Lipoprotein measurements in a group of 29 patients with massive protei
nuria and without hypoalbuminemia, were compared with those observed i
n matched controls and patients with overt nephrotic syndrome to asses
s the influence of plasma albumin concentration and proteinuria in mod
ulating blood lipid levels. Plasma apoprotein B and apo B containing l
ipoproteins were not increased in proteinuric normoalbuminemic patient
s. There was a good correlation between plasma albumin and oncotic pre
ssure (r = 0.937; P < 0.001). Plasma oncotic pressure was inversely co
rrelated with plasma apoprotein B in nephrotic patients (r = -0.44, P
= 0.017) but not in normoalbuminemics (r = 0.17, P = 0.369), suggestin
g that plasma albumin affects apoprotein B secretion. Other findings,
however, indicate that multiple processes are ocurring simultaneously
in these patients. There was an accumulation of very low- and intermed
iate density lipoproteins in normoalbuminemics, suggesting a residual
defect in the lipoprotein removal. Also, raised (P < 0.05) lipoprotein
(a) levels respect to controls (median, 0.15 g/l) were noted in both,
normoalbuminemics (median, 0.72 g/l) and hypoalbuminemics (median, 0.8
4 g/l) with similar degree of proteinuria (6.4 vs, 6.6 g/24 h), sugges
ting that other mechanisms may be operative in lipoprotein(a) derangem
ents. Our findings suggest that there is no unique mechanism in the pa
thogenesis of nephrotic hyperlipidemia but that both hypoalbuminemia a
nd proteinuria can have a distinct contribution, individually or in co
mbination.