| Abstract: | ![]()
The aim of this review is to focus on the possible role of reactive oxygen species (ROS) in the pathogenesis of glomerulonephritis (GN) and to review the potential mechanisms of this ROS-mediated renal injury. This paper examines the literature which demonstrates ROS as primary mediators in GN, responsible for modifications of glomerular permeability to proteins, development of morphologic lesions and alteration of glomerular haemodynamics (reduction in glomerular blood flow and glomerular filtration rate). In glomeruli, ROS are generated by both infiltrating cells (neutrophils, monocytes) and resident glomerular cells (mesangial and endothelial cells and podocytes). The participation of ROS in glomerular damage was proved in many experimental studies by detection of products of oxidant injury in renal tissue or urine and by demonstration of a protective effect of antioxidants in those lesions. |
