[Lipid metabolism in the nephrotic syndrome]

Hyperlipidemia is a common and serious complication in patients with chronic nephrotic syndrome which unremitted may result in accelerated atherosclerosis. Accumulation of lipids in glomeruli may moreover contribute to the progression of renal insufficiency in these patients.

Total cholesterol, HDL-cholesterol and its HDL2 a HDL3 subfractions, LDL-cholesterol, triglycerides, free fatty acids, apoprotein B, apoprotein A1 and lipoprotein (a) were determined before any immunosuppressive and/or hypolipidemic therapy in 15 patients (pts) with nephrotic syndrome (8 pts with proteinuria higher than 10 g/24 hrs-NS-A, 7 with proteinuria between 5 and 10 g/24 hrs-NS-B), 7 pts with glomerulonephritis with low proteinuria (GN) and 6 pts with autosomal dominant polycystic kidney disease (PKD). All pts had normal glomerular filtration rate.

Plasma cholesterol (10.26 +/- 2.22 vs. 4.75 +/- 0.66 mmol/1, p < 0.001), plasma triglycerides (4.03 +/- 1.64 vs. 2.17 +/- 0.12 mmol/1, p < 0.05), LDL-cholesterol (7.16 +/- 1.55 vs. 2.62 +/- 0.67 mmol/1, p < 0.001) and apoprotein B (1.92 +/- 0.47 vs. 1.11 +/- 0.31 g/1, p < 0.01) were significantly higher in NS-A than in PKD. There was no difference in total HDL-cholesterol and the ratio HDL2/HDL3 between investigated groups of pts. Lipoprotein (a) was higher in NS-A than in other investigated groups of pts. The differences between NS-B and PKD were less significant.

Disorder of lipid metabolism is more serious in patients with more severe nephrotic syndrome than in nephrotic patients with milder proteinuria. Hypercholesterolemia is complicated in these subjects by hypertriglyceridemia and by the increase of apoprotein B and A1 and lipoprotein (a). Metabolic and renal consequences of these disorders depend undoubtedly on their duration and probably also on other factors (e.g. age, hypertension, long-term therapy with corticosteroids., etc.).