Post‐prandial lipoprotein metabolism in nephrotic syndrome

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Abstract
Post‐prandial lipaemia was investigated in a group of nine subjects with nephrotic syndrome by following the concentrations of triglyceride and retinyl palmitate in the d< 1.006 g ml‐1 fraction of plasma after a standard oral fat load containing vitamin A. Lipoprotein lipase and hepatic triglyceride lipase activities were measured in post‐heparin plasma. Subjects with other renal disease but insignificant protein‐uria acted as controls. The time course of the lipaemic response was similar in both groups although individual patients demonstrated a prolonged lipaemia. Overall, there were no significant differences in the rise in triglyceride at 6 h (nephrotic—median 2.53 mmol 1‐1; range 0.87–4.76 vs. control 1.88; 0.38–4.12, p= 0.34), the peak concentration of retinyl palmitate (nephrotic 0.87 mg dl‐1; 0.27–2.16 vs. control 0.65; 0.24–1.89, P= 0.97) or the areas under the curve from 0.24 h for triglyceride (nephrotic 10.5 mmol. h l‐1; 2.9–43.6 vs. control 9.7; 4.3–27.0, P=l.0) or retinyl palmitate (5.5 mg.h dl‐1; 1.0–23.4 vs. 4.3; 1.5–12.4, P= 0.7). At baseline, the particles in the d < 1.006 g ml‐1 fraction of plasma from nephrotic subjects had a higher free cholesterol: phospholipid ratio but this difference was no longer apparent 6 h after the test meal. There were no differences in total heparin‐releasable lipase, lipoprotein lipase or hepatic triglyceride lipase activities between the two groups. These data suggest that impaired clearance of chylomicrons is not a major contributor to nephrotic hyperlipidae‐mia in man.