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)

Subjects with chronic renal failure have a greatly increased risk of coronary heart disease and dyslipidemia. Relatively few studies have examined the relationship of chronic renal failure to lipoprotein (Lp)(a) concentrations, an important risk factor for coronary heart disease. Diabetic subjects have been reported to have both increased Lp(a) concentrations and an increased risk of renal failure, thereby possibly confounding the Lp(a)-renal failure association. The association between Lp(a) and chronic renal failure in 359 control subjects and 111 subjects with renal failure was examined. Lp(a) (in milligrams per deciliter) was elevated in subjects with chronic renal failure, regardless of ethnicity (Mexican Americans, 19.8 +/- 2.7 versus 14.1 +/- 1.3; P = 0.03; non-Hispanic white patients, 24.9 +/- 3.0 versus 16.3 +/- 1.2; P = 0.006;). These differences persisted after adjustment for diabetes and ethnicity (P < 0.001). The type of treatment for chronic renal failure (diet, hemodialysis, or peritoneal dialysis) did not have an effect on Lp(a) concentrations. Lp(a) levels were not correlated with the level of creatinine in subjects with chronic renal failure. Thus, the elevation of Lp(a) levels in renal failure must occur early in renal failure, or alternatively, elevated Lp(a) levels may promote progression to chronic renal failure. These results indicate that Lp(a) concentrations are increased in chronic renal failure and may increase the risk for coronary heart disease in these subjects.
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PMID:Increased lipoprotein(a) concentrations in chronic renal failure. 148 54

Nephrotic syndrome causes hypercholesterolemia. Chronic renal failure results in hypertriglyceridemia, low HDL cholesterol and, more often, apolipoprotein abnormalities. This dyslipidemia is not corrected by hemodialysis. Transplantation corrects it but leads to other kinds of lipid abnormalities. Whether the treatment of these potentially atherogenetic abnormalities is beneficial of not remains unproved. There is some evidence of lipid contribution to the constitution of glomerulosclerosis in animals but it remains hypothetical in man.
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PMID:[Kidneys and lipids]. 160 59

Recent studies suggest that circulating blood monocytes may serve as a lipid clearance system in early atherosclerotic lesions. To evaluate the influence of moderate hyperlipoproteinemia on monocyte lipid concentrations, we measured fasting serum and monocyte lipid levels in 7 healthy individuals, in 7 patients with primary hypercholesterolemia and in 17 patients with secondary dyslipidemia due to chronic renal failure; 10 of these patients were treated by hemodialysis (HD) and 7 patients by continuous ambulatory peritoneal dialysis (CAPD). The hypercholesterolemic patients had elevated serum levels of total cholesterol, LDL-cholesterol and apolipoprotein (apo) B, but normal plasma triglycerides. Patients on dialysis had elevated serum levels of triglycerides, serum cholesterol (CAPD only) and VLDL- and LDL-cholesterol (CAPD only) and apo B (CAPD only), whereas HDL-cholesterol and apo A-I levels (HD only) were decreased. In monocytes, we measured the content of free cholesterol (FC), cholesteryl esters (CE) and triglycerides (TG). The normal mean intracellular concentrations of FC, CE and TG were 48.3, 1.7 and 2.4 micrograms/mg cell protein, respectively. All monocyte lipid levels were similar in patients and controls, with the exception of a decreased content of FC (30.8 micrograms/mg) in monocytes of HD patients. We conclude that moderate increases in serum lipoprotein lipid levels are not associated with lipid accumulation in monocytes.
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PMID:Lipid levels in monocytes of patients with moderate hyperlipoproteinemia. 163 66

