원발성 신증후군과 당뇨병성 신증후군 사이의 고지혈증 양상의 비교

Abstract

Hyperlipidemia and hyperlipoproteinemia are major features of the nephrotic syndrome. Two mechanis- ms might contribute to nephrotic dyslipidemia' an overproduction and an impaired catabolism of apo-B containing lipoproteins. However, few studies were performed to determine whether nephrotic syndrome due to diabetes mellitus(DM) and primary glomeru- lonephritis(GN) have similar or dissimilar patterns of dyslipidemia. We reviewed the clinical records of patients witb the nephrotic syndrome in Yonsei Medical Center from January 1, 1991 to Feburary 28, 1995. Among 89 patients, 71 patients were primary GN(45 minimal change disease(MCD), 26 non-MCD) and 18 patients were diabetic nephropathy. I@n both groups, serum total cholesterol and triglyceride levels were increased and HDL-cholesterol levels were normal. The serum total cholesterol level was significantly higher in primary GN(489.7±128.2, 410.3 ± 158.2, 308.7±55.1mg/dl in MCD, non-MCD and diabetic nephropathy, respectively)(p<0.05). There was a significant direct correlation between the increment of serum total cholesterol and the decrement of serum albumin in primary GN(p<0.05), but not in diabetic nephropathy. And the ratio of increment of serum total cholesterol to the decre- ment of serum albumin was significantly lower in diabetic nephropathy than that in primary GN. The serum triglyceride levels were increased in both groups, and there was no significant difference between the groups. In conclusion, relatively milder hypercholesterolemia in diabetic nephropathy might be due to different mechanisms for dyslipidemia from primary GN. First, hepatic overproduction of cholesterol might be relatively mild in diabetic nephropathy. Second, despite of similar degree of hepatic overproduction, the removal of apo-B con- taining lipoproteins might be more 'impaired in primary GN. And the combination of these two mechanisms might be another mechanism. Further studies will be necessary to clarify the different mechanisms by measuring the amount of urinary loss of macromolecules, the activities of 3-hydroxy- Hyperlipidemia and hyperlipoproteinemia are major features of the nephrotic syndrome. Two mechanis- ms might contribute to nephrotic dyslipidemia' an overproduction and an impaired catabolism of apo-B containing lipoproteins. However, few studies were performed to determine whether nephrotic syndrome due to diabetes mellitus(DM) and primary glomeru- lonephritis(GN) have similar or dissimilar patterns of dyslipidemia. We reviewed the clinical records of patients witb the nephrotic syndrome in Yonsei Medical Center from January 1, 1991 to Feburary 28, 1995. Among 89 patients, 71 patients were primary GN(45 minimal change disease(MCD), 26 non-MCD) and 18 patients were diabetic nephropathy. I@n both groups, serum total cholesterol and triglyceride levels were increased and HDL-cholesterol levels were normal. The serum total cholesterol level was significantly higher in primary GN(489.7±128.2, 410.3 ± 158.2, 308.7±55.1mg/dl in MCD, non-MCD and diabetic nephropathy, respectively)(p<0.05). There was a significant direct correlation between the increment of serum total cholesterol and the decrement of serum albumin in primary GN(p<0.05), but not in diabetic nephropathy. And the ratio of increment of serum total cholesterol to the decre- ment of serum albumin was significantly lower in diabetic nephropathy than that in primary GN. The serum triglyceride levels were increased in both groups, and there was no significant difference between the groups. In conclusion, relatively milder hypercholesterolemia in diabetic nephropathy might be due to different mechanisms for dyslipidemia from primary GN. First, hepatic overproduction of cholesterol might be relatively mild in diabetic nephropathy. Second, despite of similar degree of hepatic overproduction, the removal of apo-B con- taining lipoproteins might be more 'impaired in primary GN. And the combination of these two mechanisms might be another mechanisom. Further studies will be necessary to clarify the different mechanisms by measuring the amount of urinary loss of macromolecules, the activities of 3-hydroxy-3-methylglutaryl-CoA-reductase(HMG-CoA-reductase), turn-over rates of LDL-apo B, fractional catabolic rates of LDL-apo B and LDL input rates