Renal disease is accompanied by characteristic alterations of lipoprotein m
etabolism, which appear as a consequence of nephrotic syndrome or renal ins
ufficiency and are primarily reflected in an altered apolipoprotein profile
rather than elevated plasma lipid levels. Their full characterization requ
ires identification of discrete lipoprotein particles. While nephrotic synd
rome results in increased concentrations of both cholesterol- and triglycer
ide-rich apoB-containing lipoproteins, renal insufficiency is characterized
by an accumulation of intact or partially metabolised triglyceride-rich ap
oB-containing lipoproteins. The dyslipidemia has been discussed as a contri
butory factor for the progression of renal insufficiency through developmen
t of glomerulosclerosis and tubulointerstitial lesions together with accele
rated atherosclerosis.
Several experimental studies have shown that hyperlipidemia accelerates ren
al damage. Lipid-lowering treatment can reduce renal lesions and preserve r
enal function. The documentation in human nondiabetic progressive renal ins
ufficiency is more limited. We have found that increased concentrations of
triglyceride-rich, but not cholesterol-rich, apoB-containing lipoproteins a
re, associated with a more rapid loss of renal function. The underlying pat
hophysiological mechanisms for the relation between triglyceride-rich apoB-
containing lipoproteins and progression of renal insufficiency are not full
y understood. Treatment with hypolipemic drugs may attenuate the renal dysl
ipidemia, but thus far there have been no reports about controlled clinical
trials testing the possible effect of such treatment on the progression of
renal insufficiency. In summary, there is evidence to suggest that some sp
ecific lipoprotein abnormalities are a risk factor for the progression of r
enal dysfunction, but the final test of such assumptions still rests on the
results of urgently needed controlled intervention studies.