Нарушение соотношения сывороточных уровней фактора роста фибробластов-23 (FGF-23) / растворимой формы белка Клото (sKlotho) / гликопротеина склеростина – новый маркер поражения сердечно-сосудистой системы у больных хронической болезнью почек, получающих
Нарушение соотношения сывороточных уровней фактора роста фибробластов-23 (FGF-23) / растворимой формы белка Клото (sKlotho) / гликопротеина склеростина – новый маркер поражения сердечно-сосудистой системы у больных хронической болезнью почек, получающих
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Аннотация
Цель исследования. Изучить роль нарушения соотношения фактора роста фибробластов-23 (FGF-23) / растворимой формы белка Клото (sKlotho) / гликопротеина склеростина (FGF-23/sKlotho/склеростин) в определении сердечно-сосудистого риска у больных хронической болезнью почек (ХБП) на регулярном гемодиализе (ГД) и гемодиафильтрации (ГДФ) on line.
Материалы и методы. Обследовано 42 пациента с ХБП 5Д стадии в возрасте 18–55 лет, получавших лечение ГД или ГДФ online длительностью ≥6 мес. Лечение традиционным ГД получали 22 (52,3%) больных, остальные 20 (47,7%) – ГДФ online. У всех больных, помимо общеклинического обследования, исследовали сывороточный уровень FGF-23, sKlotho, склеростина (ELISA), их ассоциацию с факторами сердечно-сосудистого риска – гипертрофией левого желудочка (ГЛЖ), острым коронарным синдромом (ОКС), повышением уровня тропонина I; видом диализной терапии. Всем больным с помощью прибора SphygmoCor измеряли центральное (аортальное) артериальное давление (ЦАД), показатель субэндокардиального кровотока (СЭК), проводили электро- и эхокардиографию (с расчетом индекса массы миокарда левого желудочка, относительной толщины стенок левого желудочка и оценкой диастолической функции левого желудочка).
Результаты и обсуждение. Установлено независимое влияние FGF-23 на риск развития ГЛЖ, а также на повышение уровня тропонина I в сыворотке крови у больных терминальной ХБП (β=3,576; p<0,01, и β=1,115; p<0,05). Сывороточный уровень Klotho был фактором, наиболее ассоциированным с уровнем ЦАД (β=-0,023; p<0,001). Повышенный уровень склеростина коррелировал с меньшей частотой выявления сниженного СЭК (r=0,492; p<0,05), симптомов ишемической болезни сердца (r=-0,449; p<0,05) и нарушений ритма (r=-0,446; p<0,05). Наряду с этим у диализных больных более высокие показатели FGF-23 и низкие sKlotho и склеростина в сыворотке крови связаны с синдромом неадекватного диализа (Kt/V <1,1; r=0,463; p<0,05), хронического воспаления
(С-реактивный белок >10 мг/л; r=0,612; p<0,01), а также со снижением сывороточного уровня альбумина (<35 г/л; r=0,459; p<0,05). Нарушение соотношения FGF-23/sKlotho/склеростин в сыворотке крови более выражено у больных, получавших лечение традиционным ГД, чем у больных, леченных ГДФ online. Вне зависимости от вида диализной терапии установлена прямая корреляция (r=0,445; p<0,01) между концентрацией FGF-23 и неорганического фосфора в сыворотке крови, которая более выражена у пациентов на гемодиализе (r=0,545; p<0,01).
Заключение. У больных, получающих лечение ГД или ГДФ в режиме online, более высокие сывороточные уровни FGF-23 и низкие – sKlotho и склеростина ассоциированы с развитием хронического воспаления, нутритивных нарушений, формирования вторичного гиперпаратиреоза и могут служить предикторами сердечно-сосудистых осложнений (ГЛЖ, ОКС, нарушения ритма сердца).
Ключевые слова: гиперфосфатемия, фактор роста фибробластов-23 (FGF-23), растворимая форма Клото (sKlotho), гликопротеин склеростин, гемодиализ, гемодиафильтрация, тропонин, вторичный гиперпаратиреоз.
