Our improved understanding of the mechanisms of glomerular injury has
allowed the design of novel therapeutic strategies to treat glomerulon
ephritis. While elimination of the etiologic factors continues to be a
difficult task, modulation of the inflammatory response seems more pr
omising at present. Several proinflammatory mediators have been identi
fied as therapeutic targets and their inhibition has ameliorated glome
rular injury in experimental animals. The role of anti-inflammatory mo
lecules and the phenomenon of immunotolerance have gained particular a
ttention and may prove to be useful therapeutically Mediators of tissu
e repair have been found to contribute to glomerular destruction, and
their inhibition was protective in a variety of experiments. In this r
eview we discuss some of these novel approaches which may be targeted
against human glomerulonephritis in the near future.