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Abstract
The dyslipidaemia in nephrotic-range proteinuria is believed to contribute to the
increased atherogenesis associated with the condition. Excess small dense low density
lipoprotein (LDLIII) contributes to this risk. Lipoprotein remnants (RLP) may also
be implicated but have not been studied in this population. We measured the plasma
concentration of low density lipoprotein (LDL) subfractions (by density gradient ultracentrifugation),
RLP (by immunoaffinity gel), very low density lipoprotein (VLDL) subfractions, post
heparin lipases and cholesteryl ester transfer protein (CETP) activity in 27 patients
with glomerular disease and albuminuria >2.0g. These were compared with 27 age and
sex matched controls. Proteinuric patients had increased LDLIII concentration (patients
182 (84:267) vs. controls 31 (27:62); P<0.0001) with reduced lighter LDLI (36 (24:43)
vs 69 (46:101); P<0.0005) and LDLII (124 (79:220) vs 178 (129:236); P<0.04, all mg/dl,
median+interquartile range). RLP-cholesterol (RLP-C) and triglyceride (RLP-TG) were
increased in proteinuric patients (RLP-C 18.9 (11.0:26.9) vs 7.7 (6.0:8.8); P<0.0001,
RLP-TG 35.8 (11.8:54.7) vs. 7.2 (4.3:10.0); P<0.0001, all mg/dl). Increased LDLIII
and RLP were independent of renal function. VLDL(1) and VLDL(2) concentrations were
increased by 258 and 260% (both P<0.0001). CETP activity was increased by 46% (P<0.005).
Lipoprotein and hepatic lipase activities did not differ from control values. LDLIII
concentration (r(2)=45.7%, P<0.001), RLP-C (r(2)=85.2%, P<0.001) and RLP-TG (r(2)=87.5%,
P<0.001) all correlated positively with plasma triglyceride. Moreover, increased LDLIII
was associated with both RLP-C (r(2)=31.3%, P<0.002) and RLP-TG (r(2)=33.6%, P<0.002).
Excess LDLIII and RLP are present in nephrotic-range proteinuria and add to the spectrum
of cardiovascular risk factors present in proteinuric patients. Increases in LDLIII
and RLP are closely related to plasma triglyceride. The association between excess
RLP and LDLIII suggests that RLP contribute to the increased atherogenicity attributed
to the atherogenic lipoprotein phenotype.