clinmedКлиническая медицинаClinical Medicine (Russian Journal)0023-21492412-1339ООО «Медицинское информационное агентство»10.30629/0023-2149-2021-99-4-245-258clinmed-225Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESБиомаркеры поражения сердца и сосудов в рамках минерально-костных нарушений при хронической болезни почек, воз можности коррекцииBiomarkers of heart and vascular lesions in the framework of mineral and bone disorders in chronic kidney disease, correction possibilitieshttps://orcid.org/0000-0002-5599-0350МиловановаЛ. Ю.MilovanovaL. Yu.

Милованова Людмила Юрьевна — д-р мед. наук, проф. кафедры внутренних, профессиональных болезней и ревматологии

119991, Москва

Lyudmila Yu. Milovanova — MD, PhD, Professor of the Department of Internal, Occupational Diseases and Rheumatology

119991, Moscow

Ludm.milovanova@gmail.comhttps://orcid.org/0000-0002-6377-0630БекетовВ. Д.BeketovV. D.

119991, Москва

119991, Moscow

https://orcid.org/0000-0002-2687-6161МиловановаС. Ю.MilovanovaS. Yu.

119991, Москва

119991, Moscow

https://orcid.org/0000-0002-7363-6195ТарановаМ. В.TaranovaM. V.

119991, Москва

119991, Moscow

ФилипповаА. А.FilippovaA. A.

 

119991, Москва

119991, Moscow

https://orcid.org/0000-0002-7544-3696ПасечникА. И.PasechnikA. I.

 

119991, Москва

119991, Moscow

ФГАОУ ВО «Первый Московский государственный медицинский университет им. И.М. Сеченова» Минздрава России (Сеченовский Университет)РоссияI.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University)Russian Federation202120092021994245258Copyright © Милованова Л.Ю., Бекетов В.Д., Милованова С.Ю., Таранова М.В., Филиппова А.А., Пасечник А.И., 20212021Милованова Л.Ю., Бекетов В.Д., Милованова С.Ю., Таранова М.В., Филиппова А.А., Пасечник А.И.Milovanova L.Y., Beketov V.D., Milovanova S.Y., Taranova M.V., Filippova A.A., Pasechnik A.I.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.clinmedjournal.com/jour/article/view/225

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.

Сardiovascular disease (СVD) is the most common complication of chronic kidney disease (СKD). In patients with the earlier stages of CKD, the risk of death from CVD greatly exceeds the risk of progression to end-stage renal disease. In recent years, accumulated data suggest that chronic kidney disease — mineral and bone disorders (CKD-MBD) are strongly associated with cardiovascular events and mortality. Among cardiovascular damage in CKD, both, the progressive cardiac remodeling and vascular calcifi cation, contribute immensely, and lead to an urgently high cardiovascular mortality in patients with CKD. Clarifi cation of CKD progression mechanisms and possible early markers of CVD has led to interest in studying the identifi ed factors such as fi broblast growth factor-23 (FGF-23), Klotho and sclerostin in recent years. Results of studies show that disorders in the system of FGF-23–Klotho–sclerostin correlate with the frequency and severity of hypertension, cardiac remodeling, vascular calcifi cation, anaemia, malnutrition, infl ammation, and strongly aggravate cardiovascular risk in CKD. This review represents an analysis of the available data showing the potential association of СVD with established (phosphate, parathyroid hormone (PTH), Vitamin D) and newer (FGF-23, Klotho, sclerostin) СKD-MBD biomarkers. In addition, it has been shown that renoprotective therapy, including renin-angiotensin blockers, low-protein diet with amino/keto acid supplementation, phosphate binders, erythropoiesis stimulators, vitamin D metabolites used to reach the target levels of blood pressure, serum phosphorus, haemoglobin, PTH and nutritional status disorders, can aff ect CKD-MBD biomarkers and reduce the risk of cardiovascular events in CKD patients.

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The authors declare that there are no conflicts of interest present.