Аннотация
Immunoglobulin A nephropathy is the most common primary glomerular disease worldwide and remains a leading cause of chronic kidney disease and end-stage kidney failure. The disease is characterized by mesangial deposition of galactose-deficient immunoglobulin A1 (Gd-IgA1)-containing immune complexes, which initiate complement activation, glomerular inflammation, and progressive renal fibrosis. Despite decades of research, conventional treatment strategies have largely focused on supportive therapy, including optimized blood pressure control, renin–angiotensin system blockade, and lifestyle modification. However, advances in the understanding of IgAN pathogenesis have led to the development of novel targeted therapies that address key pathogenic pathways. These include targeted-release budesonide, endothelin receptor antagonists, complement inhibitors, B-cell activating factor inhibitors, APRIL-targeted therapies, sodium-glucose cotransporter-2 inhibitors, and other emerging immunomodulatory agents. In parallel, advances in biomarker discovery, multi-omics technologies, artificial intelligence, and precision medicine are improving risk stratification and enabling individualized therapeutic approaches. This review summarizes current knowledge regarding the pathophysiology of IgA nephropathy, recent therapeutic innovations, clinical outcomes, and future directions for personalized disease management.