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)

100 Patients with chronic renal failure(CRF) were treated mainly by the mediation principle (MP). Results showed that the progression of CRF with MP was slower than that without MP. There was very significant difference (P < 0.01) between the regression coefficient. In addition, the effect of MP on the factors in promoting the progression of CRF, e.g., hypertension, albuminuria, hyperlipemia and immune function etc. was discussed in detail.
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PMID:[Study on effect of mediation principle in retarding progression of chronic renal failure]. 778 93

Plasma newly-synthesized cholesteryl ester transfer (NCET) rate and concentrations of lipids, lipoproteins and apolipoproteins A1 and B were measured in chronic renal failure patients (dialysis independent and dialysis dependent), patients with a functioning renal transplant and in healthy control subjects with comparable ages and plasma triglycerides. Plasma NCET rates and apoB concentrations were significantly higher in patients treated by continuous ambulatory peritoneal dialysis (CAPD) compared with controls. In normolipidemic subjects (cholesterol < 6.5 mmol/liter, triglycerides < 2.0 mmol/liter), plasma NCET rates did not differ significantly from rates in the corresponding control subjects. In hyperlipidemic subjects, plasma NCET rates were significantly higher than rates in the normolipidemic subgroup. Plasma NCET rates were correlated closely with plasma apoB levels in all renal patients combined (r = 0.754, N = 53, P < 0.001) and with plasma cholesteryl ester mass transfer (r = 0.853, N = 13, P < 0.001). We conclude that, in the absence of hyperlipidemia, plasma NCET rate is normal in patients with chronic renal failure irrespective of the treatment for uremia, and when hyperlipidemia is present NCET rates are raised and may contribute to elevated levels of the proatherogenic apoB-containing lipoproteins.
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PMID:Cholesteryl ester transfer in patients with renal failure or renal transplants. 786 10

1. Secondary hyperparathyroidism in chronic renal failure may contribute to abnormalities of lipid metabolism and glucose tolerance. Amelioration of secondary hyperparathyroidism has been reported to mitigate the hyperlipidaemia and improve glucose tolerance experimentally. 2. The effect of the partial suppression of hyperparathyroidism by intravenous calcitriol on lipid levels and glucose tolerance was studied in 15 haemodialysis patients with secondary hyperparathyroidism. All received intravenous calcitriol 1 microgram at the end of haemodialysis thrice weekly for eight weeks. Oral glucose tolerance test and plasma lipid profiles including triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apoprotein A-I and apoprotein B were determined simultaneously before and after eight weeks of therapy. 3. Before calcitriol treatment, uraemic patients with secondary hyperparathyroidism displayed a significant higher triglyceride and a significant lower HDL-C and apoprotein A-I as well as marked glucose intolerance with an increment of the area below the glucose curve when compared with healthy control subjects. 4. After eight weeks of calcitriol treatment, there was a significant decrement in serum intact parathyroid hormone (476.45 +/- 48.33 versus 191.37 +/- 30.17 ng/l, P < 0.001) and plasma triglyceride (2.24 +/- 0.34 versus 1.80 +/- 0.29 mmol/l, P < 0.05) as well as a significant increment of plasma apoprotein A-I (38.13 +/- 2.14 versus 44.19 +/- 2.18 mumol/l, P < 0.05), whereas there was no significant change in serum total cholesterol, LDL-C, HDL-C, and apoprotein B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of intravenous calcitriol on lipid profiles and glucose tolerance in uraemic patients with secondary hyperparathyroidism. 787 41

Chronic renal failure is associated with hyperlipidemia and atherosclerosis. The mechanism responsible for the observed increase of serum cholesterol in chronic renal disease is not certain. The objective of the present study was to characterize the effect of induced renal failure on 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase) and cholesterol 7 alpha-hydroxylase, the two rate determining enzymes of the cholesterol and bile acid biosynthetic pathways, respectively. Studies were carried out in rats with subtotal (75%) nephrectomy, which resulted in a marked elevation of blood urea nitrogen (371 +/- 44% of control, P < 0.001), and was accompanied by significant increases in the levels of serum cholesterol (133 +/- 7%, P < 0.005) and triglycerides (185 +/- 25, P < 0.01). In nephrectomized rats, an increase in the specific activity of HMG-CoA reductase (219 +/- 30% above control levels, P < 0.02) was observed. This increase occurred in the presence of elevated hepatic microsomal cholesterol concentrations (150 +/- 13% of controls, P < 0.01). Surprisingly, the increase in HMG-CoA reductase specific activity was not associated with parallel increases in HMG-CoA reductase steady-state mRNA levels and gene transcriptional activity. These uremic rats also exhibited a marked increase in the specific activity of cholesterol 7 alpha-hydroxylase (240 +/- 559% of controls, P < 0.05). There was no concomitant increase in cholesterol 7 alpha-hydroxylase steady-state mRNA levels or gene transcriptional activity. The factors responsible for the observed increases in HMG-CoA reductase and cholesterol 7 alpha-hydroxylase specific activity in renal failure remain to be determined.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-transcriptional regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase and cholesterol 7 alpha-hydroxylase in rats with subtotal nephrectomy. 796 47

