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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because diabetes confers a very high risk of cardiovascular morbility and mortality, an aggressive hypolipidemic and antiplatelet treatment has been strongly recommended in the whole diabetic population. In particular, patients who have diabetes should be considered in "secondary prevention" even before presenting cardiovascular events, because diabetes is a "coronary heart disease equivalent." Furthermore, because renal failure is a cardiovascular risk factor per se, patients with diabetes and renal disease present an even greater risk for atherosclerotic vascular events and should be treated even more intensively with hypolipidemic and antiaggregating drugs: the presence of renal impairment does not justify a nihilist therapeutical approach, even if appropriate cautions are mandatory. Finally, dyslipidemia contributes to the deterioration of renal function, a phenomenon potentially prevented by hypolipidemic therapy.
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PMID:Optimization of hypolipidemic and antiplatelet treatment in the diabetic patient with renal disease. 1468 65

Hyperuricemia (HU) is present in 5-30% of the general population, although the prevalence is higher among some ethnic groups and seems to be increasing worldwide. Classically, chronic HU has been considered a risk factor for gout or lithiasis and is associated with alcoholism, obesity, hypertension, dyslipidemia, hyperglycemia/diabetes mellitus, renal failure and intake of certain drugs. HU is also associated with cardiovascular diseases such as hypertension, vascular disease, pre-eclampsia, pulmonary arterial hypertension, stroke, heart failure, ischemic heart disease and also metabolic syndrome, renal disease and increased mortality. It is uncertain if these associations are dependent or not, especially cardiovascular and renal diseases. Patients with chronic HU and also those with gout require both medical investigation for associated diseases or drugs as well as nutritional counseling and life-style changes. HU should alert physicians to possible complications.
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PMID:Primary prevention in rheumatology: the importance of hyperuricemia. 1512 Oct 34

The reduction of cardiovascular disease risk in kidney failure involves treatment of modifiable risk factors and provision of proven interventions to patients with established disease. Volume status management is key to blood pressure control. Statins are the agents of choice for the treatment of dyslipidemia. Target hemoglobin levels should be achieved using intravenous iron and erythropoietic agents. Combinations of calcium and noncalcium-containing phosphorus binders and vitamin D and its analogues should be used to attain target parathyroid hormone, phosphorus, and calcium phosphorus product levels. beta Blockers and aspirin are recommended in patients with ischemic heart disease and angiotensin-converting enzyme inhibitors (or angiotensin II receptor blockers), and beta blockers are recommended in patients with heart failure with reduced ejection fraction. In patients who require revascularization, studies suggest a survival benefit of coronary artery bypass graft surgery over percutaneous transluminal coronary angioplasty and coronary artery stenting.
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PMID:Treating the Patient with Kidney Failure to Reduce Cardiovascular Disease Risk. 1521 21

Patients with end-stage renal disease have markedly increased risk for death from cardiovascular disease. Renal failure is associated with multiple metabolic and endocrinologic abnormalities, and these alterations are involved in advanced atherosclerosis and high cardiovascular risk. Increased insulin resistance index by homeostasis model assessment (HOMA-IR), a simple index of insulin resistance, was an independent predictor of cardiovascular mortality in nondiabetic patients on maintenance hemodialysis. Renal failure impairs lipoprotein metabolism leading to the atherogenic lipoprotein profile characterized by increased triglyceride-rich remnant lipoproteins such as intermediate-density lipoprotein, an independent factor of increased aortic stiffness. Non-high-density lipoprotein cholesterol, the sum of cholesterol of intermediate-density lipoprotein and other apoB-containing lipoproteins, is an independent factor associated with increased arterial thickness and a predictor of cardiovascular death in hemodialysis patients. The risk for cardiovascular death in hemodialysis patients is associated closely with hypertension and malnutrition, but not with obesity. The constellation of insulin resistance, dyslipidemia, hypertension, and malnutrition in renal failure suggests the presence of another type of metabolic syndrome promoting cardiovascular disease. In addition, vitamin D deficiency and abnormalities in calcium, phosphate, and parathyroid hormone levels increase the death risk from cardiovascular disease in renal failure. It is expected that treatment of these metabolic and endocrinologic alterations would improve the survival of patients with renal failure.
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PMID:Roles of metabolic and endocrinological alterations in atherosclerosis and cardiovascular disease in renal failure: another form of metabolic syndrome. 1549 Apr 3

