Abstract:
The review considers the mechanisms of podocyte damage underlying the development of proteinuria and progression of glomerulosclerosis in chronic glomerulonephritis and presents the results experimental and clinical studies on these issues. It is described that under the action of various immune and non-immune factors, podocytes form a stereotypic response to damage consisting in rearrangement of actin cytoskeleton, flattening of stem processes, detachment of podocytes
from the glomerular basal membrane and the appearance of specific podocytic proteins and/or whole
cells in the urine (podocyturia). Massive podocyturia in limited Proliferative ability of podocytes
contributes to the reduction of their total mass in the glomerulus (podocytopenia) and the development of glomerulosclerosis. The authors describe the spectrum of markers of podocytic damage, highlight the methods of their invasive and noninvasive assessment, analyze the relationship of their level with the severity of proteinuria and renal dysfunction, consider Prospects of the study of podocytic proteins in urine to assess the severity of glomerular damage, the risk of glomerulosclerosis.
