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)

Hyperlipidemia is a consistent feature of the nephrotic syndrome. In this study, low-density lipoprotein (LDL) metabolism has been investigated in nine patients with nephrotic syndrome and varying degrees of proteinuria. In subjects with moderate proteinuria (less than 10 g/d), total plasma cholesterol values were elevated to approximately 160% of normal due mainly to an increase in circulating LDL cholesterol. Metabolic studies showed that a defect in LDL clearance via the receptor pathway was responsible for its accumulation. The total amount of LDL apolipoprotein catabolized by this mechanism was only 55% of the value seen in controls; 60% more LDL was channelled into alternative, receptor-independent, catabolic pathways. Heavier proteinuria was associated with substantial increases in plasma triglyceride and very-low-density lipoprotein (VLDL) levels. The defect in LDL catabolism was aggravated by oversynthesis of the lipoprotein, which expanded the plasma LDL pool to 250% of normal. These observations indicate that the hyperlipidemia of the nephrotic syndrome is multifactorial in origin. The altered catabolism of LDL may be important in predisposing these subjects to premature atherosclerosis.
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PMID:Low-density lipoprotein metabolism in the nephrotic syndrome. 229 90

It has been established previously that nephrotic hyperlipidemia is characterized by both an increase in lipid synthesis and a defect in removal of lipoproteins. The relationship between these defects and altered albumin metabolism is uncertain. One hypothesis is that hepatic lipogenesis increases in parallel with albumin synthesis. To test this hypothesis, albumin synthesis was increased in nephrotic rats fed an 8.5% protein diet (LPN) by increasing dietary protein to 40% (HPN). Proteinuria was modulated in half of the rats fed 40% protein by enalapril (HPE). Albumin synthesis was the same in both HPN and HPE, but proteinuria was reduced in HPE compared to HPN, and so were serum cholesterol and triglycerides (TG). To examine the effect of serum albumin on lipid clearance in the absence of proteinuria, plasma clearance of chylomicrons (CM) and VLDL was measured in Nagase analbuminemic rats (NAR) and found to be no different than in normal SD rats. When proteinuria was induced in NAR and in SD rats, a severe and identical defect in both CM and VLDL clearance was acquired in both groups and blood lipid levels were increased to a similar degree in both groups. Neither hyperlipidemia nor defective removal of lipoproteins from the circulation are linked to albumin synthesis or serum albumin concentration but result, at least in part, from proteinuria. Postheparin lipoprotein lipase (LPL) activity was reduced slightly in nephrotic animals compared to nonnephrotic controls, but the most striking finding was a highly significant decrease in postheraprin LPL activity in normal NAR compared to SD rats (P less than 0.001), suggesting that reduced LPL activity is not responsible for reduced clearance of CM and VLDL in nephrotic rats.
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PMID:Proteinuria, not altered albumin metabolism, affects hyperlipidemia in the nephrotic rat. 238 6

A paediatric case of lipoprotein glomerulopathy, a new kidney disease characterized by glomerular lipoprotein thrombi, is reported. The patient had massive proteinuria from the age of 8 years, when the nephrotic syndrome was first detected. This was resistant to conventional treatment for more than 10 years. During the course of the disease, the hyperlipidaemia characteristic of hyper-pre-beta-lipoproteinaemia and elevation of apoprotein E persisted, and renal function gradually deteriorated. The renal histopathological findings from four biopsies were essentially the same, with storage of beta-lipoprotein in dilated, balloon-like glomerular capillary lumina. However, the number of glomeruli showing global sclerosis increased and tubulo-interstitial changes progressed in parallel with the gradual clinical deterioration. As in other cases reported in Japan some familial involvement has been noted.
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PMID:Long-term follow-up of a paediatric case of lipoprotein glomerulopathy. 239 77