Plasma triglycerides are increased in the majority of patients with advanced renal failure but cholesterol is not. HDL cholesterol is reduced while LDL IDL and VLDL cholesterol is increased. Lecithin:cholesterol acyltransferase (LCAT), an enzyme necessary for HDL maturation, is reduced in chronic renal failure (CRF). As a consequence, while all subtypes of HDL are reduced, the small HDL3 subtype is relatively enriched at the expense of the larger, more functional HDL2 subtype. Triglycerides are increased in all lipoprotein fractions. HDL-associated apolipoproteins, apo A-I and A-II are decreased, while apo B is increased. Lipoprotein catabolic rate is reduced, but the cause of hyperlipidemia is multifactorial; reduced lipoprotein lipase (LPL) activity, increased concentration of apo C-III (a specific inhibitor of LPL) in plasma, secondary hyperparathyroidism, insulin resistance. Hyperlipidemia is not corrected by dialysis. Lipid levels are somewhat higher in CAPD patients, possibly as a consequence of increased glucose absorption or as a consequence of transperitoneal HDL losses. Triglycerides decrease and cholesterol increases following transplantation. Oxidized lipids are increased in plasma of patients with CRF. Plasma polyunsaturated fatty acids are decreased and saturated fatty acids increased. The same changes occur in the lipid bilayers composing leukocytes and red blood cell membranes. These changes result in altered membrane fluidity, and are corrected by dialysis. While atherosclerotic disease is a leading cause of death in dialysis patients, it is not certain that the specific lipid disorders of CRF are responsible for this morbidity, nor is it recommended at this time that qualitative abnormalities be treated pharmacologically in the absence of increased lipid levels.
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PMID:Hyperlipidemia of chronic renal failure. 798 78

A 49-year-old woman with chronic renal failure was given gemfibrozil for hyperlipidemia. She developed gemfibrozil-induced myositis which precipitated an acute compartment syndrome, necessitating emergency fasciotomy. The muscle biopsy showed prominent degeneration of the skeletal muscle fibers, associated with moderate chronic inflammatory infiltration. Electron microscopy revealed myofibrillary fragmentation and mitochondrial disorganization. The clinicopathologic features of gemfibrozil-induced myositis appear to be distinct from those of clofibrate-induced muscular syndrome. Extreme caution should be exercised in the use of gemfibrozil in patients with impaired renal function.
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PMID:Gemfibrozil induced myositis: a case report with light microscopic and ultrastructural study. 800 60

Chronic renal failure is characterized by abnormalities in glucose metabolism. In fact there are present a normal fasting plasma glucose level )or mild hyperglycemia) in the presence of hyperinsulinemia, blunted decrease in the plasma glucose concentration in response to exogenous insulin administration, and diminished effect of intravenous insulin on glucose uptake in forearm perfusion studies. The glucose intolerance is not the result of reduced insulin secretion, or circulating insulin antagonists, and does not correlate with the coexisting metabolic acidosis. Glucose intolerance exists because the peripheral insulin-sensitive tissue (muscle, adipose tissue, liver) of the patients with chronic renal failure are insulin resistant. However there are two subgroups of uremic patients with regard to glucose tolerance: about half of uremic patients can augment their insulin secretion sufficiently to maintain normal glucose tolerance despite glucose intolerance. In the other half, insulin secretion following glucose loads is not different from normal values, so that glucose intolerance results. The cause of the peripheral insulin resistance remain unclear. Besides deranged renal function can result in the development of hypoglycemia. The most important predisposing mechanism to hypoglycemia is diminished glucose availability due to substrate limitation; the second important mechanism (alcohol, insulin, propranolol, etc.). Finally, in chronic renal failure persistent hyperinsulinemia can contribute hyperlipemia and to high incidence of cardiovascular disease.
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PMID:[Glucose metabolism and chronic renal insufficiency]. 801 26

