Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism leading to hyperlipidemia in the nephrotic syndrome is not fully understood but may be related in part to loss of high density lipoproteins in the urine of patients with nephrosis. To prove this hypothesis, we compared serum lipoprotein profiles with the excretion of high density lipoproteins in urine in 19 nephrotic patients. Serum cholesterol ranged from 19-152 (median value 45) mg/dl in very low density lipoproteins (VLDL), from 130-443 (median 186) mg/dl in low density lipoproteins (LDL) and from 19-64 (median 33) mg/dl in high density lipoproteins (HDL). Hyperlipoproteinemia was found in 17 patients, which was classified as phenotype IIa (Fredrickson) in 2, as phenotype IIb in 9 and as phenotype IV in 6 subjects. Two patients showed normal lipoprotein patterns. VLDL- and LDL-cholesterol were not found in detectable amounts in urine, whereas HDL-cholesterol was measured in low concentrations from 0.1-8.3 mg/24 h in all samples. There was no correlation between serum HDL-cholesterol and urinary HDL-cholesterol, but a positive correlation between serum LDL-cholesterol and urinary HDL-cholesterol (r = +0.54, p less than 0.05). However, the total amount of the daily urinary loss of HDL (less than 1% of total plasma HDL) seems not to be sufficient to explain hyperlipoproteinemia in the nephrotic syndrome.
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PMID:Relation of hyperlipidemia in serum and loss of high density lipoproteins in urine in the nephrotic syndrome. 367 14

We have evaluated the effect of the antihyperlipidemic agent probucol on hyperlipidemia in patients with nephrotic syndrome. Twelve patients with long-standing nephrotic syndrome received 500 mg of probucol daily for 12 weeks. Serum total cholesterol, triglyceride, HDL-cholesterol and LDL-cholesterol were significantly lowered with probucol treatment. There were no differences in urine protein, serum total protein, serum albumin and renal function before and after probucol treatment. No drug-related side effects were observed during our study. These results indicated that probucol was effective against hyperlipidemia and free from side effects in patients with persistent nephrotic syndrome. The use of probucol is therefore suggested to be advisable when antihyperlipidemic treatment is required in some subgroups of nephrotic syndrome.
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PMID:Effect of probucol on hyperlipidemia in patients with nephrotic syndrome. 369 30

Although hyperlipidemia is a common feature of the nephrotic syndrome, the distribution of cholesterol among the plasma lipoproteins and the mechanism of the enhanced hepatic synthesis of lipoprotein lipids are not well understood. We studied the distribution of cholesterol among the plasma lipoproteins, as well as the relation between total cholesterol and plasma albumin concentration, oncotic pressure, and viscosity in 20 consecutive adult patients with uncomplicated nephrotic syndrome. The total plasma cholesterol (mean +/- S.D., 302 +/- 100 mg per deciliter [7.8 +/- 2.6 mmol per liter]) and low-density-lipoprotein cholesterol concentrations (215 +/- 89 mg per deciliter [5.6 +/- 2.3 mmol per liter]) were elevated in most patients, but the high-density-lipoprotein cholesterol level was normal or low (46 +/- 18 mg per deciliter [1.2 +/- 0.5 mmol per liter]) in 95 per cent of the patients. Thus, many hypercholesterolemic patients with unremitting nephrotic syndrome may be at increased risk for atherosclerotic heart disease. A significant inverse correlation was found between the total plasma cholesterol concentration and both the plasma albumin concentration (r = -0.528) and the plasma oncotic pressure (r = -0.674), but not the plasma viscosity (r = +0.319). Enhanced hepatic synthesis of lipoprotein lipids may be stimulated by a decreased plasma albumin concentration or oncotic pressure but does not appear to be due to changes in plasma viscosity.
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PMID:The hyperlipidemia of the nephrotic syndrome. Relation to plasma albumin concentration, oncotic pressure, and viscosity. 385 68

A qualitative and quantitative analysis of urinary lipids in the nephrotic syndrome is presented. The following lipids were identified in the urine of patients with the nephrotic syndrome: free cholesterol, cholesterol esters, triglycerides, free fatty acids, and phospholipids. Glass paper chromatography identified the cholesterol esters as palmitate, oleate, linoleate, and arachidonate, and identified the phospholipids as phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine. Urinary lipid excretion was much greater in patients with the nephrotic syndrome than in patients with chronic renal disease and minimal proteinuria, or in patients with hyperlipidemia from other causes. Urinary lipid excretion varied widely among the 13 patients with the nephrotic syndrome studied, and no quantitative correlation with serum lipid levels was observed. However, qualitatively at least, the proportion of cholesterol esters excreted in the urine was similar to the proportion of these esters in plasma. A good correlation was found between lipid excretion and glomerular permeability. Furthermore, during steroid therapy urinary lipid excretion decreased concomitant with a decrease in proteinuria. All these observations support the idea that lipiduria in the nephrotic syndrome is related to protein loss and that most of the lipid in the urine enters the glomerular filtrate in the form of lipoproteins.
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PMID:Qualitative and quantitative analysis of urinary lipids in the nephrotic syndrome. 603 40

A thirty-year-old woman, who had onset of nephrotic syndrome during the last part of her pregnancy, experienced recurrent acute ischemia of both lower limbs, leading to three conservative surgical procedures one month after delivery. Investigations disclosed no cause of embolism and were suggestive of thrombosis. The arteriography showed a diffuse reduction in diameter of the aorta and iliac vessels without localised stenosis or other vascular lesions. This complication is presumably related to several factors associated with the reduction in arterial diameter: hypovolemia, hyperfibrinemia, hyperlipidemia and abnormalities of hemostasis.
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PMID:[Acute ischemia of the lower limbs in nephrotic syndrome in a young woman]. 631 45

