nefrНефрологияNephrology (Saint-Petersburg)1561-62742541-9439Pavlov First Saint-Petersburg State Medical University10.36485/1561-6274-2020-24-5-18-28nefr-1879Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESОбновленные механизмы кальцификации сердечно-сосудистой системы и ее коррекции при хронической болезни почекUpdated mechanisms of calcification of cardiovascular system and its correction in chronic kidney diseasehttps://orcid.org/0000-0002-7314-9063ДзгоеваФ. У.DzgoevaF. U.

Проф. Дзгоева Фатима Урузмаговна, д-р мед. наук 

Кафедра внутренних болезней №5

362040, Республика северная Осетия-Алания,г. Владикавказ, ул. Пушкинская, д. 40. Тел.: 8(918)8228345

 

Prof. Fatima U. Dzgoeva, MD, PhD, DMedSci 

Department of Internal Medicine №5

Affiliations: 362040, Republic of North Ossetia-Alania, Vladikavkaz, Pushkinskaya, 40. Phone: 8(918)8228345

fdzgoeva@mail.ruhttps://orcid.org/0000-0003-4175-5365РемизовО. В.RemizovO. V.

Проф. Ремизов Олег Валерьевич, д-р мед. наук 

кафедра лучевой диагностики с лучевой терапией и онкологией

362040, Республика северная Осетия-Алания, г. Вла­дикавказ, ул. Пушкинская, д. 40. Тел.: 8(867)530397

Prof. Oleg V. Remizov, MD, PhD, DMedSci 

Department of Radiology with radiotherapy and oncology

Affiliations: 362040, Republic of North Ossetia- Alania,Vladikavkaz, Pushkinskaya, 40. Phone: 8(867)530397

oleg_remizov@mail.ruhttps://orcid.org/0000-0001-5310-889XГолоеваВ. Г.GoloevaV. G.

Голоева Виктория Герсановна, аспирант

Кафедра внутренних болезней №5

кафедра лучевой диагностики с лучевой терапией и онкологией

362040, Республика Северная Осетия-Алания, г. Вла­дикавказ, ул. Пушкинская, д. 40. Тел.: +7(960)4015003

Victoria G. Goloeva, postgraduate student 

Department of Internal Medicine №5

Department of Radiology with radiotherapy and oncology

Affiliations: 362040, Republic of North Ossetia-Alania Vladikavkaz, Pushkinskaya, 40. Phone: +7(960)4015003

vgoloeva@yandex.ruhttps://orcid.org/0000-0002-4183-2335ИкоеваЗ. Р.IkoevaZ. R.

Икоева Зарина Руслановна, аспирант

Кафедра внутренних болезней №5

кафедра лучевой диагностики с лучевой терапией и онкологией

362040, Республика Северная Осетия-Алания, г. Владикавказ, ул. Пушкинская, д. 40. Тел.: +7(918)8304719

Zarina R. Ikoeva, postgraduate student

Department of Internal Medicine №5

Department of Radiology with radiotherapy and oncology

Affiliations: 362040, Republic of North Ossetia-Alania Vladikavkaz, Pushkinskaya, 40. Phone: +7(918)8304719

zariikosha@mail.ruСеверо-Осетинская государственная медицинская академияРоссияNorth Ossetian State Medical AcademyRussian FederationСеверо-Осетинская государственная медицинская академия; Северо-Осетинская государственная медицинская академияРоссияNorth Ossetian State Medical Academy; North Ossetian State Medical AcademyRussian Federation2020310820202451828Copyright © Дзгоева Ф.У., Ремизов О.В., Голоева В.Г., Икоева З.Р., 20202020Дзгоева Ф.У., Ремизов О.В., Голоева В.Г., Икоева З.Р.Dzgoeva F.U., Remizov O.V., Goloeva V.G., Ikoeva Z.R.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://journal.nephrolog.ru/jour/article/view/1879

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.

In chronic kidney disease (CKD), progressive decline in kidney function leads to disorders of mineral metabolism, which are usually called secondary hyperparathyroidism. An increase in the serum concentration of the parathyroid hormone is associ­ated with a decrease in the level of calcium and calcitriol and/or an increase in the level of fibroblast growth factor-23 and inorganic phosphate in serum. CKD-related disorders of mineral and bone metabolism are associated with other metabolic disorders, such as acidosis, protein-energy wasting, inflammation, and accumulation of uremic toxins. This contributes to vascular calcification, which is a consequence of an imbalance between numerous inhibitors and promoters of soft tissue min­eralization. Vascular calcification is a degenerative process characterized by the accumulation of calcium and phosphate salts in the artery wall. This is observed in almost all vascular areas and can develop in the media, intima, or both vascular layers of the arteries. Calcification of the intima usually occurs due to atherosclerosis and may be responsible for coronary ischemic events. Conversely, media calcification is non-exclusive and predominantly develops along elastic fibers. As a result, media calcification increases vascular stiffness, aortic pulse wave velocity, systolic and pulse blood pressure, contributing to the de­velopment of left ventricular hypertrophy and heart failure. This review examines the current understanding of the mechanisms that lead to the development of vascular calcification in CKD. The participation of factors such as inflammation, age glycation end products, indoxyl sulfate, and others in calcification processes is discussed. Promising therapeutic goals associated with a new understanding of the mechanisms of cardiovascular calcification in CKD are identified.

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