Materials and methods. 42 patients with ESRD, at the age of 18–55 years, treated with HD or HDF on line for at least 6 months, were examined. 22 (52.3%) patients received traditional HD, the remaining 20 (47.7%) – HDF online. In all the patients, in addition to a general examination, the serum levels of FGF-23, sKlotho, sclerostine (by ELISA), their associations with cardiovascular risk factors (left ventricular hypertrophy (LVH), acute coronary syndrome (ACS), serum troponin I levels) with the numbers of techniques (ECG; Eho-CGF (with calculation of left ventricular myocardium mass index (LVMMI), as well as the relative thickness of the walls of the left ventricle (RWT); sphygmography (central (aortal) blood pressure (CBP), subendocardial blood flow (SBF) – by «Sphygmocor»), and the effect of regular HD and HDF on serum levels of the studied markers, were assessed.
Results and discussion. An independent effect of FGF-23 on the risk of LVH, as well as on the increase of serum troponin I in the studied ESRD patients [β=3.576 p<0.01, and β=1.115, p<0.05, respectively] was found. Serum Klotho was the factor most associated with the CBP [β=-0.023; p<0.001]. The increased serum sclerostin was correlated with a lower incidence of both reduced SBF [r=0.492; p<0.05], symptoms of coronary heart disease [r=-0.449; p<0.05] and rhythm disturbances [r=-0.446; p<0.05]. In addition, in HD patients higher FGF-23 and lower Klotho and sclerostine serum levels were associated with: inadequate dialysis syndrome (Kt/V <1.1; r=0.463; p<0.05), chronic inflammation (C-reactive protein >10 mg/L; r=0.612; p<0.01), and with a decrease in serum albumin level (<35 g/l; r=0.459; p<0.05). The FGF-23/sKlotho/sclerostin ratio disturbance was more pronounced in patients treated with traditional HD then HDF online. A direct correlation (r=0.445; p<0.05) was established between FGF-23 serum levels and serum phosphorus, which was more pronounced in HD patients (r=0.545; p<0.01).
Conclusion. In HD and HDF ESRD patients, higher serum FGF-23 and lower sKlotho and sclerostin levels were associated with a chronic inflammation, malnutrition, secondary hyperparathyroidism, and may considered as predictors of cardiovascular complications such as LVH, ACS, rhythm disturbances, persisting of subincreased serum troponin I.
Keywords: hyperphosphatemia, fibroblast growth factor-23 (FGF-23), soluble Klotho, sclerostine, hemodialysis, hemodiafiltration, troponin, secondary hyperparathyroidism.
Материалы и методы. Обследовано 42 пациента с ХБП 5Д стадии в возрасте 18–55 лет, получавших лечение ГД или ГДФ online длительностью ≥6 мес. Лечение традиционным ГД получали 22 (52,3%) больных, остальные 20 (47,7%) – ГДФ online. У всех больных, помимо общеклинического обследования, исследовали сывороточный уровень FGF-23, sKlotho, склеростина (ELISA), их ассоциацию с факторами сердечно-сосудистого риска – гипертрофией левого желудочка (ГЛЖ), острым коронарным синдромом (ОКС), повышением уровня тропонина I; видом диализной терапии. Всем больным с помощью прибора SphygmoCor измеряли центральное (аортальное) артериальное давление (ЦАД), показатель субэндокардиального кровотока (СЭК), проводили электро- и эхокардиографию (с расчетом индекса массы миокарда левого желудочка, относительной толщины стенок левого желудочка и оценкой диастолической функции левого желудочка).
Результаты и обсуждение. Установлено независимое влияние FGF-23 на риск развития ГЛЖ, а также на повышение уровня тропонина I в сыворотке крови у больных терминальной ХБП (β=3,576; p<0,01, и β=1,115; p<0,05). Сывороточный уровень Klotho был фактором, наиболее ассоциированным с уровнем ЦАД (β=-0,023; p<0,001). Повышенный уровень склеростина коррелировал с меньшей частотой выявления сниженного СЭК (r=0,492; p<0,05), симптомов ишемической болезни сердца (r=-0,449; p<0,05) и нарушений ритма (r=-0,446; p<0,05). Наряду с этим у диализных больных более высокие показатели FGF-23 и низкие sKlotho и склеростина в сыворотке крови связаны с синдромом неадекватного диализа (Kt/V <1,1; r=0,463; p<0,05), хронического воспаления
(С-реактивный белок >10 мг/л; r=0,612; p<0,01), а также со снижением сывороточного уровня альбумина (<35 г/л; r=0,459; p<0,05). Нарушение соотношения FGF-23/sKlotho/склеростин в сыворотке крови более выражено у больных, получавших лечение традиционным ГД, чем у больных, леченных ГДФ online. Вне зависимости от вида диализной терапии установлена прямая корреляция (r=0,445; p<0,01) между концентрацией FGF-23 и неорганического фосфора в сыворотке крови, которая более выражена у пациентов на гемодиализе (r=0,545; p<0,01).
