronary artery disease, CCS class 2–4, Chronic heart failure, NYHA 24, myocarditis, pericarditis, arrhythmias), as well as the severe arterial hypertension (BP >160/90 mm Hg), according to the laboratory and instrumental methods of examination. The selected group of patients was studied: serum levels of FGF-23 (Human FGF-23 ELISA kit), Klotho (Human soluble Klotho with antiklotho monoclonal antibodies), troponin-I (high-sensitive assay), and also data from instrumental examination methods: electrocardiography (ECG), echocardiography (left ventricular myocardial mass index (LVMI), cardiac (valvular) calcification score (CCS) using a semi-quantitative point scale), sphygmagraphy (augmentation (stiffness) indices of vessels (AI), pulse wave velocity (PWV), central (aortic) blood pressure (CBP), blood supply of subendocardium (BSE) – using "Shygmacor" device (Australia)).
Results and discussion. The changes in serum levels of FGF-23, Klotho and troponin-I (Tr-I) depended on the stage of CKD. The following correlations were identified: FGF-23 and: Tr-I (r=0.601; p<0.01), LVMI (r=0.528; p<0.05), eccentric type of myocardial remodeling (MR; r=0.509; p<0.01), left ventricular diastolic dysfunction (DD; r=0.458; p<0.05), BSE (r=-0.499; p<0.05), PWV (r=0.514; p<0.01). Importantly, mean serum FGF-23 levels were not statistically significantly different in patients with elevated levels of CBP (CBP >120/80 mm Hg), and in patients with normal levels of CBP (CBP=90–120 / 60–79 mm Hg; p=0.071). At the same time, the serum level of Tr-I correlated with LVMI (r=0.567; p<0.05), eccentric type MR (r=0.461; p<0.01), DD (r=0.473; p<0.05), duration of CKD (r=0.512; p<0.05), BSE (r=-0.497; p<0.01), CBP (r=0.534; p<0.01). We revealed negative correlations between serum levels of Klotho and followed parameters: Tr-I (r=-0.537; p<0.01), PWV (r=-0.647; p<0.01), CCS (r=-0.612; p<0.01), LVMI (r=-0.539; p<0.01), concentric type MR (r=-0.528; p<0.01). According to multivariate analysis (logistic regression), a significant association there was only between elevated FGF-23 and elevated Tr-I in CKD patients without CVD.
Conclusion. Detectable Tr-I serum levels without clinical signs of CVD and severe AH in patients with CKD is associated mainly with elevated serum levels of FGF-23.
Key words: chronic kidney disease, FGF-23, Klotho, troponin-I (Tr-I).
Цель исследования. Установить/опровергнуть наличие причинно-следственной связи между повышенным уровнем FGF-23, сниженным уровнем Klotho и повышенным уровнем тропонина-I (Tr-I) как наиболее специфического тропонина при ХБП.
Материалы и методы. В исследование включено 130 пациентов с ХБП стадий 1–5D без клинически выраженных симптомов КВЗ (ИБС II–IV ФК, ХСН II–IV класса по NYHA, миокардит, перикардит, аритмии), а также тяжелой артериальной гипертензии (АГ; артериальное давление >160/90 мм рт. ст.) по данным лабораторных и инструментальных методов обследования. У отобранной группы больных изучены: сывороточные уровни FGF-23 (Human FGF-23 ELISA kit with antibodies to native FGF-23 molecule), Klotho (Human soluble Klotho with antiKlotho monoclonal antibodies), Tr-I (high-sensitive assay), а также данные инструментальных методов обследования: электрокардиографии, эхокардиографии [индекс массы миокарда левого желудочка (ИММЛЖ), степень кальцификации структур сердца (СКС) – с помощью полуколичественной балльной шкалы], сфигмографии [индексы аугментации (жесткости) сосудов, скорость пульсовой волны (СПВ), центральное (аортальное) давление (ЦАД), кровоснабжение субэндокарда (КСЭ) – с помощью прибора Shygmacor (Австралия)].
