The generation of reactive oxygen species (ROS) has been recognized as a common pathway of tissue damage in a wide range of seemingly unrelated disorders like atherosclerosis or reperfusion injury [1, 2]. Not surprisingly therefore a growing body of evidence suggests that ROS are also important mediators in renal disease where they have been noted to be of importance in vascular, glomerular, tubular and interstitial damage [3-7]. In this review we will give a short description of the nature of ROS, their intrarenal production as well as their degradation by local defense mechanisms. We then will focus on the impact of ROS in glomerular injury trying also to summarize the experimental as well as human data (as far as they are available) as to how 'antioxidants' might be effective drugs for the treatment of specific disorders.