[The role of oxygen radicals in the pathogenesis of glomerulonephritis]

In the pathogenesis of glomerulonephritis, acute renal failure, pyelonephritis and other diseases of the kidneys oxygen radicals are involved. Some types of glomerulonephritis are characterized by infiltration of the glomeruli by neutrophils and monocytes which can form oxygen radicals (superoxide, hydrogen peroxide). The increased amount of cAMP in glomeruli can be due to oxygen radicals. Cyclic nucleotides modulate the inflammatory or immune response in glomerular disease and play a part in the action of local mediators of the inflammation. Oxygen radicals act as second messenger for the activation of cytokines via NF-kappaB transcription factor, they stimulate the formation of TNF-alpha, IL-1, IL-6 and influence the expression of monocyte-specific cytokines (CSF-1 and MCP-1). Radicals formed by the system myeloperoxidase--hydrogen peroxide--halogen derivatives activate proteolytic enzymes (proteinases) which break down collagen and other components of the extracellular matrix present in the basal membrane of glomeruli and in the mesangium. Oxygen radicals and proteinases can cause and amplify glomerular damage. Glucocorticoid administration leads to an increased activity of endogenous antioxidant enzymes in the glomerulus and reduced the of lipid peroxidation.