Результаты и обсуждение. Изменение сывороточных уровней FGF-23, Klotho и Tr-I зависит от стадии ХБП. Выявлены следующие корреляции: FGF-23 – с Tr-I (r=0,601; p<0,01), ИММЛЖ (r=0,628; p<0,01), эксцентрическим типом ремоделирования миокарда (РМ; r=0,509; p<0,01), диастолической дисфункцией левого желудочка сердца (ДД; r=0,458; p<0,05), КСЭ (r=-0,499; p<0,05), СПВ (r=0,514; p<0,01). У пациентов, имеющих повышенный уровень ЦАД (>120/80 мм рт. ст.), и у пациентов с нормальным уровнем ЦАД (90–120/60-79 мм рт. ст.) средние уровни FGF-23 в сыворотке крови статистически значимо не различались (р=0,071). В то же время сывороточный уровень Tr-I коррелировал с ИММЛЖ (r=0,567; p<0,05), эксцентрическим типом РМ (r=0,461; p<0,01), ДД (r=0,473; p<0,05), длительностью ХБП (r=0,512; p<0,05), КСЭ (r=-0,497; p<0,01), ЦАД (r=0,534; p<0,01). Между сывороточными уровнями Klotho и Tr-I (r=-0,537; p<0,01), СПВ (r=-0,647; p<0,01), СКС (r=-0,612; p<0,01), ИММЛЖ (r=-0,539; p<0,01), концентрическим типом РМ (r=-0,528; p<0,01) мы выявили отрицательную взаимосвязь. По данным многофакторного анализа (логистическая регрессия), отмечено наличие достоверной ассоциации только между повышенным уровнем FGF-23 и повышенным уровнем Tr-I у больных ХБП, включенных в исследование.
Заключение. Умеренно повышенный уровень Tr-I в сыворотке крови у больных ХБП без клинических признаков КВЗ и тяжелой АГ ассоциирован, главным образом, с повышенным сывороточным уровнем FGF-23.
Ключевые слова: хроническая болезнь почек, FGF-23, Klotho, тропонин-I.
________________________________________________
Materials and methods. The study included 130 CKD stages 1–5D patients without clinically pronounced symptoms of СVD (Coronary artery disease, CCS class 2–4, Chronic heart failure, NYHA 24, myocarditis, pericarditis, arrhythmias), as well as the severe arterial hypertension (BP >160/90 mm Hg), according to the laboratory and instrumental methods of examination. The selected group of patients was studied: serum levels of FGF-23 (Human FGF-23 ELISA kit), Klotho (Human soluble Klotho with antiklotho monoclonal antibodies), troponin-I (high-sensitive assay), and also data from instrumental examination methods: electrocardiography (ECG), echocardiography (left ventricular myocardial mass index (LVMI), cardiac (valvular) calcification score (CCS) using a semi-quantitative point scale), sphygmagraphy (augmentation (stiffness) indices of vessels (AI), pulse wave velocity (PWV), central (aortic) blood pressure (CBP), blood supply of subendocardium (BSE) – using "Shygmacor" device (Australia)).
Results and discussion. The changes in serum levels of FGF-23, Klotho and troponin-I (Tr-I) depended on the stage of CKD. The following correlations were identified: FGF-23 and: Tr-I (r=0.601; p<0.01), LVMI (r=0.528; p<0.05), eccentric type of myocardial remodeling (MR; r=0.509; p<0.01), left ventricular diastolic dysfunction (DD; r=0.458; p<0.05), BSE (r=-0.499; p<0.05), PWV (r=0.514; p<0.01). Importantly, mean serum FGF-23 levels were not statistically significantly different in patients with elevated levels of CBP (CBP >120/80 mm Hg), and in patients with normal levels of CBP (CBP=90–120 / 60–79 mm Hg; p=0.071). At the same time, the serum level of Tr-I correlated with LVMI (r=0.567; p<0.05), eccentric type MR (r=0.461; p<0.01), DD (r=0.473; p<0.05), duration of CKD (r=0.512; p<0.05), BSE (r=-0.497; p<0.01), CBP (r=0.534; p<0.01). We revealed negative correlations between serum levels of Klotho and followed parameters: Tr-I (r=-0.537; p<0.01), PWV (r=-0.647; p<0.01), CCS (r=-0.612; p<0.01), LVMI (r=-0.539; p<0.01), concentric type MR (r=-0.528; p<0.01). According to multivariate analysis (logistic regression), a significant association there was only between elevated FGF-23 and elevated Tr-I in CKD patients without CVD.
