Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic renal disease is accompanied by characteristic abnormalities of lipid metabolism, which appear as a consequence of nephrotic syndrome or renal insufficiency and are reflected in an altered apolipoprotein profile as well as elevated plasma lipid levels. Experimental and clinical studies have suggested a correlation between the progression of renal disease and dyslipidemia. High cholesterol and triglyceride plasma levels have been demonstrated to be independent risk factors for progression of renal disease in humans. The underlying pathophysiologic mechanisms for the relationship between lipid levels and progression of renal disease are not yet fully understood, although there are data that oxidative stress and insulin resistance may mediate the lipid-induced renal damage. In the animal model, lipid-lowering agents seem to ameliorate glomerular damage, preventing glomerulosclerosis and interstitial fibrosis. Although evidence from clinical studies indicates that statin therapy is associated with significant benefit in individuals with established chronic renal failure, whether lipid reduction can slow the renal functional decline awaits a primary renal outcome lipid-lowering therapy study.
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PMID:Lipids and renal disease. 1656 40

Dyslipoproteinemia is common in lupus patients. In this study, we investigated the pattern of dyslipoproteinemia in the course of active systemic lupus erythematosus (SLE) in possible association with anti-double-stranded DNA (anti-dsDNA) antibodies. Forty-six lupus patients under 45 years old who fulfilled the American College of Rheumatology revised criteria for the classification of SLE were selected. The exclusion criteria were renal failure, nephrotic syndrome, thyroid or liver disease, diabetes mellitus, obesity, pregnancy and taking drugs that induce dyslipidemia. Disease activity was measured by Systemic Lupus Erythematosus Disease Activity Index (SLEDAI). Comparison of the lipid profiles, between active and inactive groups determined high levels of serum TG and VLDL and low levels of serum HDL in active group in comparison with inactive group (P < 0.05). The results indicated that the levels of TG and VLDL were significantly elevated in the patients with positive anti-dsDNA (P < 0.05). Although, the mean of serum HDL levels was also lower in patients with positive anti-dsDNA, the difference was not significant. This pattern of dyslipoproteinemia in active SLE may be associated with the autoimmune mechanisms especially in relation to the presence of anti-dsDNA antibodies.
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PMID:Dyslipoproteinemia during the active course of systemic lupus erythematosus in association with anti-double-stranded DNA (anti-dsDNA) antibodies. 1694 55

Dyslipidemia is a potent cardiovascular (CV) risk factor in the general population. Elevated low-density lipoprotein cholesterol (LDL-C) and/or low high-density lipoprotein (HDL-C) are well-established CV risk factors, but more precise determinants of risk include increased apoprotein B (ApoB), lipoprotein(a) [Lp(a)], intermediate and very low-density lipoprotein (IDL-C, VLDL-C; "remnant particles"), and small dense LDL particles. Lipoprotein metabolism is altered in association with declining glomerular filtration rate such that patients with non dialysis-dependent chronic kidney disease (CKD) have lower levels of HDL-C, higher triglyceride, ApoB, remnant IDL-C, remnant VLDL-C, and Lp(a), and a greater proportion of oxidized LDL-C. Similar abnormalities are prevalent in hemodialysis (HD) patients, who often manifest proatherogenic changes in LDL-C in the absence of increased levels. Patients treated with peritoneal dialysis (PD) have a similar but more severe dyslipidemia compared to HD patients due to stimulation of hepatic lipoprotein synthesis by glucose absorption from dialysate, increased insulin levels, and selective protein loss in the dialysate analogous to the nephrotic syndrome. In the dialysis-dependent CKD population, total cholesterol is directly associated with increased mortality after controlling for the presence of malnutrition-inflammation. Treatment with statins reduces CV mortality in the general population by approximately one third, irrespective of baseline LDL-C or prior CV events. Statins have similar, if not greater, efficacy in altering the lipid profile in patients with dialysis-dependent CKD (HD and PD) compared to those with normal renal function, and are well tolerated in CKD patients at moderate doses (<or=20 mg/day atorvastatin or simvastatin). Statins reduce C-reactive protein as well as lipid moieties such as ApoB, remnants IDL and VLDL-C, and oxidized and small dense LDL-C fraction. Large observational studies demonstrate that statin treatment is independently associated with a 30%-50% mortality reduction in patients with dialysis-dependent CKD (similar between HD- and PD-treated patients). One recent randomized controlled trial evaluated the ability of statin treatment to reduce mortality in type II diabetics treated with HD ("4D"); the primary end point of death from cardiac cause, myocardial infarction, and stroke was not significantly reduced. However, results of this trial may not apply to other end-stage renal disease populations. Two ongoing randomized controlled trials (SHARP and AURORA) are underway evaluating the effect of statins on CV events and death in patients with CKD (including patients treated with HD and PD). Recruitment to future trials should be given a high priority by nephrologists and, until more data are available, consideration should be given to following published guidelines for the treatment of dyslipidemia in CKD. Additional consideration could be given to treating all dialysis patients felt to be at risk of CV disease (irrespective of cholesterol level), given the safety and potential efficacy of statins. This is especially relevant in patients treated with PD, given their more atherogenic lipid profile and the lack of randomized controlled trials in this population.
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PMID:Statins for treatment of dyslipidemia in chronic kidney disease. 1729 64