The mechanisms responsible for hyperfiltration in diabetes mellitus (DM) as well as for the initiation and progression of diabetic nephropathy are not fully elucidated. Enhanced prostaglandin E2 (PGE2) production has been invoked in the former and thromboxane (TXB2) and hyperlipidemia in the latter. Fish oil (FO)-enriched diets can favorably alter eicosanoid synthesis and serum lipid profiles. We therefore examined the effects of a FO-enriched diet on glomerular filtration (GFR), proteinuria, glomerular eicosanoid production, and serum lipids in rats with streptozotocin-induced DM (STZ-DM). Groups of 5-8 rats with STZ-DM were maintained on low insulin and then pair-fed with isocaloric diets enriched with either FO (20% w/w) or beef tallow (BT; 20% w/w). GFR was determined in the same animals at onset of diet and after 8 and 20 weeks on the respective diets by [14C]inulin clearance using implanted osmotic minipumps each time. Significant hyperfiltration was present initially and GFR did not change on either diet for 20 weeks, in spite of a significant and greater than 50% decrease in all prostaglandins (PGE2, TXB2, PGF2 alpha, 6-keto, PGF1 alpha) produced by glomeruli isolated from DM/FO as compared to DM/BT or control rats. FO diet completely corrected the hypertriglyceridemia of diabetes and significantly reduced the mild and early proteinuria of DM. The decrease in proteinuria and the correction of hyperlipidemia of DM by a FO-enriched diet may be beneficial in the long term not only for the development of diabetic glomerulopathy, but also for the accelerated atherosclerosis of DM.
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PMID:Effects of fish oil on glomerular function in rats with diabetes mellitus. 240 55

In the last few years, remarkable advances have been made in the understanding of lipoprotein metabolism in the pathogenesis of renal disease in animal models and in vitro cell culture. Central to this work is the problem of the progression of renal disease in humans. This review recapitulates the theory (Lancet 1982; II: 1309-1312) that the progression of disease depends in part on the damage inflicted on the glomerulus by lipoproteins. The glomerular environment of high or low pressure, basement membrane damage, and destruction or damage of the mesangial and epithelial cells permits the filtration of protein, the consequence of which is hyperlipidemia. Whatever the therapeutic measures employed, if proteinuria persists, hyperlipidemia will follow. This suggest that lipoprotein toxicity may contribute to the final common path of renal damage in progressive renal disease. "Lipoprotein toxicity" in arteries is called atherosclerosis, but this term ignores the complexity of the glomerulus and the possible tubular damage that might be caused by filtered lipoprotein. It is clear there is insufficient knowledge of the metabolism of the damaged kidney to confidently attribute the pathology of progression of disease to any single process.
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PMID:Glomerular structures and lipids in progressive renal disease. 248 39

Progressive deterioration in renal function frequently occurs in the absence of the original cause of injury. During the past decade, intense investigations into the factors responsible for progressive nephron destruction have demonstrated that hemodynamic stresses and metabolic and coagulation abnormalities participate in glomerular injury. Hyperlipidemia is a common abnormality in renal disease and is frequently aggravated by protein-uria. Experimentally, therapy with the lipid-lowering agents clofibric acid or lovastatin reduced circulating lipids, particularly cholesterol, decreased proteinuria, and prevented glomerular damage in normotensive and hypertensive models of progressive renal disease. These beneficial effects occurred independently of changes in systemic blood pressure or glomerular injury, supporting the notion that cholesterol or its accompanying changes, or both, were central in lipid modulation of glomerulosclerosis. Clinically, lipid abnormalities are common in patients with renal disease, and atherosclerotic cardiovascular disease is the most frequent cause of death in these patients. Although the role of lipids in atherosclerotic disease has been well established, whether a similar effect of lipids occurs in the microvasculature of the kidney is unknown. Whether therapeutic approaches directed at reducing hyperlipidemia in patients with renal disease will provide a measure of renal protection, as has been seen in experimental models of renal disease, is also unknown.
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PMID:Therapeutic implications of lipid-lowering agents in the progression of renal disease. 248 40

The authors described the clinical, biologic and histologic particularities of two cases of congenital nephrotic syndrome, Finnish type. Clinically, the hydropic syndrome was represented by anasarca: biologically by marked proteinuria, hypoproteinemia with dysproteinemia and hyperlipemia with dyslipemia. Histologically both cases presented microcystic dilatation of the proximal tubuli contorti. The evolution was unfavorable and ended in death.
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PMID:[The Finnish-type congenital nephrotic syndrome. Comments on 2 cases]. 250 64

