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)

Case 1, a 60-year-old man and case 2, a 70-year-old man had several year history of chronic renal failure with hypertension and hyperlipidemia due to diabetes mellitus. Treatment of hyperlipidemia was started by oral bezafibrate intake 1,200 mg per day in case 1 and 400 mg per day in case 2 respectively. Three to fourteen days later, both patients noticed symmetrical muscle pain and weakness. Then the symptoms worsened and they were hospitalized. At the time of admission, both patients revealed weakness in the proximal muscles of their upper and lower limbs and the serum creatine kinase and myoglobin levels were remarkably elevated. Myoglobinuria was also noted. Routine light microscopic examination of biopsied quadriceps femoris muscles of two patients showed scattered necrotic muscle fibers, some of which were under phagocytosis. The symptoms of the patients were immediately resolved after the drug was discontinued. Serum concentration of bezafibrate was remarkably elevated during treatment. Thus the diagnosis was established as having bezafibrate induced myopathy and, as far as we know, this is the first report of bezafibrate induced myopathy in Japan. On the basis of the above description, bezafibrate may induce muscle damage if dose is excess over the renal capacity. Extreme caution is warranted when the patient is placed on bezafibrate and has renal dysfunction. Strict dose adjustment is necessary in taking account of renal function to avoid muscle damage including rhabdomyolysis.
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PMID:[Bezafibrate myopathy in two patients with chronic renal failure]. 129 Nov 64

The incidence of end-stage renal disease is increasing and this results in an enhanced requirement of renal replacement therapy facilities. This brings about a significant burden on health care budgets and makes strategies that slow down or even prevent deterioration of the renal function mandatory. Although large scale randomized, controlled and prospective clinical trials on the effect of blood pressure control on the course of renal function are lacking, there is circumstantial evidence from animal, epidemiological and clinical studies to state that treatment of hypertension to blood pressure values well within the normal range is most important to ameliorate the downhill course of renal function in patients with chronic renal failure. Moreover, treatment of hypertension is critical to reduce morbidity and mortality of cardiovascular disease in these patients, who have an increased risk for such events. Low-protein diets, if possible with ketoacid supplement, are advocated to slow down the deterioration of renal function. However, based on the results of recent studies, low-protein diets may only have a moderate effect in patients with diabetic nephropathy and, possibly, in patients with chronic glomerulonephritis. The possibility of influencing renal ammoniagenesis by protein restriction or calcium carbonate administration, and an attenuation of alternative complement pathway activation and tubulo-interstitial injury, are challenging. Finally, in animal studies it has been found that abnormalities in serum lipid profile contribute to the progression of chronic renal failure, which may be prevented by pharmacological treatment of hyperlipidemia. Studies in humans concerning this subject are lacking at this moment, but treatment of hyperlipidemia is proper to reduce cardiovascular events.
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PMID:Clinical strategies for arresting progression of renal disease. 140 61

Uremic hyperlipidemia was recently suggested to contribute to progression of chronic renal failure (CRF). To investigate the relationship between lipoprotein abnormalities and decline of renal function, plasma lipids with apoproteins A1, B, E, CII, CIII, CII/CIII and E/CIII ratios, parathyroid hormone (PTH), insulin and glucose levels were examined in 72 patients with different degrees of CRF and compared to 28 patients of a reference group. A significant decrease of CII/CIII ratio was already evident below a Ccr of 60 ml/min, while increased apo-CIII and triglycerides (TG) with reduced HDL-cholesterol (HDL-C) levels occurred below a Ccr of 30 ml/min. Both TG and apo-CIII showed a positive correlation with creatinine levels. On the contrary, apo-CII/apo-CIII and HDL-C inversely correlated with the progression of renal failure. PTH and insulin showed a positive correlation with TG, the former being also inversely related to apo-CII/apo-CIII ratio. Our results point to early apolipoprotein changes in the course of CRF. Elevated apo-CIII and reduced apo-CII/apo-CIII ratio may be considered the most typical features of uremic hyperlipidemia and likely account for the impaired TG removal and the hypertriglyceridemia (HTG). Secondary hyperparathyroidism may contribute to reduce peripheral lipolytic activity and cause HTG. A contributory role of hyperlipidemia in the progression of renal disease is also supported.
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PMID:Lipids and apolipoproteins change during the progression of chronic renal failure. 145 39