Advances in our understanding of the mechanisms of proteinuria in humans have depended on a variety of animal models. Most of these have been partially satisfactory because they require pretreatment of the animal with chemicals or toxins or they depend on an aging-related glomerular protein leakiness. The strain in this study was obtained by Koletsky after selective inbreeding of the offspring from a hypertensive Kyoto-Wistar and a normotensive Sprague-Dawley rat. The affected animals appear in 25% of the litters, indicating an autosomal recessive gene, and present with a spontaneous and progressive nephrotic syndrome detected as early as 3-5 weeks and associated with obesity, hypertension, hypoalbuminemia, hypercholesterolemia, and hyperlipidemia. Preliminary morphologic and immunofluorescence studies of their kidneys show progressive glomerular segmental sclerotic lesions and prominent mesangial deposition of IgM, a picture which resembles a steroid-resistant form of idiopathic nephrotic syndrome in humans, namely, focal glomerular sclerosis.
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PMID:Spontaneous nephrotic syndrome in a genetic rat model. 650 87

Chronic renal disease with secondary hyperlipidemia is highly atherogenic. In uremia and patients on chronic hemodialysis there is a high incidence of atherosclerotic complications whereas the incidence of atherosclerotic disease is relatively low in the nephrotic syndrome. This is surprising, as nephrosis produces type-II hyperlipidemia, which is usually highly atherogenic. In this study 10 patients (5 male, 5 female) with a newly diagnosed nephrotic syndrome were compared to 10 controls (5 male, 5 female). As laboratory parameters, lipids, lipoproteins (VLDL, IDL, LDL, HDL2 and HDL3 by rate zonal centrifugation) and the percentage composition of the major apolipoproteins in VLDL, HDL2 and HDL3, as well as lipoprotein lipase (LPL), hepatic lipase (HTGL) and lecithin-cholesterol-acyl-transferase (LCAT) were measured. In nephrotic patients significantly higher plasma levels of cholesterol, triglycerides, phospholipids, VLDL, IDL and LDL were found, whereas HDL-chol, HDL2 and HDL3 were unchanged. LPL and HTGL were both significantly impaired, whereas LCAT was distinctly increased. The percentage composition of apolipoproteins in HDL2 and HDL3 was normal. In nephrotic VLDL, apo-AI was distinctly increased at the expense of a decrease in apo-CII, and increased LCAT was explained by the relative rise of apo-AI in nephrotic VLDL. The increase in apo-AI in VLDL is discussed as a possible reason for the low atherogenic risk of secondary hyperlipidemia in nephrotic syndrome.
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PMID:[Lipoproteins, apolipoproteins, lipoprotein lipase, hepatic triglyceride lipase and lecithin cholesterol acyltransferase in patients with nephrotic syndrome]. 661 72

We investigated the severity and duration of hyperlipidemia in 59 nephrotic children during relapse and remission. Serum total cholesterol and triglyceride values were greater than or equal to 95th percentile for age and sex in all patients with minimal change nephrotic syndrome in relapse and in patients with non-MCNS and persistent proteinuria. Most of these patients also had a significant elevation of low- and very-low-density lipoproteins. A significant number of children with MCNS during prolonged remission had elevated serum concentrations of total cholesterol (46%), triglycerides (42%), LDL (29%), and VLDL (40%). Persistence and severity of lipid changes correlated well with duration of disease and frequency of relapses. Significantly decreased HDL and HDL/LDL were found in patients with non-MCNS and persistent proteinuria. Our results suggest that nephrotic children may have prolonged periods of hyperlipidemia even after clinical remission. In addition, some of these children with significantly decreased HDL/LDL may be at increased risk of developing premature atherosclerosis.
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PMID:Persistence of serum lipid abnormalities in children with idiopathic nephrotic syndrome. 669 Jun 76

Serum total cholesterol and triglycerides were measured in 18 nephrotic and 14 control children. The values of the two lipids were significantly elevated in nephrotic children. The control values also were elevated when compared with normal values in Nigerian adults. There was a positive linear correlation between serum total cholesterol and triglycerides, so that one of them could be used for follow-up of patients. Hyperlipidaemia constitutes an additional factor in the poor prognosis of Nigerian children with nephrotic syndrome. Longitudinal studies of serum lipids in nephrotic children are advocated.
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PMID:Serum cholesterol and triglycerides in childhood nephrotic syndrome in northern Nigeria. A preliminary report. 672 84

Plasma lipids and 6 plasma apolipoproteins (apoA-I, apoA-II, apoB, apoC-I, apoC-II and apoC-III) were studied in 23 patients with nephrotic syndrome. The elevated total cholesterol, triglyceride and apoB levels in nephrotic patients decreased gradually, after the disappearance of proteinuria. During the acute stage high density lipoprotein cholesterol, as well as the sum of apoA-I and apoA-II were similar in the patients and the controls. ApoA-I and apoA-II were transiently elevated during the recovery stage. All three apoC proteins (apoC-I, apoC-II and apoC-III) were elevated during the acute stage. A significant decrease in apoC-I, apoC-II and apoC-III was observed during the first 3 weeks after normalization of the urine protein. The ratio of apoC-II/apoC-III was reduced during the first 4 weeks after normalization of urine protein and then returned to the control level. The results suggest that as far as total levels are concerned, changes of apoC-II, apoC-III and the ratio of apoC-II/apoC-III appear to have no effect on the development of hyperlipidemia in th nephrotic syndrome.
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PMID:Lipid and apolipoprotein levels in patients with nephrotic syndrome. 679 92


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