nefrНефрологияNephrology (Saint-Petersburg)1561-62742541-9439Pavlov First Saint-Petersburg State Medical University10.24884/1561-6274-2009-13-4-28-36nefr-1188Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESПОЧЕЧНЫЕ ГЕМОДИНАМИЧЕСКИЕ МЕХАНИЗМЫ ФОРМИРОВАНИЯ ГИПЕРТОНИЧЕСКОЙ НЕФРОПАТИИRENAL HEMODYNAMIC MECHANISMS DEVELOPMENT OF THE HYPERTENSIVE NEPHROPATHYКузьминО. Б.KuzminO. B.

кафедра фармакологии

460040, Оренбург, тел.: (3532) 77­ 49-66

o.kuzmin.orgma@yandex.ruБучневаН. В.BuchnevaN. V.

кафедра фармакологии

ПугаеваМ. О.PugaevaM. O.

кафедра фармакологии

Оренбургская государственная медицинская академияRussian Federation2009100420091342836Copyright © Кузьмин О.Б., Бучнева Н.В., Пугаева М.О., 20092009Кузьмин О.Б., Бучнева Н.В., Пугаева М.О.Kuzmin O.B., Buchneva N.V., Pugaeva M.O.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/1188

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.

In the review are examined the contemporary concepts about the mechanisms of development and progression of hypertensive nephropathy, which is of the main reasons for the chronic kidney disease. Hypertensive nephropathy is the consequence of disruption of the work of renal hemodynamic mechanisms, which protect glomeruli from the damaging action increased arterial pressure. As a result in the kidneys are developed two principally different pathologic processes – ischemic and hypertrophic damage of the glomeruli, which lead to the formation of focal-segmental glomerulosclerosis and increasing loss of renal function. The reason for the first of them is the excessive autoregulatory reaction, which is complicated by obstructive hyalinosis of afferent arterioles, by the ischemic damage of glomeruli and by the loss of the part of functioning nephrons. Simultaneously the ischemic damage of the kidney in the preserved nephrons compensating by its nature phenomenon of hyperfiltration, which leads to the loss of renal autoregulation and steadfast glomerular hypertension, which becomes the major factor for future progression of the glomerular damage, is developed. As a result these hemodynamic disturbances in the kidney is developed hypertrophic (proliferating) glomerulosclerosis. The key role in its formation plays the hyperactivity of the cellular RAS of podocytes, which accompanied by the excess produce of TGF-β1 , VEGF and PDGF, causing profibrotic structural-functional reconstruction of podocytes and mesangial cells. The significant contribution to this pathologic process introduces also the direct mechanical damage of podocytes and mesangial cells, the facilities their sclerotic regeneration and development of inflammatory reaction in the surrounding mesangial tissue.

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