Using a complex stimulating mixture containing ADP, epinephrine and collagen, a significantly (p less than 0.002) enhanced platelet aggregability, expressed as platelet sensitivity factor (PSF) was noted in platelet rich plasma of patients with proteinuria (PSF = 472 +/- 125), as against normal weight normolipidemic control subjects (PSF = 32.76 +/- 2.67). A significantly negative correlation (r. -0.579; p less than 0.001) was found between serum albumin concentration and the logarithmic values of platelet sensitivity factor. Plasma von Willebrand factor activity expressed as a percentage of normal was also significantly (p less than 0.001) higher in proteinuric patients (287% +/- 25.8) than in control subjects (99% +/- 5.02), but this hemostatic variable did not correlate with the logarithm of platelet sensitivity factor. Platelet aggregability was higher in hyperlipidemic nephrotic patients than in proteinuric patients with normal serum lipids, while renal failure led to a decrease of platelet function. The raised plasma levels of von Willebrand factor noted in proteinuric patients were not influenced by either hyperlipidemia or by chronic renal failure. It is concluded that changes affecting platelet function in the nephrotic syndrome are produced by other mechanisms than these leading to an increase of endothelia-derived von Willebrand factor. Both changes may, however, contribute to the thrombotic tendency of nephrotic patients.
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PMID:Plasma von Willebrand factor antigen and activity and platelet aggregability in patients with proteinuria. 261 81

The available data indicate that in chronic renal failure (CRF) loss of renal function usually progresses at a constant rate toward end-stage renal disease. Although immunological events might be responsible for initiating most glomerular diseases, certain clinical and experimental observations suggest that the rate of progression of these diseases is influenced by several non immunological factors. These factors include systemic hypertension, proteinuria, hyperlipidemia, high protein intake, and probably conditions leading to glomerular hypertrophy. Interventions designed to minimize the potential contribution of these factors to the progression of renal insufficiency may halt or slow the loss of function at early and late stages of CRF.
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PMID:[Mechanisms of progression of glomerular sclerosis in chronic renal diseases in man]. 270 30

It is known that chronic alcoholics and type II diabetics show hyperlipidemia, characterized by hypertriglyceridemia and in a minor degree by hypercholesterolemia. The mechanisms underlying the effect of ethanol and carbohydrates on plasma lipids seem to be different; therefore in diabetic subjects chronic alcohol consumption could produce a more severe hyperlipidemia and so accelerate atherosclerotic events. In order to verify it we have measured plasma cholesterol, HDL-cholesterol, and triglycerides and investigated the presence of micro- and macroangiopathy in two groups of non-insulin-dependent diabetics, differing each other for daily alcohol intake (18 chronic male alcoholics and 30 male subjects consuming respectively more than 150 g and less than 50 g of alcohol daily). In alcoholics, no clinical features, laboratory and echographic findings of cirrhosis and pancreatic disease were present. In order to avoid a possible interference of other factors on the metabolism of plasma lipids, in our study patients were selected with the following criteria: 1) only male subjects; 2) age 40-60 years; 3) nonsmokers; 4) moderate coffee drinkers; 5) average physical activity; 6) with BMI less than 28; 7) in good diabetic control (HbA1c less than 6%, n.v. 4.4%-5.6%); 8) normal kidney function (plasma creatinine less than 1.3 mg%) and 24 hr proteinuria absent;) 9) in treatment with diet alone or diet plus low doses of sulphonylureas or biguanides. The data were analyzed by Student's "t" and chi-squared tests. No significant differences could be detected (alcoholics/occasional drinkers, means +/- 1 SD) either in the plasma levels of cholesterol (181.7 +2- 39.3/198.2 +/- 32.5), HDL-cholesterol (43.4 +/- 12.7/38.5 +/- 11.9), and triglycerides (105.5 +/- 56.4/159.7 +/- 114.8) and in the frequency of micro (22.2%/16.6%) and macroangiopathy (16.6%/26.6%) between the two studied groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of chronic alcohol consumption on blood lipid levels and angiopathy in diabetics]. 274 71


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