Cardiovascular complications in patients with chronic renal failure have been associated with the hyperlipidemia present in many of these patients. Since a protein-restricted diet is often prescribed in an attempt to preserve renal function, we performed a randomized controlled study in children with chronic renal failure on the effect of a protein-restricted diet on fat intake and serum lipid profiles. Although total fat intake did not change, we found a lower cholesterol intake and a higher polyunsaturated/saturated fat ratio in the patients with the protein-restricted diet. This is probably caused by the restriction of animal protein which results in the replacement of animal fat by vegetable fat in the protein-restricted group. Moreover, we observed an increase of plasma cholesterol and low-density lipoprotein cholesterol in patients with a normal protein intake which was absent in the protein-restricted group. This suggests a favourable effect of the institution of a protein-restricted diet on lipid intake and plasma profile.
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PMID:Protein restriction affects fat intake and serum lipids in children with chronic renal failure. 146 60

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

Disorders of lipid metabolism during chronic renal failure (CRF) play a crucial role in the pathogenesis of early cardiovascular complication of this syndrome. In addition, some experimental evidence suggests that hyperlipidemia may accelerate progression of renal disease. We have studied 65 patients with CRF (S-creatinine 1.5-9.0 mg/dl), 52.3% of whom were hypertensive. Patients were divided in 2 groups matched for age, sex and degree of renal failure: group 1 was kept for 36 +/- 8 months on a free diet; group 2 was kept for 39 +/- 6 months on a low-protein diet with an elevated polyunsaturated/saturated fatty acid (PUFA/SFA) ratio. We found significantly higher levels of triglycerides (TG) and lower levels of esterified cholesterol in high density lipoprotein (HDL-C) in group 1 than in group 2. Patients on the diet had a lower percentage of membrane SFA and a higher percentage of PUFA than patients on free diet. Only in group 1 a direct correlation between cholesterol/phospholipid (Chol/P) ratio and age was observed; in group 2, a negative correlation between levels of PUFA and TG and between linoleic/oleic (Lin/Ol) ratio and serum Chol was shown. S-creatinine levels were directly correlated with Chol/P ratio in group 1 and indirectly with Lin/Ol ratio and PUFA in group 2. These data show that a low-protein diet, containing an elevated PUFA/SFA ratio, is able to counteract lipid abnormalities in patients with CRF and the normalization of this pattern is associated with significant improvement of membrane lipid composition and, presumably, of "functional" activity of cell membranes with a better control of supposed "renal lipoprotein toxicity".
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PMID:Modification of serum and membrane lipid composition induced by diet in patients with chronic renal failure. 207 70

We report the results of a study to assess the glomerular filtration rate in the elderly population seen at the center and to investigate the prevalence of cardiovascular risk factors and use of drugs in this age group. The glomerular filtration rate could be measured in 64.6% of the elderly population. In 94 (17.6%) of the 825 evaluated individuals the clearance values were 50 ml/min or lower. Only 6 of them had previously known chronic renal failure. A high prevalence of concomitant cardiovascular risk factors was found (48.7% were hypertensive, 25.1% diabetic, 19% smokers, 24.1% had hyperlipidemia and 38.8% were obese). The rate of drug use was also high (69.6% took two or more drugs sustainedly). These findings indicate the need to evaluate the renal function in elderly people before prescribing drug therapy.
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PMID:[Determination of the degree of renal functioning and cardiovascular risk factors in an aged population seen at a health center]. 210 55

