Glomerulonephritis is a significant factor fueling the rapid increase in th
e population of patients with end-stage renal disease. Novel therapeutic st
rategies targeting specific mechanisms of glomerular destruction are the mo
st reasonable approaches to arrest ongoing injury. In this review, we summa
rize some of our results obtained in our effort to characterize the role of
15-lipoxygenase activation as one of the mechansisms operative during the
early, prefibrotic stage of glomerular immune injury. We also summarize the
effects of cytokines released during these processes, as well as the activ
ation by aspirin of the synthesis of 15-R-HETE (see text). Finally, we will
propose a clinical approach to this group of disorders, based on emerging
concepts of the pathophysiology of glomerulonephritis from our work and tha
t of several other investigators. Copyright (C) 2000 S. Karger AG, Basel.