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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipid abnormalities have been postulated to contribute to renal insufficiency by a mechanism that is analogous to atherogenesis. The majority of patients treated for chronic renal failure die of cardiovascular complications. Lipid abnormalities in this group are thought to contribute to this high mortality. Proving a causal association between dyslipidemia and accelerated atherosclerosis in the end-stage renal disease population has been confounded by the presence of other pro-atherogenic conditions in this population. The current study compiles the lipid data we have accumulated from our renal population for the years 1987 to 1989. The report is divided into three main parts: The first is a survey of lipid levels and atherogenicity indicators in groups with different types of renal disease or modalities of treatment. The second is a multivariate analysis of the relationship of clinical and biochemical variables (and their interactions) to the serum lipid and apolipoprotein levels and their ratios and their change over time in a large dialysis population. In the third study, we quantitate the peritoneal clearances of apolipoproteins A-I and B in patients undergoing continuous ambulatory peritoneal dialysis and assess the relationship of these clearances to serum lipid and lipoprotein levels and risk ratios.
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PMID:Cholesterol and lipid disturbances in renal disease: the natural history of uremic dyslipidemia and the impact of hemodialysis and continuous ambulatory peritoneal dialysis. 248 49

The Authors have analyzed the complex problems of the possible binding between uric acid and plasma proteins using two methods consisting of serum ultrafiltration at 22 degrees C or electrophoresis on different supports with successive specific coloration of the free and bound uric acid. The percentage of free and bound uric acid was established in serum from normal subjects, patients with primary gout, patients with renal insufficiency treated by dialysis and subjects with type IV dyslipidemia. The Authors discuss the results obtained as regards the possible role played by urate-plasma proteins binding in the interpretation of a genetic defect present in gouty patients involving a diminished uric acid binding capacity of plasma proteins.
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PMID:[Study of the binding between uric acid and plasma proteins (author's transl)]. 745 62

Renal insufficiency is frequently associated with both quantitative and qualitative abnormalities in lipid and hemorheologic profiles. Although this may lead to increased risk of cardiovascular disease, a number of studies have also shown dyslipidemia to be a significant risk factor for the progression of renal insufficiency in human chronic renal disease. This double-blind, placebo-controlled trial aimed to assess the effect of fluvastatin, a synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on these parameters in dyslipidemic patients with or without chronic renal insufficiency. After a 6-week placebo run-in, 42 patients who had been previously stratified into 2 groups on the basis of creatinine clearance levels (0.5-1.0 mL/sec or > 1.0-1.5 mL/sec) were randomized to treatment with fluvastatin (40 mg daily) or matching placebo. Significant differences (on analysis of variance with repeated measures) were seen between fluvastatin and placebo treatment groups for changes in total cholesterol (-15% vs 1%, respectively; p < 0.001), low density lipoprotein cholesterol (LDL-C; -21% vs -5%; p < 0.001), very low density lipoprotein cholesterol (-14% vs 14%; p = 0.017), very low density lipoprotein triglycerides (-1% vs 29%; p = 0.014) and total triglycerides (-7% vs 24%; p < 0.001). These effects on cholesterol levels were reflected in a significant decrease in apolipoprotein B levels with fluvastatin therapy (p < 0.001). Apolipoprotein A-I levels increased (p = 0.054) despite no significant change in the levels of high density lipoprotein cholesterol. Response to therapy did not differ between the 2 renal function groups for any of the lipid, lipoprotein, and apolipoprotein variables. Hemorheologic parameters were not altered with fluvastatin therapy, regardless of renal function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fluvastatin for dyslipoproteinemia, with or without concomitant chronic renal insufficiency. 760 9

Atherosclerosis develops rapidly in patients with diabetes or renal insufficiency. Plasma lipoprotein profiles are frequently abnormal in these conditions and reflect an elevation in the level of the apoprotein B (ApoB)-containing components very low density lipoprotein (VLDL) and low density lipoprotein (LDL). High levels of circulating advanced glycation end products (AGEs) also occur in diabetes and end-stage renal disease (ESRD). These products arise from glucose-derived Amadori products and include AGE-modified peptides (AGE-peptides) which result from the catabolism of AGE-modified tissue proteins. AGE-peptides have been shown to crosslink protein amino groups and to accumulate in plasma as a consequence of renal insufficiency. To address potential mechanisms for the dyslipidemia of diabetes and ESRD, we investigated the possibility that circulating AGEs react directly with plasma lipoproteins to prevent their recognition by tissue LDL receptors. AGE-specific ELISA showed a significantly increased level of AGE-modified LDL in the plasma of diabetic or ESRD patients compared with normal controls. AGE-LDL formed readily in vitro when native LDL was incubated with either synthetic AGE-peptides or AGE-peptides isolated directly from patient plasma. LDL which had been modified by AGE-peptides in vitro to the same level of modification as that present in the plasma of diabetics with renal insufficiency exhibited markedly impaired clearance kinetics when injected into transgenic mice expressing the human LDL receptor. These data indicate that AGE modification significantly impairs LDL-receptor-mediated clearance mechanisms and may contribute to elevated LDL levels in patients with diabetes or renal insufficiency. This hypothesis was further supported by the observation that the administration of the advanced glycation inhibitor aminoguanidine to diabetic patients decreased circulating LDL levels by 28%.
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PMID:Modification of low density lipoprotein by advanced glycation end products contributes to the dyslipidemia of diabetes and renal insufficiency. 793 86

