nefrНефрологияNephrology (Saint-Petersburg)1561-62742541-9439Pavlov First Saint-Petersburg State Medical University10.36485/1561-6274-2021-25-3-36-42nefr-1973Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESЭпидемиология и патофизиология гемолитико-уремического синдрома, ассоциированного с шига-токсином (обзор литературы)Epidemiology and pathophysiology of hemolytic uremic syndrome associated with shiga toxin (literature review)https://orcid.org/0000-0001-5860-856XБайкоС. В.BaikoS. V.

 Байко Сергей Валерьевич, д-р мед наук, проф. 1-я кафедра детских болезней

220016,  г. Минск, пр. Дзержинского, д. 83.

Тел.: +375 (17) 250-37-61 

Sergey V. Baiko MD, PhD, DMedSci, Prof.  1st Department of Pediatric

220016,  Minsk, Dzerginskogo Av. 83

Phone: +375(17)2503761

baiko@yandex.ruБелорусский государственный медицинский университетБеларусьBelarusian State Medical UniversityBelarus2021220420212533642Copyright © Байко С.В., 20212021Байко С.В.Baiko S.V.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/1973

Гемолитико-уремический синдром (ГУС), ассоциированный с шига-токсином Е. coli(STEC), относится к наиболее частым причинам острого почечного повреждения у детей раннего возраста. Доля STEC-ГУС среди всех вариантов ГУС составляет до 90 %. Не все STEC являются патогенными для человека, а те, которые вызывают заболевание (геморрагический колит, ГУС), относятся к энтерогеморрагическим E. coli(EHEC). К основным патогенам, вызывающим STEC-ГУС, относится серотип E. coli О157:Н7, реже серотипы O26, O80, О103, O121, O145. EHEC присутствуют в виде нормальной микробиоты у крупного рогатого скота, но также может обнаруживаться у коз, овец, свиней, цыплят, собак, крыс. Заражение может произойти при употреблении недостаточно термически обработанного говяжьего фарша, непастеризованного молока, воды, включая водопроводную и из открытых водоемов и бассейнов, от инфицированного человека и при посещении ферм, зоопарков. Эпидемиологический анамнез должен тщательно оцениваться у каждого пациента с ГУС, учитывая ежегодные вспышки данного заболевания в различных регионах мира. В последние годы активно обсуждается вопрос о переносе шига-токсина (Stx) из кишечника в кровь и из крови к органам-мишеням в виде микровезикул, стенкой которых является наружная оболочка E. coliи клеток крови. Это позволяет Stx избежать ответа иммунной системы человека. В статье подробно изложены механизмы заражения и экспрессии генов патогенности EHEC, описано влияния Stx на эндотелиальные клетки, экспрессию молекул адгезии и воспалительных хемокинов, активацию альтернативного пути комплемента, которые обуславливают развитие ГУС.

Hemolytic uremic syndrome (HUS) associated with shiga toxin E. coli(STEC) is one of the most common causes of acute kidney injury in young children. The share of STEC-HUS among all HUS variants is up to 90%. Not all STECs are pathogenic to humans, and those that cause disease (hemorrhagic colitis, HUS) are referred to as enterohemorrhagic E. coli(EHEC). The main pathogens causing STEC-HUS include the serotype E. coliO157: H7, less often serotypes O26, O80, O103, O121, O145. EHEC exist as normal microbiota in cattle, but can also be found in goats, sheep, pigs, chickens, dogs, and rats. Infection can occur when using undercooked ground beef, unpasteurized milk, water, including tap water and from open ponds and pools, from an infected person and when visiting farms and zoos. The epidemiological history should be carefully assessed in each patient with HUS, taking into account the annual outbreaks of this disease in different regions of the world. In recent years actively discussed the issue of the transfer of shiga toxin (Stx) from the intestine to the blood and from the blood to target organs in the form of microvesicles, the wall of which is the outer shell of E.coliand blood cells. This allows Stx to escape the response of the human immune system. The article describes in detail the mechanisms of infection and expression of pathogenic genes of EHEC, the effect of Stx on endothelial cells, on expression of adhesion molecules and inflammatory chemokines, activation of the alternative complement pathway, which determine the development of HUS.

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