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)

Patients with chronic renal failure retain Na+ and H2O, and they retain K- and acid. This disordered homeostasis results in hypertension, edema, hyperkalemia and acidosis. Diuretics may be used to favorably modify these disturbances. However, because of the limited filtered load of water and electrolytes, and the low renal blood flow, measures need to be taken to maximize the response to diuretics. These measures include: (a) the use of the most bioavailable drug, torasemide, when using the oral route; (b) the use of the drug with the least hepatic elimination, furosemide, when using the intravenous route; (c) the use of combinations of loop- and distal tubule-acting diuretics; (d) the use of the maximum effective diuretic dose; and (e) the use of repeated doses or constant infusion. In benefiting hypertension, vascular congestion and hyperkalemia diuretics appear to exert their effects not only on the kidneys but also on extrarenal sites, such as the vascular tree and the gastrointestinal tract. The use of diuretics, however, is not without complications, which include: intravascular volume depletion and azotemia, ototoxicity (when using loop-acting diuretics), hyperlipidemia, acute pancreatitis, hyperkalemia (when using K(+)-sparing agents), and acidosis (when using carbonic anhydrase inhibitors).
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PMID:Use of diuretics in chronic renal failure. 918 1

We compared plasma lipid and lipoprotein parameters between 210 chronic renal failure patients treated by hemodialysis and 223 age- and sex-matched healthy control subjects to examine whether atherogenic lipoprotein changes were present in hemodialysis patients in the absence of hyperlipidemia. The hemodialysis group showed higher levels of plasma triglycerides, very low density lipoprotein (VLDL) cholesterol, and intermediate density lipoprotein (IDL) cholesterol and a lower level of high density lipoprotein (HDL) cholesterol. Low density lipoprotein (LDL) cholesterol of the hemodialysis group was not elevated but their LDL was significantly more triglyceride-enriched than that of controls. Subjects were then divided into five categories according to their plasma triglyceride levels at an interval of 50 mg/dl, and comparison was made between the two groups in the same range of plasma triglycerides. Hemodialysis patients again showed higher levels of VLDL- and IDL-cholesterol, and lower levels of HDL-cholesterol than the control group even in the plasma triglycerides-matched comparisons. Similarly, higher VLDL- and IDL-cholesterol levels in hemodialysis patients were significant in plasma total cholesterol-matched subgroup comparisons. Multiple regression analysis indicated that the relationship between plasma lipid concentrations and individual lipoprotein levels were substantially altered in uremic state. The 95th percentile level of IDL-cholesterol in the nonuremic controls was 15 mg/dl, and 45% of hemodialysis patients exceeded this level. Decreased HDL-cholesterol levels < or = 35 mg/dl were seen in 6% of the control and 38% of the hemodialysis group. Elevated IDL-cholesterol and decreased HDL-cholesterol were persistently found in hemodialysis patients with normal lipid levels. It is concluded that hemodialysis patients exhibited more atherogenic lipoprotein profile than nonuremic subjects with comparable levels of plasma triglycerides and total cholesterol. Especially, increased IDL- and decreased HDL-cholesterol levels in hemodialysis patients persisted even at very low levels of plasma lipids. Since elevated IDL and decreased HDL-cholesterol are implicated in the progression of atherosclerosis, these findings are of clinical importance in the diagnosis of lipoprotein disorder in chronic renal failure.
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PMID:Atherogenic lipoprotein changes in the absence of hyperlipidemia in patients with chronic renal failure treated by hemodialysis. 919 76

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

The anorexia of chronic renal failure (CRF) is frequently managed with enteral feeds using combinations of commercial preparations, glucose polymers and fat emulsions. Such feeds might predispose to atherogenic blood lipid profiles. Our aim, therefore, was to compare the blood lipid profiles of enterally fed and non-enterally fed children. Plasma lipid subfractions were measured in 37 children with CRF managed conservatively and 10 managed with peritoneal dialysis (PD); 10 of the children were tube fed, 5 of whom were on PD. Results were compared between these groups. Overall, triglycerides (TGs, mean +/- SD) were high (2.3 +/- 1.4 mmol/l) and total cholesterol (TC) was at the upper limit of normal (5.2 +/- 1.5 mmol/l). Low-density lipoprotein (LDL), high-density lipoprotein (HDL), apoprotein A1 (apo A1), A2 (apo A2) and B (apo B), and lipoprotein (a) [Lp(a)] were within the normal range. There was an inverse correlation between TGs and glomerular filtration rate (P = 0.0001). There were no differences in the levels of TC, TG, LDL, HDL, apo A1, apo A2 or Lp(a) between tube-fed and non-tube-fed children. We conclude that enteral feeding does not enhance hyperlipidaemia.
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PMID:Effect of enteral feeding on lipid subfractions in children with chronic renal failure. 968 60

