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)

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

Plasma fibronectin (PF) concentrations, were investigated in normolipidaemic and hyperlipidaemic (type IV) patients with chronic renal failure treated with hemodialysis (n = 29) and in controls (n = 34). Mean PF was significantly reduced in both subsets of dialysed patients. Among the hemodialysed patients the presence of hyperlipidaemia did not modify PF levels, which resulted, on the contrary, significantly higher in hyperlipidaemic controls as compared with the normolipidaemic group. In controls, according to a multivariate analysis model, PF was directly related with age and inversely with HDL-cholesterol. In the hemodialysed patients total cholesterol was the unique significant PF related variate, being this group, therefore, characterized by the lack of any inverse relation between PF and HDL-cholesterol. Finally, no PF modifications were observed in hemodialyzed patients affected by arterial hypertension or clinically evident atherosclerotic lesions.
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PMID:Plasma fibronectin in normolipidaemic and hyperlipidaemic uraemic patients treated with haemodialysis. 367 26

To elucidate the pathogenesis of hyperlipidemia in chronic renal disease in children and adolescents, we have measured serum triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-C) and activities of postheparin plasma lipoprotein lipase and hepatic triglyceride lipase (EC 3.1.1.3) in nine patients with transplants, and nine hemodialyzed and 18 conservatively treated patients with chronic renal failure. In 29 of 36 patients, serum insulin levels both in fasting and in response to oral glucose load were measured. The lipase activities were measured separately, utilizing antiserum against hepatic triglyceride lipase. All groups of patients had hypertriglyceridemia. The patients with endogenous creatinine clearance less than 20 ml/min/m2 had a low HDL-C level. The HDL-C level was correlated inversely with serum triglyceride level and positively with glomerular filtration rate. The lipoprotein lipase activities were low in patients with endogenous creatinine clearance less than 20 ml/min/m2. Although hepatic triglyceride lipase activities were not significantly low in any groups of patients, they were correlated with glomerular filtration rates in the conservatively treated patients with chronic renal failure. A defective triglyceride removal due to low lipase activities may contribute to uremic hypertriglyceridemia in these patients. On the other hand, patients with transplants had almost normal lipase activities and exhibited hyperinsulinemia; overproduction of triglyceride due to hyperinsulinemia may contribute to their hypertriglyceridemia.
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PMID:Lipid profiles and lipase activities in children and adolescents with chronic renal failure treated conservatively or with hemodialysis or transplantation. 638 39

Serum lipids, apoprotein and lecithin-cholesterol acyltransferase activities were studied in 27 renal transplant recipients with stable and normal renal function (serum creatinine 0.16 mM/l or less) sustained for more than 1 year following grafting. Hypertriglyceridemia, which was characteristic of hyperlipidemia in 18 hemodialyzed patients with chronic renal failure, was no longer manifest in transplant recipients. On the other hand, de novo hypercholesterolemia was observed posttransplant with mean serum levels of 5.82 +/- 1.34 versus 5.01 +/- 0.88 mM/l in 575 normal controls. As to the high-density lipoprotein metabolism, the cholesterol content (1.72 +/- 0.56 mM/l) was significantly higher in transplant patients than in hemodialyzed patients (0.82 +/- 0.31 mM/l). In contrast, no variation in apoprotein A-I levels was found between both groups of patients, which produced an elevated high-density lipoprotein cholesterol:apoprotein A-I ratio. Thus, derangement in the serum lipid profile, although qualitatively different, continued to be present following transplantation, and its relevance to the cardiovascular morbidity in these patients remains to be evaluated.
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PMID:De novo development of hypercholesterolemia and elevated high-density lipoprotein cholesterol: apoprotein A-I ratio in patients with chronic renal failure following kidney transplantation. 641 53

Chronic renal disease with secondary hyperlipidemia is highly atherogenic. In uremia and patients on chronic hemodialysis there is a high incidence of atherosclerotic complications whereas the incidence of atherosclerotic disease is relatively low in the nephrotic syndrome. This is surprising, as nephrosis produces type-II hyperlipidemia, which is usually highly atherogenic. In this study 10 patients (5 male, 5 female) with a newly diagnosed nephrotic syndrome were compared to 10 controls (5 male, 5 female). As laboratory parameters, lipids, lipoproteins (VLDL, IDL, LDL, HDL2 and HDL3 by rate zonal centrifugation) and the percentage composition of the major apolipoproteins in VLDL, HDL2 and HDL3, as well as lipoprotein lipase (LPL), hepatic lipase (HTGL) and lecithin-cholesterol-acyl-transferase (LCAT) were measured. In nephrotic patients significantly higher plasma levels of cholesterol, triglycerides, phospholipids, VLDL, IDL and LDL were found, whereas HDL-chol, HDL2 and HDL3 were unchanged. LPL and HTGL were both significantly impaired, whereas LCAT was distinctly increased. The percentage composition of apolipoproteins in HDL2 and HDL3 was normal. In nephrotic VLDL, apo-AI was distinctly increased at the expense of a decrease in apo-CII, and increased LCAT was explained by the relative rise of apo-AI in nephrotic VLDL. The increase in apo-AI in VLDL is discussed as a possible reason for the low atherogenic risk of secondary hyperlipidemia in nephrotic syndrome.
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PMID:[Lipoproteins, apolipoproteins, lipoprotein lipase, hepatic triglyceride lipase and lecithin cholesterol acyltransferase in patients with nephrotic syndrome]. 661 72