Conclusion. Detectable Tr-I serum levels without clinical signs of CVD and severe AH in patients with CKD is associated mainly with elevated serum levels of FGF-23.
Key words: chronic kidney disease, FGF-23, Klotho, troponin-I (Tr-I).
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2. Levin A, Stevens PE, Bilous RW, et al. Kidney disease: Improving global outcomes (KDIGO) CKD work group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. Suppl. 2013;3:1-150. doi: 10.1038/kisup.2012.73
3. Hu MC, Shiizaki K, Kuro-o M, et al. Fibroblast Growth Factor 23 and Klotho: Physiology and Pathophysiology of an Endocrine Network of Mineral Metabolism. Annu Rev Physiol. 2013;75:503-33. doi: 10.1146/annurev-physiol-030212-183727
4. Scialla JJ, Xie H, Rahman M, et al. Fibroblast Growth Factor-23 and Cardiovascular Events in CKD, the Chronic Renal Insufficiency Cohort (CRIC) Study Investigators. J Am Soc Nephrol. 2014;25(2):349-60. doi: 10.1681/ASN.2013050465
5. Milovanova L, Fomin VV, Lysenko (Kozlovskaya) LV, et al. Disorders in the System of Mineral and Bone Metabolism Regulators – FGF-23, Klotho and Sclerostin – in Chronic Kidney Disease: Clinical Significance and Possibilities for Correction. Chapter in the book “Chronic Kidney Disease”. INTECH. 2017. ISBN 978-953-51-5463-1. http// dx.doi.org/10.5772/66239
6. Kardami E. Fibroblast growth factor 23 isoforms and cardiac hypertrophy. Cardiovasc Res. 2004;63(3):458-66. doi: 0.1016/j.cardiores.2004.04.024
7. Hu MC, Kuro-o M, Moe OW. Klotho and Chronic Kidney Disease. Contrib Nephrol. 2013;180:47-63. doi: 10.1159/000346778
8. Kuro-o M. Klotho in chronic kidney disease – What's new? Nephrol Dialysis Transplant. 2009;24(6):1705-8. doi: 10.1093/ndt/gfp069
9. Hu MC, Shi M, Zhang J, et al. Klotho deficiency causes vascular calcification in chronic kidney disease. Am J Soc Nephrol. 2011;22(1):124-36. doi: 10.1681/ASN.2009121311
10. Hu MC, Kuro-o M, Moe OW. Renal and Extra-Renal Actions of Klotho. Semin Nephrol. 2013;33(2):118-29. doi: 10.1016/j.semnephrol.2012.12.013
11. Milovanova LY, Milovanov YS, Kozlovskaya LV. Nephro-cardioprotective role of the circulating forms of the KLOTHO protein in chronic kidney disease. Clin Nephrol. 2013;3:7-10. doi: https://doi.org/10.18454/IRJ.2016.51.074
12. Chen S, Huang H, Wu B, et al. Cardiac Troponin I in Non- Acute Coronary Syndrome Patients with Chronic Kidney Disease. PLoS One. 2013;8(12):12-9. doi: 10.1371/journal.pone.0082752
13. Abbas NA, John RI, Webb MC, et al. Cardiac troponins and renal function in nondialysis patients with chronic kidney disease. Clin Chem. 2005;51(11):2059-66.
