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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been postulated that hyperlipidemia in the nephrotic syndrome is due to overproduction of lipoproteins and that low colloid osmotic pressure (due to hypoalbuminemia) triggers this. Secretion of very low density lipoproteins (VLDL) by cultured rat hepatocytes has been shown to be inhibited by albumin, globulins, and dextrans, but the effect did not correlate with osmolarity. In the present studies we tested the hypothesis that viscosity rather than osmolarity might be the parameter determining the effectiveness of macromolecules in inhibiting VLDL synthesis and secretion by cultured rat hepatocytes. Synthesis and secretion of VLDL was measured in terms of incorporation of [3H] glycerol into medium triglycerides and also from changes in the mass of secreted VLDL triglycerides and apoproteins. The viscosity of the culture medium was increased by addition of dextran-500, gelatin or methylcellulose MX 880. Synthesis and secretion of VLDL was inhibited in direct proportion to increasing viscosity. At a viscosity of 2, which is about that of normal plasma, VLDL secretion was reduced by 20%. An inhibition of 60-70% in secretion and 30-40% in synthesis of VLDL lipid and protein components was observed at a relative viscosity of approximately 3.7. This viscosity was obtained by addition of any of the following: 3% dextran, 3% gelatin, 0.2% methylcellulose, or a combination of 0.1% methylcellulose plus 2% gelatin. Thus, similar viscosities resulted in similar degrees of inhibition despite differences of up to 16-fold in mass concentration and up to 20-fold in osmolarity.
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PMID:Viscosity of culture medium as a regulator of synthesis and secretion of very low density lipoproteins by cultured hepatocytes. 706 16

There is current debate as to whether or not the hyperlipidaemia seen in patients (1) with chronic renal insufficiency, (2) on regular dialysis treatment and (3) after successful renal transplantation should be specifically treated. The reduced HDL cholesterol fraction suggests that the risk of cardiovascular complications may be increased. Therapeutic possibilities include increased physical exercise and a reduction of carbohydrate intake. If these measures fail, then treatment with clofibrate or bezafibrate should be considered. The recommended dosage of clofibrate is 1.0-1.5 g/week (with CPK-control), and of bezafibrate is 400-500 mg/week in patients with chronic renal insufficiency (creatinin-clearance below 20 ml/min). In patients on regular dialysis treatment plasma lipids are reduced by adding carnitine. Most investigators believe that a specific therapy of the hypercholesterolaemia and hypertriglyceridaemia of patients with nephrotic syndrome is not necessary since the disturbances in fat metabolism are associated with an increased levels of HDL-cholesterol. With remission of the nephrotic syndrome an improvement of the hyperlipoproteinaemia is observed. If patients with acute renal failure are under parenteral nutrition fat infusion is recommended once per week to avoid a deficiency of essential fatty acids which is augmented by daily dialysis therapy.
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PMID:[Fat and renal failure--therapeutic aspects]. 713 29

Plasma-mediated inhibition of normal lymphoproliferation is an unexplained immunologic abnormality frequently observed in nephrotic syndrome. Since hyperlipidemia, also common in nephrotic syndrome, has been linked with in vitro and in vivo immunodeficiency in other diseases, we have quantitated plasma-mediated inhibition of lymphoproliferation and related it to the degree of hyperlipidemia in 19 patients with nephrotic syndrome. Fifteen patients were hyperlipidemic; the plasma of 9 of these 15 caused greater than 60% inhibition of antigen-specific proliferative responses of normal lymphocytes. None of the four normolipidemic plasmas, nor a hyperlipidemic plasma depleted of lipoproteins by ultracentrifugation, was inhibitory. A highly significant correlation between the degree of inhibition and the plasma triglyceride levels in patients with nephrotic syndrome was observed (P less than 0.001). The results suggest that elevated plasma lipids may be the cause of the plasma-mediated inhibition of lymphoproliferation in nephrotic syndrome.
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PMID:Plasma inhibition of lymphocyte proliferation in nephrotic syndrome: correlation with hyperlipidemia. 714 66