Secondary dyslipidemias may develop as a result of other diseases or some major exogenous influences. The most common are secondary dyslipidemias due to the following diseases: poorly controlled diabetes mellitus, hypothyreosis, hyperfunction of suprarenal glands, cholestasis, chronic renal diseases (chronic renal failure, nephrotic syndrome), acute infectious diseases. A very common cause of secondary dyslipidemia is abuse of alcohol. Also some drugs may induce dyslipidemias: corticosteroids, immunosuppressive drugs, less frequently also thiazide diuretics and non-selective beta-blockers. Secondary dyslipidemia is physiologic during pregnancy. If causal treatment of secondary dyslipidemia is possible, hypolipidemic drugs are not indicated. The decision to initiate treatment with hypolipidemic drugs depends on the degree of risk of a fatal cardiovascular event rather than on the blood lipids level. When hypolipidemic treatment is indicated, the choice of the drug and its dose also depends on the type of the primary disease and its severity.
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PMID:[Secondary dyslipidemias and their treatment]. 1757 73

Hyperlipidemia has been well recognized as a striking feature of nephrotic syndrome and other renal diseases. However, the underlying pathophysiological mechanisms still have not yet been elucidated. In this study, we evaluated acylation-stimulating protein (ASP) and complement component 3 (C3) in children (n=48) with various forms of proteinuric renal disease [nephrotic syndrome, acute poststreptococcal infection glomerulonephritis (APSGN), and lupus nephritis (LN)] in comparison with age- and gender-matched controls (n=279). In children with proteinuric renal disease, various aberrations in plasma lipids were noted, including increased triglyceride, cholesterol, and low-density lipoprotein cholesterol (LDL-C) (all p<0.0001). Whereas C3 was not altered in children with nephrotic syndrome (1.05+/-0.05 g/L vs. 1.29+/-0.04 controls), the decrease was pronounced in children with LN and APSGN (0.42+/-0.11, p<0.05 and 0.30+/-0.06, p<0.001, respectively). Plasma C3 correlated positively with lipid parameters [triglyceride, cholesterol, LDL-C, apolipoprotein B (apoB), high-density lipoprotein cholesterol (HDL-C) and apoA1] and inversely with total protein, blood urea nitrogen, and creatinine. By contrast, plasma ASP was significantly elevated in all proteinuric renal diseases (101.4+/-7.1 nmol/L nephrotic syndrome, 90.9+/-14.1 LN, and 81.8+/-7.2 APSGN vs. 44.3+/-1.5 controls, p<0.05 to p<0.001), and this increase was correlated with changes in lipid parameters (triglycerides and apoA1). In summary, these results demonstrate alterations in C3 and ASP that may contribute to or compensate for dyslipidemia.
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PMID:Increased plasma acylation-stimulating protein in pediatric proteinuric renal disease. 1825 59