Заключение. У больных, получающих лечение ГД или ГДФ в режиме online, более высокие сывороточные уровни FGF-23 и низкие – sKlotho и склеростина ассоциированы с развитием хронического воспаления, нутритивных нарушений, формирования вторичного гиперпаратиреоза и могут служить предикторами сердечно-сосудистых осложнений (ГЛЖ, ОКС, нарушения ритма сердца).
Ключевые слова: гиперфосфатемия, фактор роста фибробластов-23 (FGF-23), растворимая форма Клото (sKlotho), гликопротеин склеростин, гемодиализ, гемодиафильтрация, тропонин, вторичный гиперпаратиреоз.
________________________________________________
Materials and methods. 42 patients with ESRD, at the age of 18–55 years, treated with HD or HDF on line for at least 6 months, were examined. 22 (52.3%) patients received traditional HD, the remaining 20 (47.7%) – HDF online. In all the patients, in addition to a general examination, the serum levels of FGF-23, sKlotho, sclerostine (by ELISA), their associations with cardiovascular risk factors (left ventricular hypertrophy (LVH), acute coronary syndrome (ACS), serum troponin I levels) with the numbers of techniques (ECG; Eho-CGF (with calculation of left ventricular myocardium mass index (LVMMI), as well as the relative thickness of the walls of the left ventricle (RWT); sphygmography (central (aortal) blood pressure (CBP), subendocardial blood flow (SBF) – by «Sphygmocor»), and the effect of regular HD and HDF on serum levels of the studied markers, were assessed.
Results and discussion. An independent effect of FGF-23 on the risk of LVH, as well as on the increase of serum troponin I in the studied ESRD patients [β=3.576 p<0.01, and β=1.115, p<0.05, respectively] was found. Serum Klotho was the factor most associated with the CBP [β=-0.023; p<0.001]. The increased serum sclerostin was correlated with a lower incidence of both reduced SBF [r=0.492; p<0.05], symptoms of coronary heart disease [r=-0.449; p<0.05] and rhythm disturbances [r=-0.446; p<0.05]. In addition, in HD patients higher FGF-23 and lower Klotho and sclerostine serum levels were associated with: inadequate dialysis syndrome (Kt/V <1.1; r=0.463; p<0.05), chronic inflammation (C-reactive protein >10 mg/L; r=0.612; p<0.01), and with a decrease in serum albumin level (<35 g/l; r=0.459; p<0.05). The FGF-23/sKlotho/sclerostin ratio disturbance was more pronounced in patients treated with traditional HD then HDF online. A direct correlation (r=0.445; p<0.05) was established between FGF-23 serum levels and serum phosphorus, which was more pronounced in HD patients (r=0.545; p<0.01).
Conclusion. In HD and HDF ESRD patients, higher serum FGF-23 and lower sKlotho and sclerostin levels were associated with a chronic inflammation, malnutrition, secondary hyperparathyroidism, and may considered as predictors of cardiovascular complications such as LVH, ACS, rhythm disturbances, persisting of subincreased serum troponin I.
Keywords: hyperphosphatemia, fibroblast growth factor-23 (FGF-23), soluble Klotho, sclerostine, hemodialysis, hemodiafiltration, troponin, secondary hyperparathyroidism.