The overall cardiovascular mortality in patients with chronic renal failure is about 30 per cent of which 10 per cent is attributed to myocardial infarction. This prevalence led some workers to propose a hypothesis of "accelerated atherosclerosis" due to the hyperlipidaemia observed in 30 to 70 per cent of patients. However, the concept of accelerated atherosclerosis, which was based essentially on clinical studies, has been questioned. Pericardial effusion is a common complication of chronic renal failure and has been reported in over 62 per cent of patients in echocardiographic studies. There are many causes and symptoms are often mild; systematic echocardiographic examination of patients with renal failure undergoing haemodialysis has shown 32 per cent of pericardial effusions to be asymptomatic. There are two potential complications: cardiac tamponade and, lesser frequently, constrictive pericarditis. Cardiac failure is a common cause of death in patients undergoing long-term dialysis. The myocardial histological appearances are those of fibrosis, the etiology of which is not fully understood although the dialysis membranes and hypotensive episodes occurring during haemodialysis have been thought to play a role. Left ventricular hypertrophy and fibrosis may give rise to ventricular arrhythmias which could explain some of the cases of sudden death observed in patients with renal failure and often wrongly attributed to ischemic heart disease. Another form of myocardial disease which is observed later is characterised by an alteration of systolic function with left ventricular dilatation and hypokinesia and increased end diastolic pressures without an increase in left ventricular wall thickness. Valvular heart disease may also result from renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[So-called uremic heart diseases]. 210 35

Patients with chronic renal failure treated by maintenance dialysis often have nutritional disorders, metabolic disorders concerning lipids, proteins and carbohydrates, and disorders of endocrine systems involved in the regulation of these metabolisms. These disorders are difficult to diagnose, as their clinical symptoms are few and of little pathognomonic value. Hence the need for anthropometric measurements as well as biochemical and physiological exploration of metabolic pathways for intermittent overall evaluation and longitudinal follow-up. These patients have reduced subcutaneous fat reserves, intolerance to carbohydrates by resistance to insulin (partially corrected by haemodialysis), low levels of plasma aminoacids, notably valine, type IV hyperlipidaemia with low levels of essential fatty acids, fragile immune system and increased requirements for vitamins B, especially B6. Dietary recommendations include: food energy 35 kiloCal/kg bodyweight/day; proteins 1 to 1.2 g/kg bodyweight/day (50 p. 100 of which must be complete proteins) and supplements of vitamins. Dialysis must be optimal for clearance of nitrogen compounds and body homeostasis.
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PMID:[Nutrition, metabolic and endocrine complications during extrarenal dialysis]. 210 47

Lipoprotein [a] (Lp[a]) is known to show high values in patients with ischemic heart disease (IHD). In the present study attempts were made to determine Lp[a] levels and to investigate the association of Lp[a] and other atherosclerotic risk factors in patients with chronic renal failure treated by hemodialysis. Lp[a] concentrations were measured in 30 hemodialysis patients in the age range 34 to 77 years. Mean (+/- SD) levels of serum Lp[a] were not elevated in the hemodialysis patients compared to controls (19.3 +/- 18.0 mg/dl vs. 18.3 +/- 10.4 mg/dl, respectively). We found no statistically significant correlation of Lp[a] with either cholesterol, triglycerides, HDL-C or apoproteins. However, compared with controls, more than fivefold as many of those hemodialysis patients had high risk (greater than 30 mg/dl) concentrations of Lp[a]. Lp[a] tended to increase in hemodialysis patients with diabetes mellitus and/or ischemic heart disease. In patients with high levels of Lp[a] (greater than 30 mg/dl), Lp[a] tended to correlate positively with cholesterol, LDL-, HDL-C, apo B or apo B/AI. Incidence of IHD was also elevated in these patients. Along with other known risk factors such as hyperlipidemia and hypertension, an increased concentration of Lp[a] may play an important role in accelerating development of atherosclerosis in this condition.
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PMID:[A study of clinical significance of Lp[a] lipoprotein in patients with chronic renal failure treated by hemodialysis]. 214 55


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