The relative importance of increased lipoprotein synthesis and decreased lipoprotein catabolism is examined in 13 patients with untreated nephrotic syndrome by the use of intravenous fat tolerance tests analysed in relation to other parameters of lipid metabolism. Increased lipoprotein synthesis in nephrotic patients was indicated by the fact that at a given fractional clearance rate of Intralipid (K2), nephrotic patients had higher serum TG concentrations than did control subjects. A defect in lipoprotein catabolism was also suggested by the frequent finding of intermediate density lipoproteins on electrophoresis and the marginally low (p = 0.05) mean K2 in nephrotic patients. A highly significant (p less than 0.001) positive correlation between HDL-cholesterol concentrations and postheparin fractional clearance rates (K'2) of Intralipid led to the speculation that in the severe nephrotic state (albumin less than 20 g/l) the loss of high density lipoproteins may contribute to the hyperlipidaemia.
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PMID:Hyperlipidaemia in untreated nephrotic syndrome, increased production or decreased removal? 731 85

Variations in lipid metabolism were studied in 20 children with chronic glomerulonephritis (CGN) associated with the nephrotic syndrome and 14 children with chronic renal insufficiency given protein deficient therapeutic diets. Suggestive abnormalities of lipid metabolism involved hyperlipidemia, hypercholesterinemia and hypertriglyceridemia (more sharply pronounced in patients with CGN associated with the nephrotic syndrome) as well as hyperlipoproteidemia, chiefly of types IY and IIB. Disproportions in lipoproteid spectra of the plasma towards increase in atherogenous beta- and pre-beta-lipoproteids are characteristic for patients of both groups but sharply pronounced in CRI. These patients also show a reduced metabolization efficacy coefficient (MEC) of essential fatty acids of food to the lipid structures of erythrocyte membranes. As a results of the treatment the lipid metabolism returned to normal in most patients with CGN and in part of the patients with CRI. In order to raise the efficacy of therapeutic diets during normalization of lipid metabolism in CRI it is recommended that the fat and carbohydrate components of the diet may be changed qualitatively with due regard for the types of hyperlipoproteidemia.
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PMID:[Changes in lipid metabolic indices in children with chronic kidney diseases under the influence of diet therapy]. 736 72

Diminished autologous LCAT activity was found in patients with proteinuria. This was due to substrate limitation and albumin appeared the most likely limiting factors. It is suggested that low albumin can contribute to the hyperlipidaemia of nephrotic syndrome through its role on the LCAT reaction. Evidence of the ability of triglyceride to enhance homologous LCAT activity was also noted.
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PMID:The mechanism of hyperlipidaemia in nephrotic syndrome--role of low albumin and the LCAT reaction. 738 46

Patients with analgesic nephropathy are reported to have a higher risk of atherosclerosis. One possible reason for this is a high incidence of hyperlipaemia in patients with analgesic nephropathy. In a retrospective study, serum cholesterol and serum triglyceride concentrations of patients with analgesic nephropathy and moderately restricted renal function were significantly higher compared to a control group with other renal diseases of similar age and degree of renal insufficiency. Hyperlipaemia in analgesic nephropathy is not explained by end-stage renal failure on one side or protein loss as in nephrotic syndrome on the other side. Some possible mechanisms for hyperlipaemia in analgesic nephropathy are discussed.
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PMID:Hypercholesterolaemia and hypertriglyceridaemia in patients with analgesic nephropathy. 741 66

Hyperlipidemia is one of the main features of nephrotic syndrome (NS), which has been reported to be important in the pathogenesis of mesangial cell proliferation. In an attempt to understand if LDL of the NS patients is more nephrotoxic on the development of mesangial cell proliferation, serum lipoprotein composition of normal controls, patients of NS untreated and treated with steroid drugs were measured, moreover, the influence of LDL from each group of patients on the proliferation of human mesangial cell (HMC) were observed. Lipoprotein composition was measured by enzymic methods. LDL was prepared by ultracentrifugation and used within three weeks. HMC was cultured and identified by classical methods, mesangial cell proliferation was observed by 3H-TdR incorporation according to the dose of LDL from 20-1000 micrograms/ml and time from 24 hours to 72 hours. Our results indicated that: 1. Both the NS patients untreated and treated with steroid drugs showed hypercholesterolemia and hypertriglyceride, serum low-density lipoprotein cholesterol (LDL-ch) concentration were higher in these patients than in the normal control group but there was no significant difference between NS untreated and treated groups. 2. LDL from normal controls or NS patients had biphasic effect on HMC proliferation. Low concentration stimulated HMC proliferation in concentration dependent and time-dependent manner, where as high concentration inhibited HMC proliferation. There was no significant difference on the effect of HMC proliferation between NS untreated and treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of LDL on human mesangial cell proliferation]. 760 Aug 66