The indices of cardiac performances were compared between 31 continuous ambulatory peritoneal dialysis (CAPD) and 20 long-term hemodialysis (HD) patients. They were subdivided into three groups according to dialysis duration: L-CAPD (n = 16, mean age and CAPD duration were, respectively, 53 +/- 8 [SD] years and 77 +/- 13 months); S-CAPD (n = 15; 52 +/- 12 years, 28 +/- 12 months); HD (n = 20; 51 +/- 10 years, 162 +/- 52 months). The diabetic HD patients (DM-HD; n = 13; 60 +/- 13 years of age, 22 +/- 11 months) were chosen separately. Thirteen normotensive subjects with normal kidney function (mean age, 57 +/- 9 years) were selected as an age-matched control group. There were no significant differences between groups in age, gender, incidence of original kidney disease, or serum biochemical data. The blood pressure and the cardiothoracic ratio in L-CAPD were highest among groups. The indices of left ventricular (LV) hypertrophy as well as LV performance by means of echocardiography or pulsed Doppler were compared. Among nondiabetic dialysis patients, the calculated LV mass index (LVMI) of 166.4 +/- 84.3 g/m2 and the ratio of the peak atrial filling velocity to the peak diastolic flow velocity of 1.25 +/- 0.4 in L-CAPD were greatest, and the left ventricular fractional shortening (%FS) of 34.2 +/- 10.8% in L-CAPD was smallest. LVMI or %FS of L-CAPD was the same as DM-HD of 161.0 +/- 40.7 g/m2 or 31.6 +/- 8.2%. Possibly, poor control of hypervolemia, which is caused by peritoneal problems induced by either peritonitis or chronic exposure to high-glucose dialysate, causes a substantial cardiac preload leading to incipient cardiac failure in L-CAPD. According to the similar results of L-CAPD and DM-HD, it may be that hypertension, hyperlipidemia, or long-term constant glucose loading of CAPD fluids in addition to impaired glucose tolerance by chronic renal failure is more or less related to the progression of LV hypertrophy and latent cardiac dysfunction in long-term CAPD patients. In this context, CAPD of more than 5 years' duration is disadvantageous for preserving cardiac function as compared with HD.
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PMID:Disadvantage of long-term CAPD for preserving cardiac performance: an echocardiographic study. 974 Jan 66

Homocysteine (Hcy) represents a branching point between the transsulfuration and transmethylation pathway of methionine. A large increase of plasma concentration of Hcy is observed in patients with inherited hyperhomocysteinemia. A moderated increase (above 10 microM) is also observed in various pathological conditions, such as arterial occlusion, hypertension, hyperlipidemia and chronic renal failure. While amino acids were largely studied using capillary electrophoresis with UV or laser-induced fluorescence detection (LIF), thiol-amino acids were not. In this work we present a new approach for testing homocysteine in human plasma using CE-LIF and fluorescein isothiocyanate. The low fluorescence yield of the fluorescein thiocarbamyl (FTC) thiol-amino acids limits, probably, the sensitivity of the detection to 8 x 10(-10) M (instead of 10(-12) M for FTC-arginine).
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PMID:Quantitation of homocysteine in human plasma by capillary electrophoresis and laser-induced fluorescence detection. 976 92