14. Cheng H-M, Chuang S-Y, Sung S-H, et al. Derivation and validation of Diagnostic thresholds for Central Blood Pressure Measurements based on Long-Term Cardiovascular Risks. J Amer Coll Cardiol. 2013; 62(19):1780-7. doi: 10.1016/j.jacc.2013.06.029
15. Mancia G, De Backer G, Dominiczak A, et al. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J. 2013;34: 34 (28): 2159–2219. doi: 10.1093/eurheartj/eht151
16. Ermolenko VM, Volgina GV, Dobronravov VA, et al. National recommendations on mineral and bone disorders in chronic kidney disease. Russian Dialysis Society (May 2010). Nephrologia i Dialis. 2011;13(1):33-51 (In Russ)
17. Milyagin V.A., Komissarov V.B. Methods for determining the stiffness of blood vessels. Arterial hypertension. 2010; 16 (2): 134-43]. doi: https://doi.org/10.18705/1607-419X-2010--2-
18. Townsend RR, Wilkinson IB, Schiffrin EL, et al. American Heart Association Council on Hypertension. Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness. A Scientific Statement from the American Heart Association. J Hypertension. 2015;66(3):698-722.
19. Consistent opinion of Russian experts on arterial stiffness assessment in clinical practice (RCO Congress, 2015). Kardiovaskulyarnaya terapiya i profilaktika. 2016;15(2):4-19 (In Russ.) doi: 10.15829/1728-8800-2016-2-4-19
20. McMurray JJ, Uno H, Jarolim P, et al. Predictors of fatal and nonfatal cardiovascular events in patients with type 2 diabetes mellitus, chronic kidney disease, and anemia: an analysis of the Trial to Reduce cardiovascular Events with Aranesp (darbepoetin-alfa) Therapy (TREAT). Am Heart J. 2011;162(4):748-55. doi: 10.1016/j.ahj.2011.07.016
21. Smith K, de Filippi C, Isakov T, et al. Fibroblast Growth Factor 23, High-Sensitivity Cardiac Troponin, and Left Ventricular Hypertrophy in CKD. Am J Kidney Dis. 2013;61(1):67-73. doi: 10.1053/j.ajkd.2012.06.022
22. Faul C, Amaral AP, Oskouei B, et al. FGF23 induces left ventricular hypertrophy. J Clin Invest. 2011;121:4393-408. doi: 10.1172/JCI46122
23. Shinichiro N, Yoshitaka I, Takaharu Y, et al. Renocardiovascular Biomarkers: from the Perspective of Managing Chronic Kidney Disease and Cardiovascular Disease. Front Cardiovasc Med. 2017;4:10. doi: 10.3389/fcvm.2017.00010
24. Scialla JJ, Lau WL, Reilly MP, et al. Fibroblast growth factor 23 is not associated with and does not induce arterial calcification. Kidney Int. 2013;83:1159-68. doi: 10.1038/ki.2013.3
25. Marthi A, Donovan K, Haynes R, et al. Fibroblast Growth Factor-23 and Risks of Cardiovascular and Noncardiovascular Diseases: A Meta-Analysis. JASN. 2018;29(7):2015-27; doi: 10.1681/ASN.2017121334
26. Sze J, Mooney J, Barzi F. Cardiac troponin and its relationship to cardiovascular outcomes in community populations – a systematic review and meta-analysis. Heart Lung Circ. 2016;25:217-28. doi: 10.1016/j.hlc.2015.09.001
27. Jacobs LH, van de Kerkhof J, Mingels AM, et al. Haemodialysis patients longitudinally assessed by highly sensitive cardiac troponin T and commercial cardiac troponin T and cardiac troponin I assays. Ann Clin Biochem. 2009;46:283-90. doi: 10.1258/acb.2009.008197
28. Stacy SR, Suarez-Cuervo C, Berger Z, et al. Role of troponin in patients with chronic kidney disease and suspected acute coronary syndrome: a systematic review. Ann Intern Med. 2014;161:502-12. doi: 10.7326/M14-0746