Список литературы
1. Go AS, Chertow GM, Fan D, et al. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004;351:1296-305.
2. Kumar S, Bogle R, Banerjee D. Why do young people with chronic kidney disease die early? World J Nephrol. 2014;3(4):143-55. doi: 10. 5527/wjn.v3.i4.143
3. Milovanova L, Plotnikova A.Phosphorus and Calcium Metabolism Disorders Assosiated with Chronic Kidney Disease Stage III-IV (Systematic Rewiew and Meta-Analysis). In: Manisha Sahay, editor. Chronic Kidney Disease and Renal Transplantation. INTECH; 2012. P. 95-118.
4. Milovanova L, Fomin VV, Mukhin NA. Nutritional status disorders in Chronic Kidney Disease: practical aspects. In: Chronic Kidney Disease. INTECH; 2017. P. 95-118. ISBN 978-953-51-5463-1.
5. Gutierrez O, Mannstadt M, Isakova T, et al. Fibroblast Growth Factor 23 and Mortality among Hemodialysis Patients. N Engl J Med. 2008;359:584-92.
6. Seifert ME, Hruska KA. The Kidney-Vascular-Bone Axis in the Chronic Kidney Disease-Mineral Bone Disorder. Transplantation. 2016;100(3): 497-505. doi: 10.1097/TP.0000000000000903
7. Milovanova LYu, Milovanov YuS, Kudryavtseva (Kryukova) DV, Markina MM, Milovanova SYu, Lebedeva MV, Beketov DV, Moiseev SV, Kozlovskaya LV, Mukhin NA, Fomin VV. The role of morphogenetic proteins (fibroblast growth factor – 23 – FGF-23, Klotho) and glycoprotein sclerostin in assessing cardiovascular risk and the prognosis of chronic kidney disease. Terapevticheskiy Arhiv. 2015;(4):46-54.
8. Isakova T, Wahl P, Vargas GS, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int. 2011;79:1370-8.
9. 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
10. Semba RD, Cappola AR, Sun K, et al. Plasma klotho and mortality risk in older community-dwelling adults. J Gerontol A Biol Sci Med Sci. 2011;66:794-800.
11. Donate-Correa J, Martín-Núñez E, Mora-Fernández C, et al. Klotho in cardiovascular disease: Current and future perspectives. World J Biol Chem. 2015;6(4):351-7. doi: 10.4331/wjbc.v6.i4.351
12. Cejka D, Herberth J, Branscum AJ, Fardo DW, Monier-Faugere MC, Diarra D, et al. Sclerostin and Dickkopf-1 in renal osteodystrophy. Clin J Am Soc Nephrol. 2011;6:877-82. doi: 10.2215/CJN.06550810
13. Lips L, de Roij van Zuijdewijn CLM, ter Wee PM, Bots ML, Blankestijn PJ, van den Dorpel MA, Fouque D, de Jongh R, Pelletier S, Vervloet MG. Serum sclerostin: relation with mortality and impact of hemodiafiltration. Nephrol Dial Transplant. 2017;32(7):1217-23.
doi: 10.1093/ndt/gfw246
14. Milovanova L, Fomin VV, Lysenko (Kozlovskaya) LV. 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. In: Chronic Kidney Disease.
INTECH; 2017. ISBN 978-953-51-5463-1
15. Grabner A, Amaral AP, Schramm K, et al. Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy. Cell Metab. 2015;22(6):1020-32. doi: 10.1016/j.cmet. 2015.09. 002
16. Di Marco GS, Reuter S, Kentrup D, Grabner A, Amaral AP, Fobker M, Stypmann J, Pavenstadt H, Wolf M, Faul C, Brand M.Treatment of established left ventricular hypertrophy with fibroblast growth factor receptor blockade in an animal model of CKD. Nephrol Dial Transplant. 2014;10:1-8.
17. Smith K, Defilippi C, Isakova T, Gutiérrez OM, Laliberte K Seliger S, Kelley W, Duh SH, Hise M, Christenson R, Wolf M. Fibroblast growth factor-23, high-sensitivity cardiac troponin, and left ventricular hypertrophy in CKD. J Am Kidney Dis. 2013;61(1):67-73.
18. Hu MC, Shi M, Zhang J, et al. Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease. J Am Soc Nephrol. 2011;22(1):124-36. doi: 10.1681/ASN.2009121311
19. Bruzzese A, Lacquaniti A, Cernaro V, Ricciardi CA, Loddo S, Romeo A. Sclerostin levels in uremic patients: a link between bone and vascular disease. J Renal Failure. 2016;38(5):123-9.