It has been proposed that nephrotic syndrome is a consequence of an imbalance between oxidant/antioxidant statuses. The present study aimed to assess oxidant and antioxidant status in relation to dyslipidemia in children during remission and relapse phases of steroid sensitive nephrotic syndrome (SSNS). The study dealt with 40 children diagnosed as SSNS. They were categorized into two subgroups. The first subgroup included 25 children during remission stage. The second subgroup included 15 children during relapse. Control group consisted of age and gender-matched 15 healthy children. Significantly higher serum levels of malondialdehyde, oxidized LDL, total cholesterol, LDL cholesterol, triglycerides, apolipoprotein A-I, and apolipoprotein-B were observed in patients with SSNS especially in the relapsers. The serum levels of albumin, glutathione peroxidase activity, vitamin C, A, and E, and HDL cholesterol were significantly lower in patients especially among relapsers. In conclusion, a strong relationship between the oxidant/antioxidant status and dyslipidemia is documented in patients with SSNS, especially among relapsers. No normalization of the biochemical indices was observed despite the use of glucocorticoids. Therefore, the combined use of steroid, antioxidant therapy, and lipid lowering therapy can be recommended in such children.
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PMID:Oxidative modification of low-density lipoprotein in relation to dyslipidemia and oxidant status in children with steroid sensitive nephrotic syndrome. 1835 47

Hyperlipidemia is one of the major features of nephrotic syndrome (NS). Although many factors have been implicated in the pathogenesis of NS-related dyslipidemia, the underlying mechanisms remain largely uncharacterized. The present study was designed to examine the gene profile associated with lipid metabolism in the livers of nephrotic rats. NS was created in male Sprague-Dawley rats (n = 6) receiving sequential intraperitoneal injections of puromycin aminonucleoside. Analysis by Affymetrix assay, quantitative RT-PCR, and Northern and Western blotting revealed 21 genes associated with cholesterol and fatty acid metabolism. Eight genes involved in cholesterol metabolism, Apo A-I, Acly, Acat, Mpd, Fdps, Ss, Lss, and Nsdhl, were significantly upregulated under NS. Four genes involved in fatty acid biosynthesis, Acc, FAS, ELOVL 2, and ELOVL6, and three critical for triglyceride biosynthesis, Gpam, Agpat 3, and Dgat 1, were significantly upregulated, whereas two genes involved in fatty acid oxidation, Dci and MCAD, were downregulated. Expression of several genes in sterol-regulatory element-binding protein (SREBP)-1 activation was also aberrantly altered in nephrotic livers. The expression and transcriptional activity of SREBP-1 but not SREBP-2 were increased in nephrotic rats as assessed by real-time PCR, immunoblotting, and gel shift assays. The upregulation of hepatic genes involved in cholesterol biosynthesis may play an important role in the pathogenesis of hypercholesterolemia, whereas upregulation of genes participating in hepatic fatty acid and triglyceride biosynthesis and downregulation of genes involved in hepatic fatty acid oxidation may contribute to hypertriglyceridemia in nephrotic rats. Activation of SREBP-1 transcription factor may represent an underlying molecular mechanism of hyperlipidemia in NS.
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PMID:Expression profiling of hepatic genes associated with lipid metabolism in nephrotic rats. 1861 21

The nephrotic syndrome is associated with an increased risk ofatherosclerosis and endothelial dysfunction. Endothelial dysfunction was assessed and correlated with dyslipidemia and markers of inflammation in patients with nephrotic syndrome. 20 patients were divided into two groups: group A (10 patients with primary nephrotic syndrome) and group B, 10 controls. The endothelial function was assessed by means of flow mediated dilation on brachial artery, using B-mode ultrasonography. The values of flow mediated dilation were 4 +/- 1.49% (group A) and 11.95 +/- 0.24% (group B), p<0.01. There was a very strong inverse correlation between flow mediated dilation and LDL-cholesterol (r=-0.9650, p<0.001), total cholesterol (r=-0.9399, p<0.001), and fibrinogen (r=-0.7127, p<0.001), and a weak correlation with triglycerides (r=-0.2880. p<0.01), and positive correlation with respective HDL-cholesterol (r=0.4020, p<0.001). The most important factors involved in the endothelial dysfunction in the nephrotic syndrome are LDL-cholesterol, total cholesterol and fibrinogen and their treatment is necessary to prevent atherosclerosis in patients with nephrotic syndrome.
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PMID:Endothelial dysfunction in the nephrotic syndrome. 1892 61