A 61-year-old woman with hyperlipidemia was treated with gemfibrozil. She also had insulin-treated diabetes mellitus and chronic renal failure and was admitted because of severe chest pain. The ST segment was depressed and creatine kinase levels were elevated. The original diagnosis was acute myocardial infarction. In the presence of increasing chest pain, the onset of limb muscle tenderness, and increasing levels of creatine kinase, the diagnosis of myopathy secondary to gemfibrozil therapy was made and the drug was discontinued. All symptoms then subsided and creatine kinase levels returned to normal. Myopathy is a well-known complication of blood lipid-lowering drugs, especially in patients with renal failure.
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PMID:[Gemfibrozil-induced myopathy]. 825 19

Catabolism of low-density lipoprotein is altered in experimental chronic renal failure. In patients with chronic renal failure, cardiovascular disease accounts for a significant proportion of all deaths. Several factors contribute to the "accelerated" atherosclerosis in this population, including hyperlipidemia, the pathogenesis of which is multifactorial. We investigated low-density lipoprotein (LDL) metabolism in a remnant model of chronic renal failure in the guinea pig. After one and two-thirds nephrectomy, creatinine clearance decreased to one-sixth normal. Plasma cholesterol and triglyceride (TG) levels increased with induction of renal failure. Analysis of lipoprotein composition disclosed significant TG enrichment of both uremic very-low-density lipoprotein (VLDL) and uremic LDL compared with control lipoproteins. Plasma clearance of homologous LDL was evaluated in turnover studies in control and uremic guinea pigs. To discriminate between differences in catabolism related to the uremic lipoprotein particle and to the uremic host milieu, a crossover protocol was used comparing the fractional catabolic rate (FCR) after simultaneous injection into control and uremic animals of 125I-control LDL and 131I-uremic LDL. The FCR of native LDL was slower in uremic animals than in controls. In addition, FCR of uremic LDL was significantly less than that of control LDL in both groups. Degradation studies in cultured fibroblasts indicated substantially reduced degradation of uremic LDL compared with control LDL. These results suggest dual abnormalities of LDL catabolism in renal failure that are not only related to alterations in clearance mechanisms in the uremic environment, but also suggest important functional differences in the LDL particle itself isolated from uremic animals.
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PMID:Catabolism of low-density lipoprotein is altered in experimental chronic renal failure. 847 12

The purpose of this review has been to summarize the effects of lipids on the progression of renal disease in chronic renal failure. Animal studies show that hypercholesterolemia as induced by a high cholesterol diet can aggravate the progression of renal disease in experimental models of chronic renal failure. Hypolipidemic treatment, when given to animals with chronic nephropathy associated with endogenous hyperlipidemia such as in reduced renal mass, obese Zucker rat, PAN nephrosis and the Dahl salt-sensitive rat, results in a reduction in serum lipids levels concomitant with a decrease in the renal damage. Enrichment of the diet with omega-6 PUFA given to rats with reduced kidney mass leads to a reduction in renal damage, probably due to beneficial changes in renal fatty acid composition, while supplementation of a fish oil diet to rats with immune complex nephritis resulted in a similar beneficial effect, probably due to a suppression in the local immunologic processes. The pathogenesis of this effect is still only partially understood. Lipid deposition and oxidation in the renal mesangium, migration of circulatory monocytes into the renal mesangium and their transformation to foam cell, and alterations in renal PUFA metabolism and composition are the main known alterations that accompany lipid-induced renal damage. These alterations, which are similar to those observed in atherosclerosis, lead to alterations in the normal biologic processes in the renal mesangium and terminate in glomerulosclerosis. Extrapolating the data from experimental studies to human renal diseases, it may be assumed that lipid metabolism has a significant impact on the gravity and progression of renal disease in a selected patient population, namely in patients with chronic renal disease. If so, hypolipidemic treatment or administration of certain types of PUFA can be important in the prevention of progression of the renal disease in these patients. Clinical studies are needed to elucidate this issue.
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PMID:Role of lipids in the progression of renal disease in chronic renal failure: evidence from animal studies and pathogenesis. 849 78


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