20. Kanbay M, Solak Y, Siriopol D, Aslan G, Afsar B, Yazici D, Covic A. Sclerostin, cardiovascular disease and mortality: a systematic review and meta-analysis. Int Urol Nephrol. 2016;48(12):2029-42.
21. Register TC, Hruska KA, Divers J, Bowden DW, Palmer ND, Carr JJ, et al. Sclerostin is positively associated with bone mineral density in men and women and negatively associated with carotid calcified atherosclerotic plaque in men from the African American-Diabetes Heart Study. J Clin Endocrinol Metab. 2013 Epub 2013.11.02. doi: 10.1210/ jc.2013-3168
2. Kumar S, Bogle R, Banerjee D. Why do young people with chronic kidney disease die early? World J Nephrol. 2014;3(4):143-55. doi: 10. 5527/wjn.v3.i4.143
3. Milovanova L, Plotnikova A.Phosphorus and Calcium Metabolism Disorders Assosiated with Chronic Kidney Disease Stage III-IV (Systematic Rewiew and Meta-Analysis). In: Manisha Sahay, editor. Chronic Kidney Disease and Renal Transplantation. INTECH; 2012. P. 95-118.
4. Milovanova L, Fomin VV, Mukhin NA. Nutritional status disorders in Chronic Kidney Disease: practical aspects. In: Chronic Kidney Disease. INTECH; 2017. P. 95-118. ISBN 978-953-51-5463-1.
5. Gutierrez O, Mannstadt M, Isakova T, et al. Fibroblast Growth Factor 23 and Mortality among Hemodialysis Patients. N Engl J Med. 2008;359:584-92.
6. Seifert ME, Hruska KA. The Kidney-Vascular-Bone Axis in the Chronic Kidney Disease-Mineral Bone Disorder. Transplantation. 2016;100(3): 497-505. doi: 10.1097/TP.0000000000000903
7. Milovanova LYu, Milovanov YuS, Kudryavtseva (Kryukova) DV, Markina MM, Milovanova SYu, Lebedeva MV, Beketov DV, Moiseev SV, Kozlovskaya LV, Mukhin NA, Fomin VV. The role of morphogenetic proteins (fibroblast growth factor – 23 – FGF-23, Klotho) and glycoprotein sclerostin in assessing cardiovascular risk and the prognosis of chronic kidney disease. Terapevticheskiy Arhiv. 2015;(4):46-54.
8. Isakova T, Wahl P, Vargas GS, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int. 2011;79:1370-8.
9. 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
10. Semba RD, Cappola AR, Sun K, et al. Plasma klotho and mortality risk in older community-dwelling adults. J Gerontol A Biol Sci Med Sci. 2011;66:794-800.
11. Donate-Correa J, Martín-Núñez E, Mora-Fernández C, et al. Klotho in cardiovascular disease: Current and future perspectives. World J Biol Chem. 2015;6(4):351-7. doi: 10.4331/wjbc.v6.i4.351
12. Cejka D, Herberth J, Branscum AJ, Fardo DW, Monier-Faugere MC, Diarra D, et al. Sclerostin and Dickkopf-1 in renal osteodystrophy. Clin J Am Soc Nephrol. 2011;6:877-82. doi: 10.2215/CJN.06550810
13. Lips L, de Roij van Zuijdewijn CLM, ter Wee PM, Bots ML, Blankestijn PJ, van den Dorpel MA, Fouque D, de Jongh R, Pelletier S, Vervloet MG. Serum sclerostin: relation with mortality and impact of hemodiafiltration. Nephrol Dial Transplant. 2017;32(7):1217-23.
doi: 10.1093/ndt/gfw246
14. Milovanova L, Fomin VV, Lysenko (Kozlovskaya) LV. 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. In: Chronic Kidney Disease.
INTECH; 2017. ISBN 978-953-51-5463-1
15. Grabner A, Amaral AP, Schramm K, et al. Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy. Cell Metab. 2015;22(6):1020-32. doi: 10.1016/j.cmet. 2015.09. 002
16. Di Marco GS, Reuter S, Kentrup D, Grabner A, Amaral AP, Fobker M, Stypmann J, Pavenstadt H, Wolf M, Faul C, Brand M.Treatment of established left ventricular hypertrophy with fibroblast growth factor receptor blockade in an animal model of CKD. Nephrol Dial Transplant. 2014;10:1-8.
