Lipoprotein metabolism in nephrotic syndrome in childhood.

In nine patients with proteinuric nephrotic syndrome (NS), significant negative correlations were shown between plasma albumin and cholesterol (r=-0.85, p less than 0.005) and between plasma albumin and low density lipoprotein (LDL)-apoprotein B (ApoB) (r=-0.84, p less than 0.005), whereas there was no such correlation in ten matched ntrol patients. LDL-ApoB (182.8 +/141.2 MG/DL), cholesterol (249.3 +/-190.2 mg/dl) and triglycerides (40.8 +/- 23.5 mg/dl) were all elevated above controls. Control values: LDL-ApoB: 75.4 +/-25.0 mg/dl, -cholesterol: ll9.3 +/-27.6 mg/dl and -triglycerides: 29.2-17.9 mg/dl. The patients with proteinuric NS also exhibited a negative correlation between plasma triglyceride levels and plasma lipoprotein lipaseactiveiy (r=-0.79, p less than 0.02), which was not observed in controls. The hepatic triglycerice lipase (H-TGL) showed a mean activity of 22.2 +/- 10.7 mumol/ml FFA, which was not different form the control value of 21.2 +/-3.9 mumol/ml FFA. Not only LDL-cholesterol values were elevated in the patients with proteinuric NS, but high density lipoprotein (HDL)-cholesterol as well. HDL-cholesterol in proteinuric NS: 68.6 +/- 29.0 mg/dl, controls: 45.7 +/- 8.5 mg/dl. Twelve patients with NS in remission showed no correlation between plasma albumin and cholesterol and plasma albumin and LDL-ApoB respectively. The concentrations of LDL-ApoB (92.2 +/- 24.5 mg/dl),-cholesterol (121.7 +/- 37.1 mg/dl) and -triglycerides (28.9 +/-18.9 mg/dl) were within the normal range. No significan correlation was found between plasma triglyceride levels and plasma lipoprotein lipase activity (r=0.38, p greater than 0.2), and H-TGL activity, at 24.1 +/-9.3 mumol/ml FFA, was not different from control. In contrast to the complete normalization of LDL-cholesterol level, the HDL-cholesterol level remained slightly above control (HDL-cholesterol: 57.0 +/- 17.6 mg/dl). The hyperlipoproteinaemia in NS represents a combination of an increasents a combination of an increased hepatic lipoprotein synthesis and a decreased catabolism of triglyceride rich lipoproteins as indicated by an insufficiency of the lipoprotein lipase. The simultaneous elevation of LDL- and HDL-cholesterol suggests at most a moderate degree of atherogeneity of the hyperlipoproteinemia in NS.