The beneficial effects of HMG-CoA reductase inhibition in models of pr
ogressive glomerular injury may not all be due to reductions in circul
ating lipoproteins and decreases in glomerular lipoprotein deposition.
Indeed, HMG-CoA reductase inhibitors may have direct effects on glome
rular mesangial cells that could explain the amelioration of renal inj
ury. Specifically, HMG-CoA reductase inhibitors block the synthesis of
isoprenoids that are necessary for mesangial cell proliferation and o
ther important cell functions. Thus, protein isoprenylation may play a
critical role in the pathogenesis and treatment of lipid-induced glom
erular injury.