nidНефрология и диализNephrology and Dialysis1680-44222618-9801Российское диализное обществоnid-3276Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESНекоторые механизмы формирования тубулоинтерстициального компонента при хронических заболеваниях почек (Обзор литературы)Some mechanisms of the pathogenesis of tubulointerstitial damage in chronic renal diseasеsКартамышеваН. Н.KartamyshevaN. N.noemail@neicon.ruЧумаковаО. В.TchumakovaO. V.noemail@neicon.ruНИИ Педиатрии НЦЗД РАМН, МоскваRussian Federation20012806202533314317Copyright © Картамышева Н.Н., Чумакова О.В., 20252025Картамышева Н.Н., Чумакова О.В.Kartamysheva N.N., Tchumakova O.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.nephro.ru/jour/article/view/3276

Тубулоинтерстициальный компонент является важным признаком прогрессирования хронических заболеваний почек. Формирование изменений тубулоинтерстициальной ткани включает в себя инфильтрацию интерстиция воспалительными клетками, склероз интерстиция и атрофию канальцевого эпителия. В генезе воспалительных и иммунных механизмов при этом значительная роль принадлежит действию цитокинов и факторов роста, в частности моноцитарного хемоаттрактантного протеина 1 и трансформирующего фактора роста β. Последние исследования патогенеза изменений тубулоинтерстициальной ткани расширяют представление о механизмах хронического почечного поражения, результатом которых возможно окажется выявление новых подходов к диагностике и лечению хронических заболеваний почек.

Tubulointerstitial changes are important factor of progression of chronic renal diseases. The pathogenesis of the tubulointerstitial injury includes the influx of inflammatory cells in the renal interstitium, interstitial scarring and tubular atrophy. Cytokines and growth factors play an important role in this process, in particular monocyte chemoattractant protein 1, transforming growth factor β. Resent data on the pathogenesis of tubulointerstitial changes provide new understanding of the mechanisms of the chronic kidney damage. New observations regarding maneuvers which downregulate such injurious renal responses may direct further studies to develop new diagnostic and therapeutic modalities.

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