References

nid

Нефрология и диализ

Nephrology and Dialysis

1680-44222618-9801

Российское диализное общество

nid-585

Research Article

ОБЗОРЫ И ЛЕКЦИИ

REVIEWS AND LECTURES

Медиаторы воспаления при остром повреждении почек (Обзор литературы)

Mediators of inflammation in acute kidney injury

Хван

М. А.

Khvan

M. A.

khvanmarina@gmail.com

Национальный научный центр материнства и детстваРоссияNational institute for motherhood and childhood, Astana, KazakhstanRussian Federation

2013

20092024

152106115

2024

Хван М.А.

Khvan M.A.

Данная работа распространяется под лицензией Creative Commons Attribution 4.0.

This work is licensed under a Creative Commons Attribution 4.0 License.

https://journal.nephro.ru/jour/article/view/585

Острое повреждение почек (ОПП) является независимым фактором риска заболеваемости и летальности. По современным представлениям основную роль в патофизиологии ОПП играет воспаление. В различных моделях почечного повреждения (ишемических, септических, нефротоксических) продемонстрированы морфологические и/или функциональные изменения сосудистого эндотелия и/или канальцевого эпителия, сопровождающиеся привлечением в очаг повреждения лейкоцитов, включая нейтрофилы, макрофаги, натуральные киллеры и лимфоциты, с последующей инфильтрацией этими клетками ткани почки. Повреждающие факторы индуцируют синтез эндотелием и канальцевым эпителием воспалительных медиаторов, таких как цитокины и хемокины, что усиливает привлечение лейкоцитов в почечную ткань. Таким образом, воспаление является определяющим механизмом в инициации ОПП и обуславливает его длительность. В данном обзоре представлены современные сведения о медиаторах воспаления, участвующих в патогенезе ОПП.

Acute kidney injury (AKI) remains an independent risk factor for mortality and morbidity. Inflammation plays a major role in the pathophysiology of AKI. In ischemia, sepsis and nephrotoxic models the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leucocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokines by tubular and endothelial cells which contribute to the recruiting of leukocytes into the kidney. Thus, inflammation plays an important role in the initiation and extension phases of AKI. This review focuses on the inflammation mediators which contribute to the pathogenesis of AKI.

острое повреждение почеквоспалениецитокиныacute kidney injuryinflammationcytokines

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