29. Bansal N, Hyre Anderson A, Yang W, et al. High-sensitivity troponin T and N-terminal pro-B-type natriuretic peptide (NT-proBNP) and risk of incident heart failure in patients with CKD: the chronic renal insufficiency cohort (CRIC) study. J Am Soc Nephrol. 2015;26:946-56. doi: 10.1681/ASN.2014010108
2. Levin A, Stevens PE, Bilous RW, et al. Kidney disease: Improving global outcomes (KDIGO) CKD work group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. Suppl. 2013;3:1-150. doi: 10.1038/kisup.2012.73
3. Hu MC, Shiizaki K, Kuro-o M, et al. Fibroblast Growth Factor 23 and Klotho: Physiology and Pathophysiology of an Endocrine Network of Mineral Metabolism. Annu Rev Physiol. 2013;75:503-33. doi: 10.1146/annurev-physiol-030212-183727
4. Scialla JJ, Xie H, Rahman M, et al. Fibroblast Growth Factor-23 and Cardiovascular Events in CKD, the Chronic Renal Insufficiency Cohort (CRIC) Study Investigators. J Am Soc Nephrol. 2014;25(2):349-60. doi: 10.1681/ASN.2013050465
5. Milovanova L, Fomin VV, Lysenko (Kozlovskaya) LV, et al. Disorders in the System of Mineral and Bone Metabolism Regulators – FGF-23, Klotho and Sclerostin – in Chronic Kidney Disease: Clinical Significance and Possibilities for Correction. Chapter in the book “Chronic Kidney Disease”. INTECH. 2017. ISBN 978-953-51-5463-1. http// dx.doi.org/10.5772/66239
6. Kardami E. Fibroblast growth factor 23 isoforms and cardiac hypertrophy. Cardiovasc Res. 2004;63(3):458-66. doi: 0.1016/j.cardiores.2004.04.024
7. Hu MC, Kuro-o M, Moe OW. Klotho and Chronic Kidney Disease. Contrib Nephrol. 2013;180:47-63. doi: 10.1159/000346778
8. Kuro-o M. Klotho in chronic kidney disease – What's new? Nephrol Dialysis Transplant. 2009;24(6):1705-8. doi: 10.1093/ndt/gfp069
9. Hu MC, Shi M, Zhang J, et al. Klotho deficiency causes vascular calcification in chronic kidney disease. Am J Soc Nephrol. 2011;22(1):124-36. doi: 10.1681/ASN.2009121311
10. Hu MC, Kuro-o M, Moe OW. Renal and Extra-Renal Actions of Klotho. Semin Nephrol. 2013;33(2):118-29. doi: 10.1016/j.semnephrol.2012.12.013
11. Milovanova LY, Milovanov YS, Kozlovskaya LV. Nephro-cardioprotective role of the circulating forms of the KLOTHO protein in chronic kidney disease. Clin Nephrol. 2013;3:7-10. doi: https://doi.org/10.18454/IRJ.2016.51.074
12. Chen S, Huang H, Wu B, et al. Cardiac Troponin I in Non- Acute Coronary Syndrome Patients with Chronic Kidney Disease. PLoS One. 2013;8(12):12-9. doi: 10.1371/journal.pone.0082752
13. Abbas NA, John RI, Webb MC, et al. Cardiac troponins and renal function in nondialysis patients with chronic kidney disease. Clin Chem. 2005;51(11):2059-66.
14. Cheng H-M, Chuang S-Y, Sung S-H, et al. Derivation and validation of Diagnostic thresholds for Central Blood Pressure Measurements based on Long-Term Cardiovascular Risks. J Amer Coll Cardiol. 2013; 62(19):1780-7. doi: 10.1016/j.jacc.2013.06.029
15. Mancia G, De Backer G, Dominiczak A, et al. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J. 2013;34: 34 (28): 2159–2219. doi: 10.1093/eurheartj/eht151
16. Ермоленко В.М., Волгина Г.В., Добронравов В.А. и др. Национальные рекомендации по минеральным и костным нарушениям при хронической болезни почек. Российское диализное общество (май 2010). Нефрология и диализ. 2011;13(1):33-51 [Ermolenko VM, Volgina GV, Dobronravov VA, et al. National recommendations on mineral and bone disorders in chronic kidney disease. Russian Dialysis Society (May 2010). Nephrologia i Dialis. 2011;13(1):33-51 (In Russ)].