Hyperlipidemia (HLP), a common complication, is very prevalent in children with primary nephrotic syndrome (PNS). HLP not only significantly increases the cardiovascular risk in adulthood, but also accelerates the progression of renal disease. Proteinuria as the most important pathophysiological change can reduce serum colloid osmotic pressure, which leads to an increase in the synthesis of serum proteins including lipoproteins in the liver for export to the serum. Thus, the severity of lipid abnormalities may correlate with the degree of proteinuria. A total of 378 children with PNS were divided into three groups according to their urinary protein excretion (UPE), group A (50 mg/kg/d < or = proteinuria <100 mg/kg/d, 125 cases), group B (100 mg/kg/d < or = proteinuria <200 mg/kg/d, 132 cases) and group C (proteinuria > or =200 mg/kg/d, 121 cases). In addition, 200 healthy volunteers with neither allergic nor renal disease between 3 and 14 years of age were recruited as the control group. Fasting serum levels of lipoprotein (a) [Lp(a)], total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (apoA1), apoB, and albumin (Alb) were measured. Serum low density lipoprotein cholesterol (LDL-C) was calculated by the Friedewald formula. As expected, when all patients were compared with healthy children in this study, UPE and the serum concentrations of Lp(a), TC, TG, HDL-C, LDL-C, and apoB were higher in the PNS than in the control group (p<0.01), whereas for apoA1/B ratio the opposite was observed (p<0.01). Furthermore, patients in group C exhibited significantly higher Lp(a), TC, TG, LDL-C, and apoB concentrations than those in group A or B (p<0.01), whereas for apoA1/B ratio the opposite was found (p<0.01). The increase in serum lipids was accompanied by a significant augmented UPE in all patients (p<0.05). More specifically, positive correlations were observed between serum levels of TC (r=+0.80, p<0.01), HDL (r=+0.49, p<0.01), LDL (r=+0.79, p<0.01), ApoB (r=+0.62, p<0.01) and log proteinuria in group B; additionally, a negative correlation was observed between apoA1/B ratio and log proteinuria in group B (r=-0.38, p<0.01). However, no correlation of serum lipid profiles with UPE was determined in group A and C, respectively (p>0.05). Serum Alb was negatively correlated with Lp(a) (r=-0.96, p<0.01), TC (r=-0.78, p<0.01), TG (r=-0.78, p<0.01), LDL-C (r=-0.88, p<0.01), apoA1 (r=-0.26, p<0.01), and apoB (r=-0.71, p<0.01), while positively correlated with apoA1/B (r=+0.27, p<0.01) in all nephrotic children. Furthermore, no correlation existed between serum lipid profiles and Alb in group A, B and C, respectively (p>0.05). In Conclusion, secondary dyslipidemia in children with PNS is in parallel with the degree of UPE. There are diverse characteristics of lipid metabolism under different UPE. As for the patients with medium-UPE, positive correlation between serum lipids and proteinuria is presented.
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PMID:Characteristics of lipid metabolism under different urinary protein excretion in children with primary nephrotic syndrome. 1946 31

Nephropathic subjects show an increased tendency to develop cardiovascular diseases, mainly as the consequence of several risk factors including increased oxidative stress, inflammation, physical inactivity, anemia, vascular calcification, and endothelial dysfunction. The alterations in lipid metabolism represent a relatively lesser important cause of genesis and progression of atherosclerosis. Unfortunately, in these patients the atherogenic potential of dyslipidemia may depend more on apolipoproteins than on lipid abnormalities, and may not always be recognized by measurement of plasma lipids alone. The aim of this review was therefore to analyze the main lipid alterations that can occur in nephropathic patients, as well as their causes and their effects on the cardiovascular system. The clinical evidence and recommendations for the use of lipid-regulating drugs in patients with chronic kidney disease, nephrotic syndrome, in patients undergoing hemo- and peritoneal dialysis and in transplanted patients was also reviewed. Moreover, we analyzed the link between dyslipidemia and kidney disease onset and progression and the role of statins in preventing it.
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PMID:Alterations of lipid metabolism in chronic nephropathies: mechanisms, diagnosis and treatment. 2035 96


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