ПОЧЕЧНЫЕ ГЕМОДИНАМИЧЕСКИЕ МЕХАНИЗМЫ ФОРМИРОВАНИЯ ГИПЕРТОНИЧЕСКОЙ НЕФРОПАТИИ

В обзоре рассматриваются современные представления о механизмах развития и прогрессирования гипертонической нефропатии, которая является одной из главных причин хронической болезни почек. Гипертоническая нефропатия является следствием нарушения работы почечных гемодинамических механизмов, защищающих клубочки от повреждающего действия повышенного артериального давления (АД). В результате в почках развиваются два принципиально разных патологических процесса – ишемическое и гипертрофическое повреждение клубочков, которые ведут к формированию фокально-сегментарного гломерулосклероза и нарастающей потере почечной функции. Причиной первого из них является избыточная ауторегуляторная реакция, осложняющаяся обструктивным гиалинозом афферентных артериол, ишемическим повреждением клубочков и потерей части функционирующих нефронов. Одновременно с ишемическим повреждением почек в сохранившихся нефронах развивается компенсаторный по своей природе феномен гиперфильтрации, ведущий к потере почечной ауторегуляции и стойкой гломерулярной гипертензии, которая становится главным фактором дальнейшего прогрессирования повреждения клубочков. В результате этих гемодинамических нарушений в почках развивается гипертрофический (пролиферативный) гломерулосклероз. Ключевую роль в его формировании играет гиперактивность клеточной РАС подоцитов, которая сопровождается избыточной продукцией TGF-β₁ , VEGF и PDGF, вызывающих профибротическую структурно-функциональную перестройку подоцитов и мезангиальных клеток клубочков. Существенный вклад в этот патологический процесс вносит также прямое механическое повреждение подоцитов и мезангиальных клеток, способствующее их склеротическому перерождению и развитию воспалительной реакции в окружающей мезангиальной ткани.

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