Apolipoprotein B turnover in dialysis patients: its relationship to pathogenesis of hyperlipidemia.

Exogenously labelled Iodine-125-VLDL (very low density lipoprotein) was given intravenously to twelve dialysis patients and four normal controls. Specific activities of I-125-VLDL apoB (apolipoprotein B) and I-125-IDLapoB (intermediate density lipoprotein apolipoprotein B) were measured for forty-eight hours. Synthesis rates (flux) and fractional catabolic rates (FCRs) of VLDLapoB and IDLapoB for hyperlipidemic (n = 8), normolipidemic (n = 4) dialysis patients and controls (n = 4) were calculated. Dialysis patients had lower VLDLapoB FCRs than controls (p less than 0.05); hyperlipidemic dialysis patients had marginally raised VLDLapoB flux over normolipidemics (p = 0.0508), suggesting apoB production might play a greater role in the pathogenesis of hyperlipidemia. Hyperlipidemics had lower IDLapoB FCRs than controls (p = 0.01). IDLapoB flux was similar in all three groups. The discrepancy in VLDLapoB fluxes between hyperlipidemics and normolipidemics with similar IDLapoB fluxes suggested that VLDLapoB could be directly catabolized in hyperlipidemics. ApoB concentration was increased in VLDL, IDL of hyperlipidemics when compared with normolipidemics (p less than 0.05) and controls (p = 0.01). Hyperlipidemic VLDL plasma levels were relatively enriched with cholesterol when compared with controls, p less than 0.01, and normolipidemics, p less than 0.05. These factors might all contribute towards accelerated atherogenesis in hyperlipidemic dialysis patients.