17. Милягин В.А., Комиссаров В.Б. Современные методы определения жесткости сосудов. Артериальная гипертензия. 2010;16(2):134-143 [Milyagin V.A., Komissarov V.B. Methods for determining the stiffness of blood vessels. Arterial hypertension. 2010; 16 (2): 134-43]. doi: https://doi.org/10.18705/1607-419X-2010--2-
18. Townsend RR, Wilkinson IB, Schiffrin EL, et al. American Heart Association Council on Hypertension. Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness. A Scientific Statement from the American Heart Association. J Hypertension. 2015;66(3):698-722.
19. Согласованное мнение российских экспертов по оценке артериальной жесткости в клинической практике (конгресс РКО, 2015). Кардиоваскулярная терапия и профилактика. 2016;15(2):4–19. [Consistent opinion of Russian experts on arterial stiffness assessment in clinical practice (RCO Congress, 2015). Kardiovaskulyarnaya terapiya i profilaktika. 2016;15(2):4-19 (In Russ.)]. doi: 10.15829/1728-8800-2016-2-4-19
20. McMurray JJ, Uno H, Jarolim P, et al. Predictors of fatal and nonfatal cardiovascular events in patients with type 2 diabetes mellitus, chronic kidney disease, and anemia: an analysis of the Trial to Reduce cardiovascular Events with Aranesp (darbepoetin-alfa) Therapy (TREAT). Am Heart J. 2011;162(4):748-55. doi: 10.1016/j.ahj.2011.07.016
21. Smith K, de Filippi C, Isakov T, et al. Fibroblast Growth Factor 23, High-Sensitivity Cardiac Troponin, and Left Ventricular Hypertrophy in CKD. Am J Kidney Dis. 2013;61(1):67-73. doi: 10.1053/j.ajkd.2012.06.022
22. Faul C, Amaral AP, Oskouei B, et al. FGF23 induces left ventricular hypertrophy. J Clin Invest. 2011;121:4393-408. doi: 10.1172/JCI46122
23. Shinichiro N, Yoshitaka I, Takaharu Y, et al. Renocardiovascular Biomarkers: from the Perspective of Managing Chronic Kidney Disease and Cardiovascular Disease. Front Cardiovasc Med. 2017;4:10. doi: 10.3389/fcvm.2017.00010
24. Scialla JJ, Lau WL, Reilly MP, et al. Fibroblast growth factor 23 is not associated with and does not induce arterial calcification. Kidney Int. 2013;83:1159-68. doi: 10.1038/ki.2013.3
25. Marthi A, Donovan K, Haynes R, et al. Fibroblast Growth Factor-23 and Risks of Cardiovascular and Noncardiovascular Diseases: A Meta-Analysis. JASN. 2018;29(7):2015-27; doi: 10.1681/ASN.2017121334
26. Sze J, Mooney J, Barzi F. Cardiac troponin and its relationship to cardiovascular outcomes in community populations – a systematic review and meta-analysis. Heart Lung Circ. 2016;25:217-28. doi: 10.1016/j.hlc.2015.09.001
27. Jacobs LH, van de Kerkhof J, Mingels AM, et al. Haemodialysis patients longitudinally assessed by highly sensitive cardiac troponin T and commercial cardiac troponin T and cardiac troponin I assays. Ann Clin Biochem. 2009;46:283-90. doi: 10.1258/acb.2009.008197
28. Stacy SR, Suarez-Cuervo C, Berger Z, et al. Role of troponin in patients with chronic kidney disease and suspected acute coronary syndrome: a systematic review. Ann Intern Med. 2014;161:502-12. doi: 10.7326/M14-0746
29. Bansal N, Hyre Anderson A, Yang W, et al. High-sensitivity troponin T and N-terminal pro-B-type natriuretic peptide (NT-proBNP) and risk of incident heart failure in patients with CKD: the chronic renal insufficiency cohort (CRIC) study. J Am Soc Nephrol. 2015;26:946-56. doi: 10.1681/ASN.2014010108
