Abstract:
AIM:To determine the nature of changes in fibroblast growth factor 23 (FGF-23) and other bone mineral metabolism parameters detectable in the blood of patients with end-stage chronic renal failure (CRF) and to analyze their links to the development of cardiovascular events in uremic intoxication. SUBJECTS AND METHODS:A total of 75 patients (45 men and 30 women) aged 23 to 66 years (mean age, 53±2.1 years) with Stage VD CKF were examined. The levels of parathyroid hormone (PTH), calcium, phosphorus, the morphogenetic protein FGF-23, and the cardiospecific protein troponin I were investigated. Doppler echocardiography was performed on an Aloka 4000 machine. Left ventricular (LV) mass index (LVMI), LV systolic and diastolic function, and peak systolic blood flow velocity in the aortic arch (Vps) were estimated. RESULTS:As LVMI became higher, there were increases in the level of PTH and that of FGF-23 that plays a significant role in the processes of bone remodeling and vascular calcification. Analysis of correlations between a change in FGF-23 concentrations depending on the morphological and functional parameters of the cardiovascular system (CVS) revealed a strong direct correlation between FGF-23 levels and LVMI (r=0.746; p<0.01), a significant inverse correlation between FGF-23 and ejection fraction (r=-0.901; p<0.05), and a direct correlation of FGF-23 and troponin I (r=0.544; p<0.05). CONCLUSION:FGF-2 increasing from moderate to very high levels indicates that there is a high risk for remodeling processes in the CVS even in the absence of baseline echocardiographic signs of myocardial hypertrophy, normal aortic pulse wave velocity, and compensation of other risk factors, such as hypertension, uremia, hyperparathyroidism, even without increasing the markers of cardiovascular events, such as hyperphosphatemia. The elevated level of FGF-23 suggests that there is a need for cardioprotective therapy, the goal of which is to correct of the level of this factor. :Цель исследования. Определение характера изменений 23-го фактора роста фибробластов (FGF-23), других показателей костно-минерального обмена, выявляемых в крови у больных с терминальной стадией хронической почечной недостаточности (ХПН), и анализ их связей с развитием сердечно-сосудистых осложнений в условиях уремической интоксикации. Материалы и методы. Обследовали 75 больных ХБП (VD-стадии): 45 мужчин и 30 женщин в возрасте от 23 до 66 лет (средний возраст 53±2,1 года). Исследованы уровни паратиреоидного гормона (паратгормона - ПТГ), кальция, фосфора, морфогенетического белка FGF-23, кардиоспецифического белка тропонина I. Эхокардиографию с допплерографией выполняли на аппарате Aloka 4000. Определяли индекс массы миокарда левого желудочка - ЛЖ (ИММ ЛЖ), систолическую и диастолическую функцию ЛЖ, пиковую систолическую скорость кровотока в дуге аорты (Vps). Результаты. По мере увеличения ИММ ЛЖ отмечено повышение уровня ПТГ, уровня FGF-23, играющего значительную роль в процессах ремоделирования костной ткани и кальцификации сосудов. Анализ корреляций между изменением концентраций FGF-23 в зависимости от морфологических и функциональных показателей сердечно-сосудистой системы (ССС) выявил сильную прямую связь между уровнями FGF-23 и ИММ ЛЖ (r=0,746; p<0,01) и достоверную обратную корреляцию между FGF-23 и фракцией выброса - ФВ (r=–0,901; p<0,05), прямую зависимость FGF-23 и тропонина I (r=0,544; p<0,05). Заключение. Повышение уровня FGF-23 от умеренного до крайне высокого свидетельствует о высоком риске ремоделирующих процессов в ССС даже в отсутствие исходных эхокардиографических признаков гипертрофии миокарда, нормальной скорости пульсовой волны аорты, компенсации других факторов риска, таких как артериальная гипертония, уремия, гиперпаратиреоз даже без повышения такого маркера сердечно-сосудистых осложнений, как гиперфосфатемия. Повышение уровня FGF-23 свидетельствует о необходимости проведения кардиопротективной терапии, цель которой коррекция уровня FGF-23. :Резюме Цель исследования. Определение характера изменений 23-го фактора роста фибробластов (FGF-23), других показателей костно-минерального обмена, выявляемых в крови у больных с терминальной стадией хронической почечной недостаточности (ХПН), и анализ их связей с развитием сердечно-сосудистых осложнений в условиях уремической интоксикации. Материалы и методы. Обследовали 75 больных ХБП (VD-стадии): 45 мужчин и 30 женщин в возрасте от 23 до 66 лет (средний возраст 53±2,1 года). Исследованы уровни паратиреоидного гормона (паратгормона — ПТГ), кальция, фосфора, морфогенетического белка FGF-23, кардиоспецифического белка тропонина I. Эхокардиографию с допплерографией выполняли на аппарате Aloka 4000. Определяли индекс массы миокарда левого желудочка — ЛЖ (ИММ ЛЖ), систолическую и диастолическую функцию ЛЖ, пиковую систолическую скорость кровотока в дуге аорты (Vps). Результаты. По мере увеличения ИММ ЛЖ отмечено повышение уровня ПТГ, уровня FGF-23, играющего значительную роль в процессах ремоделирования костной ткани и кальцификации сосудов. Анализ корреляций между изменением концентраций FGF-23 в зависимости от морфологических и функциональных показателей сердечно-сосудистой системы (ССС) выявил сильную прямую связь между уровнями FGF-23 и ИММ ЛЖ (r=0,746; p<0,01) и достоверную обратную корреляцию между FGF-23 и фракцией выброса — ФВ (r=–0,901; p<0,05), прямую зависимость FGF-23 и тропонина I (r=0,544; p<0,05). Заключение. Повышение уровня FGF-23 от умеренного до крайне высокого свидетельствует о высоком риске ремоделирующих процессов в ССС даже в отсутствие исходных эхокардиографических признаков гипертрофии миокарда, нормальной скорости пульсовой волны аорты, компенсации других факторов риска, таких как артериальная гипертония, уремия, гиперпаратиреоз даже без повышения такого маркера сердечно-сосудистых осложнений, как гиперфосфатемия. Повышение уровня FGF-23 свидетельствует о необходимости проведения кардиопротективной терапии, цель которой коррекция уровня FGF-23.
journal_name
Ter Arkhjournal_title
Terapevticheskii arkhivauthors
Dzgoeva FU,Sopoev MY,Bestaeva TL,Khamitsaeva OV,Ktsoeva FA,Sageeva ROdoi
10.17116/terarkh2016881251-56subject
Has Abstractpub_date
2016-01-01 00:00:00pages
51-56issue
12eissn
0040-3660issn
2309-5342journal_volume
88pub_type
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