Chronic renal failure is associated with abnormalities in lipoprotein metabolism that may contribute to premature atherosclerosis and early mortality in patients on dialysis. In previous studies, we found that plasma clearance of radiolabelled low density lipoprotein (LDL) was retarded in nephrectomized guinea pigs left with one-sixth of normal functioning renal mass. To elucidate potential mechanisms of delayed LDL clearance, we compared binding of LDL to hepatic membranes from both normal and uremic guinea pigs. One hundred micrograms of the 8000-100,000 X g hepatic microsomal protein was incubated with 125I-labelled normal guinea pig LDL (10-150 micrograms/mL) for 1 h at 37 degrees C, and the membrane washed and pelleted by centrifugation in a Beckman Ti 42.2 rotor. Parallel incubations with excess unlabelled LDL were done to determine specific binding. LDL specific binding to uremic hepatic membranes was significantly impaired compared with normal ones. The major abnormality, as determined by Scatchard transformation of the binding data, was a reduction of the apparent maximal binding of LDL to uremic membranes, with an average Bmax of 4.1 micrograms/mg protein compared with 6.6 micrograms/mg protein for normal hepatic microsomes. The affinity of LDL for uremic liver membranes was only slightly diminished with a mean apparent Kd of 35.2 micrograms/mL in comparison with 21.8 micrograms/mL for normal liver membranes. These results provide a biochemical explanation for the diminished LDL clearance in uremia and may account for the dyslipidemia of renal failure.
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PMID:Impaired binding of low density lipoprotein to hepatic membranes from uremic guinea pigs. 166 54

Dyslipidemia of chronic renal failure is of multifactorial origin. Decreased activity of lipoprotein lipase and hepatic triglyceride lipase, peripheral insulin resistance, hyperparathyroidism and L-carnitine deficiency are the contributing factors. This results in a disturbed catabolism of chylomicron, accumulation of very-low-density (VLDL) and intermediate-density (IDL) lipoproteins as well as incompletely cleared remnant particles, whereas low-density lipoprotein (LDL) levels are diminished. There is current debate as to whether cardiovascular disease is accelerated and whether hyperlipidemia should specifically be treated. In addition, there have been few means of influencing these metabolic alterations. Drug incompatibility and consequently side effects render treatment difficult. The drugs that have been most tested for lipid lowering in chronic renal failure are the fibric acids. By their mode of action, they are the logical choice. Dose reduction overcomes major side effects such as myopathy and rhabdomyolysis. The second generation of fibric acid derivatives (gemfibrozil and beclobrate) show several advantages over formerly used derivatives. Treatment with lovastatin and simvastatin appears to be safe and is recommended in a minority of patients with predominantly elevations of LDL. HMG-CoA reductase inhibitors also lower remnant particles effectively in hemodialysis (HD) patients. L-Carnitine and low-molecular-weight heparin have been shown to influence VLDL rich in triglycerides in a subset of patients on HD. In posttransplant hyperlipidemia, diet remains the first course of action in all patients. When this approach fails, the new lipid-lowering agents, especially fibric acids, appear to be safe in short-term studies in azathioprine- and ciclosporin-treated patients. Lovastatin has been shown to be safe in stable renal transplant patients. Its toxicity seems to depend mainly on high ciclosporin whole blood through or plasma levels.
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PMID:Hyperlipoproteinemia in chronic renal failure: pathophysiological and therapeutic aspects. 186 98

Renal transplantation modifies the dyslipidemia characteristic of chronic renal failure (CRF). The change in lipoprotein and lipid values of 51 transplant recipients, on cyclosporine and corticosteroid treatment, was studied during 2 years after transplantation to examine the short- and medium-term variations of lipid metabolism. Compared with control values of (all in mg/dL) triglycerides (Tg) 111 +/- 44, very-low-density lipoprotein (VLDL) Tg 69 +/- 18, total cholesterol (Chol) 201 +/- 32, VLDL-Chol 32 +/- 9, low-density lipoprotein (LDL) Chol 118 +/- 28, and high-density lipoprotein (HDL) Chol 50 +/- 10, uremic patients pretransplantation exhibited values of Tg 200 +/- 82 (P less than .001), VLDL-Tg 133 +/- 70 (P less than .001), Chol 193 +/- 51 (NS), VLDL-Chol 52 +/- 16 (P less than .001), LDL-Chol 100 +/- 37 (P less than .007), HDL-Chol 40 +/- 16 (P less than .001), which changed to Tg 118 +/- 18 (P less than .001), VLDL-Tg 64 +/- 45 (P less than .001), Chol 223 +/- 48 (P less than .006), VLDL-Chol 26 +/- 33 (P less than .001), LDL-Chol 134 +/- 43 (P less than .001), at HDL-Chol 63 +/- 21 (P less than .001) at 3 months and Tg 135 +/- 76, VLDL-Tg 81 +/- 62, Chol 218 +/- 55, VLDL-Chol 22 +/- 20, LDL-Chol 139 +/- 46, and HDL-Chol 58 +/- 18 at 24 months without evidence of a significative variations in the 3- to 24-month posttransplant period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein-apolipoprotein changes in renal transplant recipients: a 2-year follow-up. 189 57

