抄録
Recently, presence of urinary HDL, LDL, apolipoproteins and hypoalphalipoproteinemia has been indicated in nephrotic syndrome of both human and experimental rats. In order to study the mechanism of abnormal lipid metabolism in patients with nephrotic syndrome, serum concentration of HDL cholesterol, apolipoprotein AI and urinary excretion of cholesterol, apolipoprotein AI were measured in 19 patients with chronic proteinuria of 0.7-20g/24hr. for more than two years. Indirect immunofluorescence of the renal biopsy specimens was also examined.
It was found that (1) serum concentration of HDL cholesterol and apoAI were lower significantly in patient with chronic proteinuria than in normal male controls (n=15, age 25-50), (2) positive correlations were found between urinary cholesterol, apolipoprotein AI excretion and proteinuria (g/24hr.), (3) electrophoresis of urinary lipoproteins in 8 subjects with urinary cholesterol of over 5mg/24hr. revealed an existence of HDL in all eight cases, and negative correlations were found between the serum concentration of apolipoprotein AI, HDL cholesterol and urinary excretion of apolipoprotein AI. Existence of LDL was shown in 3 of them. In prolonged nephrotic patients with urinary excretion of lipoproteins, apolipoprotein AI, CIII, B were localized in lysosomes of the tubular epithelium by fluorescent microscopy. These results suggest that HDL and LDL filtrated through damaged glomerular basement membrane were partly reabsorbed into the lysosomes of proximal tubular epithelium. Apolipoprotein deposits were not seen in the specimens from mild nephrotic patients or from non-nephrotic, chronic glomerulonephritis, suggestting that hyperpermeability and hyposelectivity due to severe damages of glomerular basement membrane have occured in prolonged nephrotic state.
