Обновленные механизмы кальцификации сердечно-сосудистой системы и ее коррекции при хронической болезни почек

При хронической болезни почек (ХБП) прогрессирующее снижение функции приводит к нарушениям минерального обмена, которые обычно называют вторичным гиперпаратиреозом. Увеличение сывороточной концентрации парати- реоидного гормона связано со снижением уровня кальция и кальцитриола и/или повышением уровня фактора роста фибробластов-23 и неорганического фосфата в сыворотке. ХБП-обусловленное нарушение минерального и костно­го метаболизма связано с другими метаболическими нарушениями, такими как ацидоз, белково-энергетическая не­достаточность, воспаление и накопление уремических токсинов. Это способствует кальцификации сосудов, которая является следствием дисбаланса между многочисленными ингибиторами и промоутерами минерализации мягких тканей. Сосудистая кальцификация является дегенеративным процессом, характеризующимся накоплением солей кальция и фосфата в стенке артерии. Это наблюдается почти во всех сосудистых областях и может развиваться в медии, интиме или обоих сосудистых слоях артерий. Кальцификация интимы обычно происходит вследствие атеро­склероза и может быть ответственна за коронарные ишемические события. И наоборот, кальцификация медии неок- клюзивна и преимущественно развивается вдоль эластических волокон. Как следствие, кальцификация медии увели­чивает жесткость сосудов, скорость пульсовой волны аорты, систолическое и пульсовое артериальное давление, спо­собствуя развитию гипертрофии левого желудочка и сердечной недостаточности. В настоящем обзоре рассмотрены современные представления о механизмах, которые приводят к развитию кальцификации сосудов в условиях ХБП. Обсуждается участие в процессах кальцификации таких факторов, как воспаление, конечные продукты гликирования, индоксилсульфат и другие. Определяются перспективные терапевтические цели, связанные с новым пониманием механизмов кардиоваскулярной кальцификации при ХБП.

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