17. Smith K, Defilippi C, Isakova T, Gutiérrez OM, Laliberte K Seliger S, Kelley W, Duh SH, Hise M, Christenson R, Wolf M. Fibroblast growth factor-23, high-sensitivity cardiac troponin, and left ventricular hypertrophy in CKD. J Am Kidney Dis. 2013;61(1):67-73.
18. Hu MC, Shi M, Zhang J, et al. Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease. J Am Soc Nephrol. 2011;22(1):124-36. doi: 10.1681/ASN.2009121311
19. Bruzzese A, Lacquaniti A, Cernaro V, Ricciardi CA, Loddo S, Romeo A. Sclerostin levels in uremic patients: a link between bone and vascular disease. J Renal Failure. 2016;38(5):123-9.
20. Kanbay M, Solak Y, Siriopol D, Aslan G, Afsar B, Yazici D, Covic A. Sclerostin, cardiovascular disease and mortality: a systematic review and meta-analysis. Int Urol Nephrol. 2016;48(12):2029-42.
21. Register TC, Hruska KA, Divers J, Bowden DW, Palmer ND, Carr JJ, et al. Sclerostin is positively associated with bone mineral density in men and women and negatively associated with carotid calcified atherosclerotic plaque in men from the African American-Diabetes Heart Study. J Clin Endocrinol Metab. 2013 Epub 2013.11.02. doi: 10.1210/ jc.2013-3168
2. Kumar S, Bogle R, Banerjee D. Why do young people with chronic kidney disease die early? World J Nephrol. 2014;3(4):143-55. doi: 10. 5527/wjn.v3.i4.143
3. Milovanova L, Plotnikova A.Phosphorus and Calcium Metabolism Disorders Assosiated with Chronic Kidney Disease Stage III-IV (Systematic Rewiew and Meta-Analysis). In: Manisha Sahay, editor. Chronic Kidney Disease and Renal Transplantation. INTECH; 2012. P. 95-118.
4. Milovanova L, Fomin VV, Mukhin NA. Nutritional status disorders in Chronic Kidney Disease: practical aspects. In: Chronic Kidney Disease. INTECH; 2017. P. 95-118. ISBN 978-953-51-5463-1.
5. Gutierrez O, Mannstadt M, Isakova T, et al. Fibroblast Growth Factor 23 and Mortality among Hemodialysis Patients. N Engl J Med. 2008;359:584-92.
6. Seifert ME, Hruska KA. The Kidney-Vascular-Bone Axis in the Chronic Kidney Disease-Mineral Bone Disorder. Transplantation. 2016;100(3): 497-505. doi: 10.1097/TP.0000000000000903
7. Milovanova LYu, Milovanov YuS, Kudryavtseva (Kryukova) DV, Markina MM, Milovanova SYu, Lebedeva MV, Beketov DV, Moiseev SV, Kozlovskaya LV, Mukhin NA, Fomin VV. The role of morphogenetic proteins (fibroblast growth factor – 23 – FGF-23, Klotho) and glycoprotein sclerostin in assessing cardiovascular risk and the prognosis of chronic kidney disease. Terapevticheskiy Arhiv. 2015;(4):46-54.
8. Isakova T, Wahl P, Vargas GS, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int. 2011;79:1370-8.
9. 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
10. Semba RD, Cappola AR, Sun K, et al. Plasma klotho and mortality risk in older community-dwelling adults. J Gerontol A Biol Sci Med Sci. 2011;66:794-800.
