Abstract
This short review of the various contributions of AA metabolites and ROS to renal injury in glomerulonephritis lets many uncertainties persist: (1) what are the respective roles of the resident glomerular cells and of the invading blood cells as sources of these mediators? (2) What is the specific role of each product, and is one of them particularly toxic? The response to the latter question will be facilitated by the use of new specific pharmacological tools, such as receptor antagonists, specific scavengers, or synthesis inhibitors apt to penetrate the cells.
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