________________________________________________
2. Levin A, Stevens PE, Bilous RW, et al. Kidney disease: Improving global outcomes (KDIGO) CKD work group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. Suppl. 2013;3:1-150. doi: 10.1038/kisup.2012.73
3. Hu MC, Shiizaki K, Kuro-o M, et al. Fibroblast Growth Factor 23 and Klotho: Physiology and Pathophysiology of an Endocrine Network of Mineral Metabolism. Annu Rev Physiol. 2013;75:503-33. doi: 10.1146/annurev-physiol-030212-183727
4. Scialla JJ, Xie H, Rahman M, et al. Fibroblast Growth Factor-23 and Cardiovascular Events in CKD, the Chronic Renal Insufficiency Cohort (CRIC) Study Investigators. J Am Soc Nephrol. 2014;25(2):349-60. doi: 10.1681/ASN.2013050465
5. Milovanova L, Fomin VV, Lysenko (Kozlovskaya) LV, et al. Disorders in the System of Mineral and Bone Metabolism Regulators – FGF-23, Klotho and Sclerostin – in Chronic Kidney Disease: Clinical Significance and Possibilities for Correction. Chapter in the book “Chronic Kidney Disease”. INTECH. 2017. ISBN 978-953-51-5463-1. http// dx.doi.org/10.5772/66239
6. Kardami E. Fibroblast growth factor 23 isoforms and cardiac hypertrophy. Cardiovasc Res. 2004;63(3):458-66. doi: 0.1016/j.cardiores.2004.04.024
7. Hu MC, Kuro-o M, Moe OW. Klotho and Chronic Kidney Disease. Contrib Nephrol. 2013;180:47-63. doi: 10.1159/000346778
8. Kuro-o M. Klotho in chronic kidney disease – What's new? Nephrol Dialysis Transplant. 2009;24(6):1705-8. doi: 10.1093/ndt/gfp069
9. Hu MC, Shi M, Zhang J, et al. Klotho deficiency causes vascular calcification in chronic kidney disease. Am J Soc Nephrol. 2011;22(1):124-36. doi: 10.1681/ASN.2009121311
10. Hu MC, Kuro-o M, Moe OW. Renal and Extra-Renal Actions of Klotho. Semin Nephrol. 2013;33(2):118-29. doi: 10.1016/j.semnephrol.2012.12.013
11. Milovanova LY, Milovanov YS, Kozlovskaya LV. Nephro-cardioprotective role of the circulating forms of the KLOTHO protein in chronic kidney disease. Clin Nephrol. 2013;3:7-10. doi: https://doi.org/10.18454/IRJ.2016.51.074
12. Chen S, Huang H, Wu B, et al. Cardiac Troponin I in Non- Acute Coronary Syndrome Patients with Chronic Kidney Disease. PLoS One. 2013;8(12):12-9. doi: 10.1371/journal.pone.0082752
13. Abbas NA, John RI, Webb MC, et al. Cardiac troponins and renal function in nondialysis patients with chronic kidney disease. Clin Chem. 2005;51(11):2059-66.
14. Cheng H-M, Chuang S-Y, Sung S-H, et al. Derivation and validation of Diagnostic thresholds for Central Blood Pressure Measurements based on Long-Term Cardiovascular Risks. J Amer Coll Cardiol. 2013; 62(19):1780-7. doi: 10.1016/j.jacc.2013.06.029
15. Mancia G, De Backer G, Dominiczak A, et al. The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J. 2013;34: 34 (28): 2159–2219. doi: 10.1093/eurheartj/eht151
16. Ermolenko VM, Volgina GV, Dobronravov VA, et al. National recommendations on mineral and bone disorders in chronic kidney disease. Russian Dialysis Society (May 2010). Nephrologia i Dialis. 2011;13(1):33-51 (In Russ)
17. Milyagin V.A., Komissarov V.B. Methods for determining the stiffness of blood vessels. Arterial hypertension. 2010; 16 (2): 134-43]. doi: https://doi.org/10.18705/1607-419X-2010--2-
18. Townsend RR, Wilkinson IB, Schiffrin EL, et al. American Heart Association Council on Hypertension. Recommendations for Improving and Standardizing Vascular Research on Arterial Stiffness. A Scientific Statement from the American Heart Association. J Hypertension. 2015;66(3):698-722.