11. Donate-Correa J, Martín-Núñez E, Mora-Fernández C, et al. Klotho in cardiovascular disease: Current and future perspectives. World J Biol Chem. 2015;6(4):351-7. doi: 10.4331/wjbc.v6.i4.351
12. Cejka D, Herberth J, Branscum AJ, Fardo DW, Monier-Faugere MC, Diarra D, et al. Sclerostin and Dickkopf-1 in renal osteodystrophy. Clin J Am Soc Nephrol. 2011;6:877-82. doi: 10.2215/CJN.06550810
13. Lips L, de Roij van Zuijdewijn CLM, ter Wee PM, Bots ML, Blankestijn PJ, van den Dorpel MA, Fouque D, de Jongh R, Pelletier S, Vervloet MG. Serum sclerostin: relation with mortality and impact of hemodiafiltration. Nephrol Dial Transplant. 2017;32(7):1217-23.
doi: 10.1093/ndt/gfw246
14. Milovanova L, Fomin VV, Lysenko (Kozlovskaya) LV. 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. In: Chronic Kidney Disease.
INTECH; 2017. ISBN 978-953-51-5463-1
15. Grabner A, Amaral AP, Schramm K, et al. Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy. Cell Metab. 2015;22(6):1020-32. doi: 10.1016/j.cmet. 2015.09. 002
16. Di Marco GS, Reuter S, Kentrup D, Grabner A, Amaral AP, Fobker M, Stypmann J, Pavenstadt H, Wolf M, Faul C, Brand M.Treatment of established left ventricular hypertrophy with fibroblast growth factor receptor blockade in an animal model of CKD. Nephrol Dial Transplant. 2014;10:1-8.
17. Smith K, Defilippi C, Isakova T, Gutiérrez OM, Laliberte K Seliger S, Kelley W, Duh SH, Hise M, Christenson R, Wolf M. Fibroblast growth factor-23, high-sensitivity cardiac troponin, and left ventricular hypertrophy in CKD. J Am Kidney Dis. 2013;61(1):67-73.
18. Hu MC, Shi M, Zhang J, et al. Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease. J Am Soc Nephrol. 2011;22(1):124-36. doi: 10.1681/ASN.2009121311
19. Bruzzese A, Lacquaniti A, Cernaro V, Ricciardi CA, Loddo S, Romeo A. Sclerostin levels in uremic patients: a link between bone and vascular disease. J Renal Failure. 2016;38(5):123-9.
20. Kanbay M, Solak Y, Siriopol D, Aslan G, Afsar B, Yazici D, Covic A. Sclerostin, cardiovascular disease and mortality: a systematic review and meta-analysis. Int Urol Nephrol. 2016;48(12):2029-42.
21. Register TC, Hruska KA, Divers J, Bowden DW, Palmer ND, Carr JJ, et al. Sclerostin is positively associated with bone mineral density in men and women and negatively associated with carotid calcified atherosclerotic plaque in men from the African American-Diabetes Heart Study. J Clin Endocrinol Metab. 2013 Epub 2013.11.02. doi: 10.1210/ jc.2013-3168
________________________________________________
2. Kumar S, Bogle R, Banerjee D. Why do young people with chronic kidney disease die early? World J Nephrol. 2014;3(4):143-55. doi: 10. 5527/wjn.v3.i4.143
3. Milovanova L, Plotnikova A.Phosphorus and Calcium Metabolism Disorders Assosiated with Chronic Kidney Disease Stage III-IV (Systematic Rewiew and Meta-Analysis). In: Manisha Sahay, editor. Chronic Kidney Disease and Renal Transplantation. INTECH; 2012. P. 95-118.
4. Milovanova L, Fomin VV, Mukhin NA. Nutritional status disorders in Chronic Kidney Disease: practical aspects. In: Chronic Kidney Disease. INTECH; 2017. P. 95-118. ISBN 978-953-51-5463-1.
5. Gutierrez O, Mannstadt M, Isakova T, et al. Fibroblast Growth Factor 23 and Mortality among Hemodialysis Patients. N Engl J Med. 2008;359:584-92.
6. Seifert ME, Hruska KA. The Kidney-Vascular-Bone Axis in the Chronic Kidney Disease-Mineral Bone Disorder. Transplantation. 2016;100(3): 497-505. doi: 10.1097/TP.0000000000000903
7. Milovanova LYu, Milovanov YuS, Kudryavtseva (Kryukova) DV, Markina MM, Milovanova SYu, Lebedeva MV, Beketov DV, Moiseev SV, Kozlovskaya LV, Mukhin NA, Fomin VV. The role of morphogenetic proteins (fibroblast growth factor – 23 – FGF-23, Klotho) and glycoprotein sclerostin in assessing cardiovascular risk and the prognosis of chronic kidney disease. Terapevticheskiy Arhiv. 2015;(4):46-54.