Cardiovascular disease remains the leading cause of death in the end-stage renal disease (ESRD), chronic renal failure, and transplant patient population. The majority of dialysis patients begin renal replacement therapy with a disproportionate cardiovascular disease risk factor burden, eg, premature atherosclerosis, hypertensive vascular disease, nonhypertensive left ventricular dysfunction, hyperlipidemia, age, and so on. Each of these accelerates the other. This report will review hypertension in the ESRD patient population. The Joint Clinical Practices Committee of the Renal Physicians Association and the American Society of Nephrology was asked to develop an evidence-based clinical practice guideline for the treatment of hypertension in chronic renal failure and the ESRD patient, to be presented to the Health Care Financing Administration (HCFA). The group was also asked to identify areas for future study and prepare an up-to-date bibliography in the field. Based on an in-depth review of the literature, the committee concluded that not enough data were available to submit an evidence-based clinical practice guideline. Thus, a treatment algorithm was not provided to the HCFA. This manuscript, based on the scientific data for the report to the HCFA, is an in-depth review of the literature on hypertension in the ESRD patient. Pathogenesis, relation to outcome, clinical therapeutic guidelines, and areas for future study are discussed. In addition, the separate exhaustive bibliography (obtainable from the National Kidney Foundation) for hypertension, renal disease, and dialysis should be a valuable resource to all nephrologists interested in clinical practice and research.
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PMID:Hypertension in the ESRD patient: pathophysiology, therapy, outcomes, and future directions. 982 Apr 38

Cardiovascular disease is the major killer in ESRD. Cardiovascular death risk is at least an order of magnitude higher in ESRD patients, even after adjusting for age and diabetic status. Cardiac failure is a rapidly lethal condition in ESRD patients which appears to mediate much of the adverse prognostic impact of ischemic heart disease. Left ventricular abnormalities are present at initiation of dialysis in about 80% of dialysis patients. These are very highly predictive of future ischemic heart disease, cardiac failure, and death after 2 years on dialysis therapy. Regression of these abnormalities improves prognosis. The associations between many classical risk factors like hyperlipidemia, smoking and hypertension and cardiac outcomes in ESRD are inconsistent. Many factors unique to ESRD and its therapy may be important. In our prospective 10 year study of 433 patients starting dialysis, the following were major risk factors for cardiac disease: hypertension (concentric LVH, LV dilatation, de novo ischemic heart disease, de novo cardiac failure, inverse relationship with mortality); anemia (LV dilatation, de novo cardiac failure and death); hypoalbuminemia (de novo ischemic heart disease, de novo cardiac failure and death). LV abnormalities tended to worsen on dialysis and improve after transplantation suggesting that a uremic environment is cardiotoxic. Many risk factors act in concert to produce cardiovascular disease in ESRD. Many can be treated, suggesting that the huge burden of disease can be reduced considerably.
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PMID:Cardiovascular disease and mortality in ESRD. 983 Dec 36

Aggressive immunosuppressive therapy should be considered for patients with proliferative lupus nephritis as the risk for progression to end stage renal disease is high. Intermittent intravenous cyclophosphamide therapy improves renal survival; longer duration of therapy is associated with fewer relapse of nephritis and decreased risk of diminished renal function. While azathioprine therapy does not differ statistically from steroids alone in prolonging renal survival, this therapy may be considered in patients with few risk factors for progression to renal insufficiency. Methylprednisolone as a single therapy does not prolong renal survival compared with regimens including cyclophosphamide. Plasmapheresis remains under study but has not shown additional benefit in treatment of severe lupus nephritis. The potential roles for cyclosporin A and mycophenylate mofetil in the therapy of proliferative lupus nephritis remain to be defined. Supportive care including rigorous control of hypertension, consideration of angiotensin receptor inhibition or blockade to reduce proteinuria and prolong renal function, control of hyperlipidemia, prevention of osteoporosis, and prevention of pregnancy remain important clinical goals. Current research efforts focus on genetic and socioeconomic factors involved in racial differences in expression of lupus nephritis, hormonal manipulation to preserve gonadal function during cyclophosphamide therapy, and the potential impact on lupus activity of estrogen-containing oral contraceptives or postmenopausal hormone replacement therapy.
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PMID:Immunosuppressive therapy of lupus nephritis. 988 1

End-stage renal disease from diabetic nephropathy, mainly due to type II diabetes, is an increasing problem in Western countries. The pathogenesis of diabetic nephropathy is still incompletely understood and much of the experimental insight has been obtained from insulinopenic animal models, resembling type I diabetes. This review therefore aims to describe available rodent models of nephropathy associated with type II diabetes. The review focusses on the metabolic as well as renal functional and structural changes. The usefulness of these rodent models to study renal involvement in type II diabetes is discussed with particular emphasis on confounding factors such as hyperlipidemia, hypertension, immunologic abnormalities, urogenital structural abnormalities and other associated pathological conditions. In addition recent observations on two rat strains, the obese Zucker (fatty) and Goto Kakizaki (GK) rat, are discussed in detail.
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PMID:Rodent models of nephropathy associated with type II diabetes. 1044 May 13


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