Биомаркеры поражения сердца и сосудов в рамках минерально-костных нарушений при хронической болезни почек, воз можности коррекции

Сердечно-сосудистые заболевания (ССЗ) часто встречаются у больных хронической болезнью почек (ХБП), при этом риск смерти от ССЗ на ранних и умеренных стадиях ХБП намного превышает риск прогрессирования ХБП до терминальной стадии почечной недостаточности (ТПН) с необходимостью диализа. В последние годы накапливается все больше данных, что наличие минеральных и костных нарушений (МКН), ХБП ассоциировано с сердечно-сосудистыми событиями и смертностью. Среди сердечно-сосудистых осложнений (ССО) при ХБП ведущую роль играют прогрессирующее ремоделирование сердца и кальцификация сосудов, в совокупности приводя к чрезвычайно высокой смертности от ССЗ у пациентов с ХБП. Уточнение механизмов прогрессирования ХБП и возможных ранних маркеров ССЗ вызвало интерес к изучению выявленных в последние годы факторов, таких как фактор роста фибробластов-23 (FGF-23), Klotho и склеростин. Результаты исследований показывают, что нарушения в системе FGF-23–Klotho– sclerostin коррелируют с частотой и тяжестью гипертонии, ремоделирования сердца, кальцификации сосудов, анемии, белково-энергетической недостаточности, воспаления и существенно усугубляют сердечно-сосудистый риск при ХБП. В данном обзоре представлен анализ имеющихся литературных данных об ассоциации ССО, связанных с ХБП, с известными — «старыми» (паратиреоидный гормон — ПТГ, фосфат, дефицит витамина D) и более новыми (FGF-23, Klotho, sclerostin) биомаркерами МКН-ХБП, а также возможностях коррекции их нарушений. Показано, что ренопротективная терапия, включая блокаторы ренин-ангиотензина, низкобелковую диету с добавлением незаменимых аминокислот/кетокислот, фосфатсвязывающие средства, стимуляторы эритропоэза, метаболиты витамина D, используемые для достижения целевых уровней артериального давления, фосфора в сыворотке крови, гемоглобина, ПТГ, может влиять на уровень биомаркеров МКН-ХБП и модулировать риск сердечно-сосудистых событий у пациентов с ХБП.

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