russjcardiolРоссийский кардиологический журналRussian Journal of Cardiology1560-40712618-7620«SILICEA-POLIGRAF» LLC10.15829/1560-4071-2021-4160russjcardiol-4160Research ArticleОБЗОРЫ ЛИТЕРАТУРЫREVIEWПричины развития и прогрессирования кардиоренального синдрома при хронической сердечной недостаточности. Методы профилактикиCauses of development and progression of cardiorenal syndrome in heart failure patients. Prevention methodshttps://orcid.org/0000-0001-7667-910XДавыдовВ. В.DavydovV. V.

Давыдов Владимир Валентинович — профессор, кафедра анестезиологии, реаниматологии и клинической фармакологии с курсом ДПО.

Барнаул

Barnaul

6davv@mail.ruhttps://orcid.org/0000-0002-7049-5585АрехинаЕ. Л.ArekhinaE. L.

Арехина Екатерина Леонидовна — зам. главного врача по медицинской части.

Барнаул

Barnaul

arehina_katerina@mail.ruФГБОУ ВО Алтайский государственный медицинский университет Минздрава РоссииРоссияAltai State Medical UniversityRussian FederationКГБУЗ Городская больницаРоссияCity HospitalRussian Federation20211702202126141604160Copyright © Давыдов В.В., Арехина Е.Л., 20212021Давыдов В.В., Арехина Е.Л.Davydov V.V., Arekhina E.L.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://russjcardiol.elpub.ru/jour/article/view/4160

Обзор включает данные о патогенезе кардиоренального синдрома (КРС) у пациентов с хронической сердечной недостаточностью (ХСН). Важной причиной его развития и прогрессирования определена почечная гипертензия. Рассмотрены механизмы ее формирования на фоне низкого сердечного выброса. В этих условиях развивалась вазокострикция в почках вследствие активации нейроэндокринных механизмов и внешняя компрессия паренхимы органа, обусловленная повышенным внутрибрюшным давлением. Оба механизма были причиной снижения скорости клубочковой фильтрации. Гипокалиемия часто сопровождала КРС. Ее связывали со снижением функции почек по механизму обратной связи. Дефицит калия в организме усугублял снижение сердечного выброса и провоцировал развитие аритмии. Это усиливало почечную гипертензию. Установлено, что избыточное применение фуросемида при терапии острой декомпенсации ХСН в некоторых случаях приводило к повреждению почек. Оно развивалось вследствие гиповолемии и гипокалиемии, при недостаточном контроле диуреза. Рассмотрены такие побочные эффекты фуросемида, как повышение активности нейроэндокринных механизмов с последующей вазоконстрикцией в органе и развитие эндотелиальной дисфункции вследствие активации окислительного стресса. Предложены два направления профилактики нефротоксических эффектов препарата. Предложенные методы профилактики показали обнадеживающие результаты.

The review includes data on the pathogenesis of cardiorenal syndrome (CRS) in patients with heart failure (HF). Renal hypertension has been identified as an important cause of its development and progression. The mechanisms of its formation in patients with low cardiac output are considered. In this setting, renal vasoconstriction, due to neuroendocrine activation, and external parenchymal compression, due to increased intra-abdominal pressure, developed. Both mechanisms were responsible for the decreased glomerular filtration rate. Hypokalemia has often accompanied by CRS. Potassium deficiency aggravated the decrease in cardiac output and provoked arrhythmias. This increased renal hypertension. High doses of furosemide in the treatment of acute decompensated HF sometimes damaged the kidneys due to hypovolemia and hypokalemia. Such side effects of furosemide as a neuroendocrine activation with subsequent vasoconstriction and the development of endothelial dysfunction due to oxidative stress are considered. Two directions of prevention of nephrotoxic effects of the drug are proposed. The proposed prevention methods have shown encouraging results.

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