Growth retardation is a common feature in children with end-stage renal failure (ESRF). Medical management of renal insufficiency rarely normalizes growth and optimistic reports on the effect of rhGH treatment on growth velocity may presage more extensive use of rhGH in pediatric nephrology. Ample evidence has shown beneficial effects of GH replacement therapy in both childhood and adolescent hypopituitarism. However, the remarkably few side effects of treatment reported in these conditions cannot necessarily be extrapolated to children with ESRF. Uremia is associated with a wide range of metabolic and hormonal derangements including decreased glucose tolerance. This is mainly due to impaired insulin-stimulated glucose disposal in peripheral tissues and insufficient insulin-induced suppression of hepatic glucose production. Insulin-stimulated glucose uptake in skeletal muscle in ESRF is reduced by 30-50% as compared to that in healthy subjects, and a reduction may be detected even in subjects with a more moderate reduction in renal function (GFR around 25 ml/min). Dialysis therapy improves the disturbed insulin action significantly. The cause of the insulin resistance in ESRF is multifactorial. Impaired physical fitness, accumulation of uremic toxins, raised levels of GH and glucagon, metabolic acidosis, dyslipidemia and the medication applied may all contribute. If exogenous GH administration is added to the already marked uremic insulin resistance, insulin action may be severely disturbed and the secondary hyperinsulinism further magnified. However, frank diabetes mellitus does not develop unless the beta cells fail to meet the enhanced demands. This will probably occur only in patients with a beta-cell genotype pivotal for the phenotypic expression of non-insulin dependent diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glucose metabolism in chronic renal failure with reference to GH treatment of uremic children. 837 90

Renal disease is accompanied by specific alterations of the lipoprotein metabolism. While marked hyperlipidemia is a characteristic finding in the nephrotic syndrome, the dyslipoproteinemia of renal insufficiency is predominantly reflected in an abnormal apolipoprotein pattern but does not necessarily include elevated plasma lipid concentrations. The specific changes in nephrotic syndrome include increased formation primarily of cholesterol-rich and to a varying extent of triglyceride-rich ApoB-containing lipoproteins in the VLDL-LDL density range with little or no change among the ApoA-containing lipoproteins in HDL. The dyslipoproteinemia of renal failure is, on the other hand, mainly characterized by a decreased catabolism of the triglyceride-rich ApoB-containing lipoproteins with increased concentrations of partially metabolized lipoproteins of intermediate and very low density and a decreased concentration of ApoA-containing lipoproteins in HDL. In addition, increased levels of Lp(a) are found both in the nephrotic syndrome and in renal failure. Dialysis treatment appears to have only a modest influence on the renal dyslipoproteinemia. Due to its atherogenic character, the dyslipidemia of renal disease may be related to the accelerated development of cardiovascular disease in these patients.
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PMID:Diagnosis and classification of dyslipidemia in renal disease. 871 66

Patients with renal disease have an increased cardiovascular mortality. Hyperlipidemia, a hallmark of renal disease, is recognized as a principal cause of atherosclerosis. However, it is difficult to prove a pathogenetic role of renal dyslipidemia per se in this increased cardiovascular risk since multiple risk factors are often present in patients with progressive renal insufficiency, e.g. hypertension, diabetes and hypercoagulability. However, evidence is accumulating demonstrating detrimental effects of hyperlipidemia during both initiation and progression of the atherosclerotic process. The present review discusses this evidence in patients with renal disease, and the possible implications for treatment.
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PMID:Mechanisms of cardiovascular injury in renal disease. 871 68