Pharmocologic treatment of the hyperlipidemia associated with the nephrotic syndrome with lovastatin has been previously shown to be safe and effective. However, there is no information on the effect of lovastatin treatment on plasma lipoprotein(a) [Lp(a)] levels in patients with the nephrotic syndrome. We administered lovastatin (40 to 80 mg/day) to 20 adult patients with unremitting nephrotic syndrome for 8 weeks to assess its effect on plasma Lp(a) and other plasma lipid concentrations. Apoprotein(a) (apo(a)) phenotype was determined in all patients. Patients were grouped according to their plasma Lp(a) levels. Those with elevated plasma Lp(a) (> or = 30 mg/dL) were placed in group I and those with normal Lp(a) levels (< 30 mg/dL) were placed in group II. Mean total cholesterol and LDL cholesterol were similarly and significantly reduced in groups I and II (-35.9% and -43.3%, P < 0.0005, P < 0.0005 group I, and -31.0% and -42.0%, P < 0.02, P < 0.03 group II, respectively). The median reduction in plasma Lp(a) was -32% (P < 0.003) in nephrotic patients in group I, whereas the median decline in plasma Lp(a) levels in nephrotic patients in group II was only -8.0% (P = 0.052). The overall frequency of the high molecular weight (M(r)) apo(a) phenotype S4 was 70% in nephrotic patients. There was no correlation between plasma Lp(a) and apo(a) phenotype. Treatment with lovastatin results in a favorable response in terms of total and low-density lipoprotein cholesterol lowering in patients with the nephrotic syndrome; however, plasma Lp(a) levels are uniformly and significantly reduced only in nephrotic patients with elevated baseline plasma Lp(a) concentrations. There was no correlation between plasma Lp(a) concentration and other lipid and biochemical parameters.
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PMID:Reduction of lipoprotein(a) following treatment with lovastatin in patients with unremitting nephrotic syndrome. 761 Dec 49

The nephrotic syndrome is characterized by reduced plasma albumin and colloid osmotic pressure (pi), urinary protein loss and hyperlipidemia. High-density lipoprotein (HDL) and the level of apo A-I, the principal apolipoprotein in HDL, is increased in nephrotic rats and rats with hereditary analbuminemia (NAR)--animals with virtually no albumin in plasma and reduced plasma pi, but without proteinuria, suggesting that urinary protein loss is not responsible for increased plasma apo A-I levels. We conducted these studies to determine the mechanism responsible for increased plasma apo A-I levels in the nephrotic syndrome and NAR and to determine whether reduced plasma pi or albumin was responsible for increased apo A-I. We first measured the clearance of 125I apo A-I HDL in NAR and rats with passive Heymann nephritis (HN) compared with normal Sprague Dawley (SD) control. Both the clearance of apo A-I and fractional apo A-I turnover rate (FTR) were significantly reduced both in HN (7.40 +/- 2.18% plasma pool/hr) and NAR (5.63 +/- 1.12) compared with SD (9.87 +/- 0.75). Total apo A-I turnover rate, which in steady state equals apo A-I synthesis rate, was also significantly increased in both HN (487 +/- 127 micrograms/100 g body weight/hr) and NAR (253 +/- 16), compared with SD (216 +/- 19). Thus decreased apo A-I catabolism and increased synthesis both contributed to increased apo A-I levels in HN and NAR. We then infused either f3p4roncotic human albumin or ficoll into two additional groups of HN for days in quantities sufficient to maintain plasma pi within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oncotic pressure on apolipoprotein A-I metabolism in the rat. 761 Dec 50


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