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a "uremic toxin" responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant "uremic toxin."
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PMID:Parathyroid hormone metabolism and its potential as a uremic toxin. 699 9

We have previously reported that the in vitro enzymatic activity of exogenous renin, plasma renin reactivity (PRR), is increased in plasma of patients with chronic renal failure, possibly due to the deficiency of a renin inhibitor. To determine whether increases PRR is related to renal failure per se or to hyperlipidemia, PRR was measured in 10 control subjects, 10 patients with renal failure, and 10 hyperlipidemic patients with normal renal function. Compared to that in control subjects (52.6 ng angiotensin I generated per ml/h +/- 3.8 SE) PRR was increased (P < 0.05) in plasma of uremic patients (65.1 +/- 4.3) and hyperlipidemic patients (71.4 +/- 10.7). Renin substrate concentration did not differ among groups, and after denaturation of endogenous substrate by acidification of plasma, PRR was still increased. A "protein-free" extract of plasma from normal subjects inhibited renin, whereas little or no inhibition occurred with a comparable extract from uremic patients and hyperlipidemic patients. Thus, alterations in lipid metabolism may account for the increased enzymatic activity of renin in uremic plasma. Increased PRR may be related to the deficiency of a normally occurring renin inhibitor.
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PMID:Increased enzymatic activity of renin and hyperlipidemia. 700 15

We performed oral fat loading tests in 10 patients with chronic renal failure (CRF) on hemodialysis (5 children and 5 adults). Fat absorption was measured by hourly determination of serum triglycerides (TG), cholesterol (CHOL), and lipoproteins (LP) after oral administration of a 'milkshake' containing 50 g of fat of dairy origin. 10 age-matched healthy volunteers with normal fasting serum TG levels and 10 subjects with fasting hypertriglyceridemia served as controls. Mean fasting serum TG levels in CRF patients were elevated compared to normal controls (177.6 +/- 14.6 mg/dl, 2.0 +/- 17 mmol/l vs. 91.0 +/- 10.5 mg/dl, 1.03 +/- 12 mmol/l). 6 patients (4 adults, 2 children) had type IV LP patterns and 2 patients (both children) showed type IIb hyperlipidemia. In only 2 patients, 1 child and 1 adult were TG, CHOL and LP electrophoresis all normal. The oral fat loading test in all CRF patients showed delayed appearance of TG and chylomicrons (CHYL) in the bloodstream i.c. impaired or slow absorption of fat from the gut. In contrast to normal and hypertriglyceridemic controls, TG and CHYL levels in CRF did not decrease by 5 h after the oral fat load. This study demonstrates impaired intestinal fat absorption in children and adults with CRF.
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PMID:Impaired intestinal fat absorption in chronic renal failure. 709 22

The effects of chitosan-coated dialdehyde cellulose (Chitosan DAC), a newly developed oral adsorbent of urea and ammonia, were examined in rats with progressive chronic renal failure (CRF) induced by adriamycin. CRF rats induced by repeated injections of adriamycin were fed a diet containing chitosan DAC (5% content) or Kremezin (5% content), an oral charcoal adsorbent (AST-120) under strict paired-feeding for four months. CRF rats that received both a normal diet and Kremezin showed progressive azotemia, hyperphosphatemia, hyperlipidemia, proteinuria, and anemia, and began to die from 9 weeks after feeding started. In contrast, chitosan DAC-treatment showed marked prolongation of the survival period and decreases in blood urea nitrogen, serum creatinine, and serum phosphate. In addition, chitosan DAC-treatment ameliorated anemia in CRF rats, although hyperlipidemia and proteinuria were not improved. Furthermore, fecal weight, fecal water content, fecal nitrogen and fecal sodium were markedly increased, and the apparent protein ratio was decreased in CRF rats fed a diet containing chitosan DAC for 9 weeks. In contrast, none of these effects were observed in CRF rats receiving Kremezin. These observations suggest the further possibility of using oral adsorbent therapy for CRF patients.
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PMID:[Pharmacological properties of chitosan-coated dialdehyde cellulose (chitosan DAC), a newly developed oral adsorbent (II). Effect of chitosan DAC on rats with chronic renal failure induced by adriamycin]. 755 38

Recent apheresis therapy is developing day by day. Now we can say that we do not achieve suitable treatment without an apheresis technology. Acute and chronic renal failure, severe hepatic failure, acute necrotic pancreatitis and MOS are not able to treat without haemodialysis (HD), haemofiltration (HF) and plasma exchange (PE). Immunomodulation for immune complex diseases and removing of pathologic antibodies are controlled by this technique. In the near future, it will play an important role for controlling of xenotransplantation. LDL apheresis for hyperlipidemia is very effective in cleaning the blood, and the prevention of ASO, angina syndrome and coronary disease is discussed. LAK therapy and immune therapy using apheresis technique have been effective for cancer and it will be developed moreover. Lastly, apheresis used to prevent aging is the music of the future.
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PMID:[Today's apheresis therapy]. 774 69


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