The metabolic effects of obesity have made this highly prevalent disease one of the most common risk factors for diabetes, hypertension, and atherosclerosis, the leading causes of end-stage renal failure. However, obesity per se, as defined by body mass index, is less predictive of the development of these diseases than is the presence of a constellation of obesity-related abnormalities now known as the metabolic syndrome. Recognition of this syndrome, which can readily be identified in clinical settings using defined threshold values for waist circumference, BP, fasting glucose, and dyslipidemia, allows for earlier intervention in these high-risk patients. Systemic insulin resistance has been implicated as one possible factor that links visceral obesity to adverse metabolic consequences; however, the mechanism whereby adipose tissue causes alterations in insulin sensitivity remains unclear. Infection and inflammation are commonly associated with insulin resistance, and visceral obesity is associated with a chronic, low-grade inflammatory state, suggesting that inflammation may be a potential mechanism whereby obesity leads to insulin resistance. Moreover, adipose tissue is now recognized as an immune organ that secretes numerous immunomodulatory factors and seems to be a significant source of inflammatory signals known to cause insulin resistance. Therefore, inflammation within white adipose tissue may be a crucial step contributing to the emergence of many of the pathologic features that characterize the metabolic syndrome and result in diabetes and atherosclerosis. This review describes the role of proinflammatory cytokines and hormones released by adipose tissue in generating the chronic inflammatory profile associated with visceral obesity.
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PMID:The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity. 1550 32

Patients with chronic kidney disease (CKD) have a substantially increased risk of cardiovascular disease (CVD) compared with the general population. The high prevalence of established traditional risk factors for atherosclerosis (diabetes, hypertension, dyslipidemia) in these patients undoubtedly contributes to the accelerated rate of vascular disease. In addition, several hypotheses have emerged to explain the high prevalence of CVD in patients with chronic renal failure. Growing evidence has been gathered over the last 15 years regarding the role of uremia-related risk factors such as inflammation and oxidant stress in the pathogenesis of atherosclerosis in subjects with renal failure. This paper will review current knowledge regarding the potential role of these non-traditional or uremia-related risk factors for atherosclerosis with special emphasis on prevalence, cardiac risk, and management in patients with CKD.
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PMID:[Vascular risk factors and renal failure]. 1558 63

The manifestations of gout can be abolished permanently by lifelong urate-lowering therapy maintaining serum urate levels under 360 mmol/l, as this ensures dissolution of pathogenic crystals of monosodium urate monohydrate. Benzbromarone has been withdrawn from the market, leaving allopurinol as the only urate-lowering drug readily available in France. Allopurinol may induce unacceptable side effects, and in patients with dose-limiting renal failure it may not be sufficiently effective. Because allopurinol can induce serious side effects when given concomitantly with purine antimetabolites, it is contraindicated in organ transplant recipients. In patients who cannot tolerate allopurinol, dietary treatment, discontinuation of diuretic agents, and use of losartan or fenofibrate to treat concomitant hypertension or dyslipidemia, respectively, may ensure adequate control of serum urate levels. Desensitization to allopurinol can be attempted in patients with mild cutaneous hypersensitivity reactions but is difficult to perform and rarely used. Uricosuric agents may be helpful in patients with normal or diminished urate excretion. Probenecid is available in France from hospital pharmacies, and benzbromarone can be prescribed via a time-limited authorization procedure. Rasburicase, an Aspergillus urate oxidase produced by genetic engineering, is indicated to prevent acute hyperuricemia induced by chemotherapy for hematological malignancies. Factors that limit the use of rasburicase include the absence of a marketing authorization, the need for parenteral administration, and the absence of validated treatment schedules. Patients with renal failure precluding the use of effective allopurinol dosages are good candidates for benzbromarone therapy. Organ transplant recipients can be given benzbromarone, within the current restrictions to its use; alternatively, mycophenolate mofetil can be substituted for calcineurin inhibitors, which elevate serum urate levels, or for azathioprine, which contraindicates the use of allopurinol.
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PMID:Current management of gout in patients unresponsive or allergic to allopurinol. 1558 27

