Lipid abnormalities are an almost universal feature of renal diseases.
Although some rare primary lipid disorders, such as lecithin-choleste
rol acyl transferase deficiency are associated with renal disease, it
is generally thought that the most common forms of dyslipemia usually
do not cause renal injury per se. Nonetheless, recent clinical and exp
erimental studies suggest that lipid abnormalities similar to those in
volved in atherogenesis may also contribute to renal damage, particula
rly when proteinuria or hypertension are also present. However, there
is a lack of adequate studies to assess whether antilipemic therapy ma
y attenuate the progression to end stage renal disease. It has been re
cently suggested that treatment with HMG-CoA reductase inhibitors may
retard the evolution of diabetic nephropathy. Recent studies show that
HMG-CoA reductase inhibitors may have direct renal beneficial effects
not mediated by their lipid lowering action. A better understanding o
f the mechanisms of lipid-induced renal injury and its modulation by a
ntilipemic agents may improve our therapeutic approach to prevent the
progression to end-stage renal disease.