8. Isakova T, Wahl P, Vargas GS, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int. 2011;79:1370-8.
9. 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
10. Semba RD, Cappola AR, Sun K, et al. Plasma klotho and mortality risk in older community-dwelling adults. J Gerontol A Biol Sci Med Sci. 2011;66:794-800.
11. Donate-Correa J, Martín-Núñez E, Mora-Fernández C, et al. Klotho in cardiovascular disease: Current and future perspectives. World J Biol Chem. 2015;6(4):351-7. doi: 10.4331/wjbc.v6.i4.351
12. Cejka D, Herberth J, Branscum AJ, Fardo DW, Monier-Faugere MC, Diarra D, et al. Sclerostin and Dickkopf-1 in renal osteodystrophy. Clin J Am Soc Nephrol. 2011;6:877-82. doi: 10.2215/CJN.06550810
13. Lips L, de Roij van Zuijdewijn CLM, ter Wee PM, Bots ML, Blankestijn PJ, van den Dorpel MA, Fouque D, de Jongh R, Pelletier S, Vervloet MG. Serum sclerostin: relation with mortality and impact of hemodiafiltration. Nephrol Dial Transplant. 2017;32(7):1217-23.
doi: 10.1093/ndt/gfw246
14. Milovanova L, Fomin VV, Lysenko (Kozlovskaya) LV. 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. In: Chronic Kidney Disease.
INTECH; 2017. ISBN 978-953-51-5463-1
15. Grabner A, Amaral AP, Schramm K, et al. Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy. Cell Metab. 2015;22(6):1020-32. doi: 10.1016/j.cmet. 2015.09. 002
16. Di Marco GS, Reuter S, Kentrup D, Grabner A, Amaral AP, Fobker M, Stypmann J, Pavenstadt H, Wolf M, Faul C, Brand M.Treatment of established left ventricular hypertrophy with fibroblast growth factor receptor blockade in an animal model of CKD. Nephrol Dial Transplant. 2014;10:1-8.
17. Smith K, Defilippi C, Isakova T, Gutiérrez OM, Laliberte K Seliger S, Kelley W, Duh SH, Hise M, Christenson R, Wolf M. Fibroblast growth factor-23, high-sensitivity cardiac troponin, and left ventricular hypertrophy in CKD. J Am Kidney Dis. 2013;61(1):67-73.
18. Hu MC, Shi M, Zhang J, et al. Klotho Deficiency Causes Vascular Calcification in Chronic Kidney Disease. J Am Soc Nephrol. 2011;22(1):124-36. doi: 10.1681/ASN.2009121311
19. Bruzzese A, Lacquaniti A, Cernaro V, Ricciardi CA, Loddo S, Romeo A. Sclerostin levels in uremic patients: a link between bone and vascular disease. J Renal Failure. 2016;38(5):123-9.
20. Kanbay M, Solak Y, Siriopol D, Aslan G, Afsar B, Yazici D, Covic A. Sclerostin, cardiovascular disease and mortality: a systematic review and meta-analysis. Int Urol Nephrol. 2016;48(12):2029-42.
21. Register TC, Hruska KA, Divers J, Bowden DW, Palmer ND, Carr JJ, et al. Sclerostin is positively associated with bone mineral density in men and women and negatively associated with carotid calcified atherosclerotic plaque in men from the African American-Diabetes Heart Study. J Clin Endocrinol Metab. 2013 Epub 2013.11.02. doi: 10.1210/ jc.2013-3168
Авторы
Л.Ю. Милованова, И.А. Добросмыслов, Ю.С. Милованов, В.В. Фомин, М.В. Таранова,
В.В. Козлов, С.Ю. Милованова, E.И. Koжевникова
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
I.M. Sechenov First Moscow State Medical University, Ministry of Health (Sechenov University), Moscow, Russia
В.В. Козлов, С.Ю. Милованова, E.И. Koжевникова
ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет), Москва, Россия
________________________________________________
I.M. Sechenov First Moscow State Medical University, Ministry of Health (Sechenov University), Moscow, Russia
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