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

Early changes in lipid metabolism and appearance of atherosclerosis risk factors play a key role in the development of cardiovascular disease of chronic renal failure (CRF). In the effort to evaluate the effects of protein restricted diet on dyslipidemia, we studied 122 patients with CRF (S-creatinine 1.3-9 mg/dl); 58.2% of whom were on antihypertensive drugs treatment. Patients had been separated into 6 groups: group 1 was kept on a free diet; groups 2, 3, 4, 5, 6 were kept on a protein-restricted diet from 12, 24, 36, 48, 60 months, respectively. We found hypertriglyceridemia, pathologic levels of esterified cholesterol in high density lipoprotein (HDL-C) and pathologic apolipoprotein A1/B ratio in group 1; the comparison with other groups--whose values were normal range after 12, 24 months of treatment--showed significant differences. The lipidic parameters were independent of the duration of CRF and of patients' age. Serum creatinine showed a significant correlation with tryglicerides and HDL-C values only in group 1. Total cholesterol and apolipoprotein B were significantly greater in hypertensives than in normotensives. In our opinion, a moderate restriction in protein intake could be effective in preventing and in halting the early alterations of lipid metabolism in CRF.
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PMID:Effect of protein-restricted diet on serum lipids and atherosclerosis risk factors in patients with chronic renal failure. 335 2

Eighteen patients with chronic renal failure (serum creatinine 173-756 mumol/l) and hyperlipidemia were treated with gemfibrozil (1200 mg/day). The drug caused a significant improvement of the dyslipidemia within one week and the effect was progressive during the 28 weeks of treatment. Very-low-density lipoprotein triglycerides and very-low-density lipoprotein cholesterol decreased by about 50% and high-density lipoprotein cholesterol increased by 30%. The lipoprotein changes occurred simultaneously with a significant activation to normal levels of postheparin plasma lipoprotein and hepatic lipases. Opposite effects were observed when gemfibrozil was discontinued and the patients were given placebo. No major harmful effects were observed.
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PMID:Normalization of lipoprotein lipase and hepatic lipase by gemfibrozil results in correction of lipoprotein abnormalities in chronic renal failure. 355 8

Dyslipidemia is one of the first metabolic dysfunction observed among patients with end stage renal disease. It can also induce acceleration of renal tissue damage. Kidney transplantation may cause recovery of some dysfunction in lipid metabolism while influencing deterioration of others. The aim of this study was to monitor dynamics of basic lipid parameters in the first year after kidney transplantation. The sample included 25 patients (9W, 16M), aged 18-59, avg. 36. We have measured concentration of the following parameters in blood serum: triglycerides (TG), total cholesterol (CH-C) and apolipoprotein B (Apo B). Simultaneously, functions of transplanted kidney were tested with use of routine methods. The immunosuppressive treatment of patients followed the scheme: cyclosporine + prednisolone + azathioprine. The treatment influence on lipid disorders was measured by relevant correlation coefficients. The obtained results point to the observation that in the first year after kidney transplantation the TG concentration gradually decreases, with simultaneous continuous increase of CH-C concentration, mainly due to LDL concentration increase. No influence of immunosuppressive treatment on lipid parameters was observed. However, lipid dysfunction, especially TG, correlated with kidney function.
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PMID:[Dynamics of changes in lipid metabolism during the first year after kidney transplantation]. 780 32


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