19. Consistent opinion of Russian experts on arterial stiffness assessment in clinical practice (RCO Congress, 2015). Kardiovaskulyarnaya terapiya i profilaktika. 2016;15(2):4-19 (In Russ.) doi: 10.15829/1728-8800-2016-2-4-19
20. McMurray JJ, Uno H, Jarolim P, et al. Predictors of fatal and nonfatal cardiovascular events in patients with type 2 diabetes mellitus, chronic kidney disease, and anemia: an analysis of the Trial to Reduce cardiovascular Events with Aranesp (darbepoetin-alfa) Therapy (TREAT). Am Heart J. 2011;162(4):748-55. doi: 10.1016/j.ahj.2011.07.016
21. Smith K, de Filippi C, Isakov T, et al. Fibroblast Growth Factor 23, High-Sensitivity Cardiac Troponin, and Left Ventricular Hypertrophy in CKD. Am J Kidney Dis. 2013;61(1):67-73. doi: 10.1053/j.ajkd.2012.06.022
22. Faul C, Amaral AP, Oskouei B, et al. FGF23 induces left ventricular hypertrophy. J Clin Invest. 2011;121:4393-408. doi: 10.1172/JCI46122
23. Shinichiro N, Yoshitaka I, Takaharu Y, et al. Renocardiovascular Biomarkers: from the Perspective of Managing Chronic Kidney Disease and Cardiovascular Disease. Front Cardiovasc Med. 2017;4:10. doi: 10.3389/fcvm.2017.00010
24. Scialla JJ, Lau WL, Reilly MP, et al. Fibroblast growth factor 23 is not associated with and does not induce arterial calcification. Kidney Int. 2013;83:1159-68. doi: 10.1038/ki.2013.3
25. Marthi A, Donovan K, Haynes R, et al. Fibroblast Growth Factor-23 and Risks of Cardiovascular and Noncardiovascular Diseases: A Meta-Analysis. JASN. 2018;29(7):2015-27; doi: 10.1681/ASN.2017121334
26. Sze J, Mooney J, Barzi F. Cardiac troponin and its relationship to cardiovascular outcomes in community populations – a systematic review and meta-analysis. Heart Lung Circ. 2016;25:217-28. doi: 10.1016/j.hlc.2015.09.001
27. Jacobs LH, van de Kerkhof J, Mingels AM, et al. Haemodialysis patients longitudinally assessed by highly sensitive cardiac troponin T and commercial cardiac troponin T and cardiac troponin I assays. Ann Clin Biochem. 2009;46:283-90. doi: 10.1258/acb.2009.008197
28. Stacy SR, Suarez-Cuervo C, Berger Z, et al. Role of troponin in patients with chronic kidney disease and suspected acute coronary syndrome: a systematic review. Ann Intern Med. 2014;161:502-12. doi: 10.7326/M14-0746
29. Bansal N, Hyre Anderson A, Yang W, et al. High-sensitivity troponin T and N-terminal pro-B-type natriuretic peptide (NT-proBNP) and risk of incident heart failure in patients with CKD: the chronic renal insufficiency cohort (CRIC) study. J Am Soc Nephrol. 2015;26:946-56. doi: 10.1681/ASN.2014010108
Авторы
М.В. Таранова, Л.Ю. Милованова, Л.В. Козловская (Лысенко), С.Ю. Милованова, Т.В. Андросова, Д.О. Зубачева, М.В. Лебедева, И.А. Добросмыслов, В.В. Козлов, А.М. Кучиева, О.A. Ли, В.А. Решетников
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
Sechenov First Moscow State Medical University of the Ministry (Sechenov University), Moscow, Russia
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
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Sechenov First Moscow State Medical University of the Ministry (Sechenov University), Moscow, Russia
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