Plasma lipoproteins (LP) may be identified on the basis of density properties or apolipoprotein (apo) composition. ApoB-containing LP occur in VLDL, IDL and LDL. There are several types of apoB-containing LP characterized by specific composition of minor apolipoproteins (apoC, apoE etc.) and lipid constituents (triglycerides and cholesterol), metabolic properties and relative atherogenicity. The alterations of lipoprotein metabolism in renal disease resulting in elevated levels of apoB-containing LP may be reflected in hyperlipidemia. Whereas nephrotic syndrome and heavy proteinuria are associated with increased formation of cholesterol-rich apoB-containing LP in LDL and VLDL, the characteristic feature in renal failure is the accumulation of intact or partially metabolised triglyceride-rich LP in IDL and VLDL. The potentially atherogenic apoB-containing LP have been linked to the pathogenic processes that result in progressive glomerular and interstitial lesions and ultimate loss of renal function. The mechanisms of injury are not fully understood. Receptor- and non-receptor mediated uptake of LP by mesangial cells may induce or accelerate proliferative and sclerotic processes in the glomerular mesangium that are analogous to atherosclerosis in the arterial wall. Changes in glomerular permeability can result in increased filtration of LP that may be internalized by tubular cells and elicit corresponding lesions in the interstitial tissues. The negative impact of proteinuria on the prognosis of renal disease could be mediated in part through an increased filtration of lipoproteins. Induction of hyperlipidemia accelerates glomerular and interstitial damage in experimental renal failure. This can be attenuated by treatment with hypolipemic agents. In patients, increased concentrations of apoB-containing LP are associated with more rapid progression of renal insufficiency in both primary renal disease and diabetic nephropathy. It is, however, presently not known to what extent treatment of the renal dyslipidemia can modify the progression of chronic renal failure. Experimental and clinical evidence suggest that apoB-containing LP may play a pathogenetic role in the progression of renal disease.
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PMID:Progression of renal failure: role of apolipoprotein B-containing lipoproteins. 940 33

Patients with diabetes and renal insufficiency (Db/ESRD), a group subject to accelerated atherosclerosis exhibit marked increases in the levels of circulating, glycation-derived reactive substances, termed advanced glycation endoproducts (AGEs). These products have been previously shown to react covalently with apoliprotein B (ApoB) to form AGE-ApoB, a modification that results in delayed low density lipoprotein (LDL) clearance and possibly to dyslipidemia. Because the effect of hemodialysis on AGE removal was shown to be unsatisfactory, based on single intradialytic studies, we examined the effect of long-term hemodialysis therapy on serum AGE-ApoB levels, as well as on total serum ApoB of 25 Db/ESRD patients treated by two types of hemodialysis filters, the Fresenius Inc. F8, as the low flux (LF), or high-flux polysulfone AN69 (HF) for two months using an AGE-specific ELISA. At the end of eight weeks, circulating AGE-ApoB levels were reduced significantly (by 35%) from baseline (P = 0.039) in patients treated by HF compared to a modest 16% reduction noted in patients treated by LF (P = 0.05) N = 12, P = 0.047). Of note, total plasma ApoB was reduced by 27% from baseline (P = 0.02) in patients treated by HF compared to a 6% reduction noted in those treated with LF (P = 0.8). In vitro comparison of AGE mass balance, and mass adsorption by the different filters revealed that the higher efficiency of HF filter was due to greater adsorption. The association of reduced AGE-ApoB levels with a decrease in total circulating ApoB by HF and not by LF dialysis suggests: (1) a causal link between AGE clearance and dyslipidemia in diabetic ESRD, and, (2) that more efficient modes of renal replacement treatment and AGE removal could significantly benefit clinical outcome.
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PMID:Reduction of plasma apolipoprotein-B by effective removal of circulating glycation derivatives in uremia. 940 12

Renal disease is accompanied by characteristic alterations of lipoprotein metabolism, which appear as a consequence of nephrotic syndrome or renal insufficiency and are primarily reflected in an altered apolipoprotein profile rather than elevated plasma lipid levels. Their full characterization requires identification of discrete lipoprotein particles. While nephrotic syndrome results in increased concentrations of both cholesterol- and triglyceride-rich apoB-containing lipoproteins, renal insufficiency is characterized by an accumulation of intact or partially metabolised triglyceride-rich apoB-containing lipoproteins. The dyslipidemia has been discussed as a contributory factor for the progression of renal insufficiency through development of glomerulosclerosis and tubulointerstitial lesions together with accelerated atherosclerosis. Several experimental studies have shown that hyperlipidemia accelerates renal damage. Lipid-lowering treatment can reduce renal lesions and preserve renal function. The documentation in human nondiabetic progressive renal insufficiency is more limited. We have found that increased concentrations of triglyceride-rich, but not cholesterol-rich, apoB-containing lipoproteins are, associated with a more rapid loss of renal function. The underlying pathophysiological mechanisms for the relation between triglyceride-rich apoB-containing lipoproteins and progression of renal insufficiency are not fully understood. Treatment with hypolipemic drugs may attenuate the renal dyslipidemia, but thus far there have been no reports about controlled clinical trials testing the possible effect of such treatment on the progression of renal insufficiency. In summary, there is evidence to suggest that some specific lipoprotein abnormalities are a risk factor for the progression of renal dysfunction, but the final test of such assumptions still rests on the results of urgently needed controlled intervention studies.
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PMID:Lipoprotein abnormalities as a risk factor for progressive nondiabetic renal disease. 1041 28


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