The results of new investigations have demonstrated that the appearance of microalbuminuria (urinary albumin excretion rate, UAER>30 mg/24 h) in patients with diabetes increases constantly in about 30% of them only, leading to development of renal failure. In the majority of patients, the contemporary methods of treatment permit the normalization of UAER or the inhibition of progression to macroalbuminuria (UAER>300 mg/24 h). Therefore the actual diagnostic criterion for diabetic nephropathy consists of demonstration of persistent macroalbuminuria (or proteinuria > 0,5 g/24h) and diabetic retinopathy when other kidney or urinary tract diseases can be excluded. Persistent micro- or macroalbuminuria are contemporary considered as the markers of generalized vascular endothelial damage, reflecting increased vascular wall permeability for albumin, which is early event in development of atherosclerosis. An association of several traditional risk factors for atherogenesis, including elevated blood pressure levels, dyslipidemia, procoagulatory state, chronic inflammation and increased production of vascular endothelial growth factor (VEGF), with micro- and macro-albuminuria, was demonstrated. The presence of multiple risk factors for atherogenesis and micro- or macro-albuminuria in patients with diabetes is associated with increased incidence of cardiovascular complications and mortality when compared to normoalbuminuric patients. The effective intervention against all factors involved in the development of vascular changes in patients with diabetes is the main target for therapeutic intervention.
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PMID:[What is new in the treatment of diabetes?--The importance of nephro- and cardioprotective management]. 1566 3

Patients with diabetic nephropathy are known to be associated with many lipoprotein abnormalities, including higher plasma levels of very low-density lipoprotein, low-density lipoprotein and triglycerides, and lower levels of high-density lipoprotein. Many studies have reported that lipids may induce both glomerular and tubulointerstitial injury through mediators such as cytokines, reactive oxygen species, chemokines, and through hemodynamic changes. Clinical studies in patients with diabetic nephropathy showed that lipid control can be associated with an additional effect of reduction in proteinuria. Experimental studies demonstrated that lipid-lowering agents exerted a certain degree of renoprotection, through both indirect effects from lipid lowering and a direct effect on cell protection. Therefore, lipid control appears to be important in the prevention and treatment of diabetic nephropathy. Diabetic nephropathy has become the leading cause of end-stage renal failure in many countries, including Taiwan. One of the major risk factors for the development and progression of diabetic nephropathy is dyslipidemia. In this paper we will review the role of lipid in mediating renal injury and the beneficial effects of lipid control in diabetic nephropathy.
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PMID:Role of lipid control in diabetic nephropathy. 1575 42

The incidence of type 2 diabetes mellitus is increasing world-wide, and is now one of the leading causes of end-stage renal disease in Western countries. Type 2 diabetes mellitus is also a major risk factor for cardiovascular events. Therefore, the early identification of patients at greatest risk, and the subsequent initiation of renal and cardiovascular protective treatments, are of the utmost importance. Microalbuminuria refers to a subclinical increase in urinary albumin excretion. By definition it corresponds to an albumin excretion rate of 20 to 200 microg/min (30 to 300 mg/day) or an albumin to creatinine ratio (mg/mmol) of 2.5 to 25 in males and 3.5 to 35 in females. Microalbuminuria is an important clinical finding because it is not only associated with an increased risk of progression to overt proteinuria (macroalbuminuria) and renal failure, but also cardiovascular events. In patients who progress to overt nephropathy, microalbuminuria usually precedes macroalbuminuria by an interval of 5 to 10 years. In patients with type 1 diabetes mellitus, blood pressure increases and renal function declines after the onset of macroalbuminuria. However, in patients with type 2 diabetes mellitus, hypertension and a decline in renal function may occur when albumin excretion is still in the microalbuminuric range. Large clinical trials have demonstrated that achieving tight glycemic (i.e. glycosylated hemoglobin < 7.0%) and blood pressure (i.e. < 130/85mm Hg) control retards the progression of renal disease. There is accumulating evidence to suggest that the use of antihypertensive agents which target the renin-angiotensin system (RAS) can slow the progression of renal disease and provide cardioprotection in patients with type 2 diabetes mellitus and microalbuminuria. Antihypertensive agents which target the RAS also appear to have advantages over and above reductions in systemic blood pressure. In summary, the annual screening of patients with type 2 diabetes mellitus for microalbuminuria, and the initiation of measures to retard the progression of renal and cardiovascular disease, are now considered part of routine clinical practice. In particular, the finding of microalbuminuria should provoke an intensified modification of the common risk factors for renal and cardiovascular disease, that is hyperglycemia, hypertension, dyslipidemia and smoking. Antihypertensive therapy in patients with microalbuminuria and type 2 diabetes mellitus should be initiated with angiotensin converting enzyme (ACE) inhibitors or angiotensin-II type 1 receptor antagonists.
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PMID:Treatment of microalbuminuria in patients with type 2 diabetes mellitus. 1579 9


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