ENDOTHELIAL DYSFUNCTION IN AUTOIMMUNE GLOMERULAR DISEASES: PATHOGENESIS AND EARLY DIAGNOSIS

Endothelial dysfunction plays a crucial role in the pathogenesis of autoimmune glomerular diseases. This thesis analyzes the structural and functional characteristics of glomerular endothelial cells and the mechanisms of their injury in autoimmune conditions. Immune complex deposition and anti-endothelial antibodies in lupus nephritis, neutrophil adhesion to endothelium in ANCA-associated vasculitis, and mesangial-endothelial interactions in IgA nephropathy are considered as primary causes of endothelial dysfunction. Complement dysregulation, oxidative stress, and cytokine effects are evaluated as common pathogenetic factors enhancing endothelial injury. The significance of early diagnostic markers of endothelial dysfunction, particularly von Willebrand factor, thrombomodulin, endothelin-1, and extracellular vesicles in blood and urine, is highlighted. Special attention is paid to the sensitivity of urinary endothelial markers in detecting local intrarenal endothelial damage and their prognostic value in the development of tubulointerstitial fibrosis. The thesis discusses the possibilities of early diagnosis and prediction of disease progression based on endothelial dysfunction markers, as well as the prospects of endothelium-targeted therapeutic strategies.