Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic nephropathy is a frequent complication in type 2 diabetic. Patients with diabetic nephropathy have a characteristic dyslipidemia profile associated increased concentrations of triglycerides, reduced levels of HDL cholesterol, and qualitative abnormalities of LDL. The dyslipidemia management in patients with diabetic nephropathy not yet in dialysis includes diet, insulin sensitizers (glitazones, metformin?), and hypolipemic agents, with statins as a first choice.
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PMID:[Management of dyslipidemia in diabetic CKD patients]. 1737 40

Apolipoprotein (apo) B48 is a structural protein of chylomicrons. Fasting serum levels of apoB48 suggest the presence of small number of remnant chylomicron particles which are thought to be an atherogenic lipoprotein. In view of the high incidence of coronary heart disease (CHD) in patients with diabetic nephropathy, we decided to measure the plasma apoB48 level in type 2 diabetics with diabetic nephropathy at various stages to ascertain how apoB48 relates to the progression of diabetic nephropathy. Patients with type 2 diabetes (n=105) were stratified into four groups: normo-albuminuria, micro-albuminuria, overt-proteinuria, and patients with end-stage renal disease (ESRD) receiving hemodialysis. Age-matched-diabetic hypertensive patients (n=24) and non-diabetic ESRD patients on hemodialysis (n=47) were also enrolled. Plasma triglyceride (TG) levels rose as diabetic nephropathy progressed to overt-proteinuria. No further elevation in TG was observed in diabetic ESRD, however, and the TG levels were normal in non-diabetic ESRD. A similar pattern was observed for remnant-like particle-cholesterol (RLP-C). In contrast to the changes observed for TG and RLP-C, the levels of apoB48 increased steadily as the diabetic nephropathy progressed (control, 3.7; normo, 5.7; micro, 6.9; overt, 10.6 mg/l, respectively). ApoB48 peaked in the diabetic ESRD (19 mg/l) and was also markedly elevated in non-diabetic ESRD (10.1mg/l). The apoB48/TG and apoB48/total-apoB ratios were substantially elevated in both diabetic and non-diabetic ESRD. These results are the first to demonstrate remarkable elevations of plasma apoB48 in patients with both diabetic and non-diabetic ESRD. The remarkably high level of apoB48 in diabetic ESRD seems to be attributable to dyslipidemia induced by both diabetic nephropathy and ESRD.
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PMID:Remarkable increase of apolipoprotein B48 level in diabetic patients with end-stage renal disease. 1746 54

Patients in different stages of diabetic nephropathy (DN) frequently present cardiac disease expressed by myocardial ischemia and/or diabetic cardiomyopathy. These changes are already present at early stages of DN, probably even before urinary albumin excretion (UAE) reaches the traditionally diagnostic levels of microalbuminuria. The cardiac changes are responsible for a significant proportion of the increased death rates in patients with DN and can be reduced through multiple intervention on the several risk factors present in these patients. Cardiac disease assessment should ideally be performed in every patient, irrespective of renal status, through specific methods to detect ischemia and myocardial dysfunction, besides routinely performing 24-h ambulatory blood pressure monitoring. In patients with advanced atherosclerosis, other arteries (aorta, carotid, renal) should be evaluated as well. Intensive treatment of arterial hypertension, and use of cardioprotective drugs, correction of the associated dyslipidemia and anemia, and use of antiplatelet agents can reduce the elevated cardiovascular mortality in patients with DN.
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PMID:[Diabetic nephropathy and cardiac disease]. 1750 31

Abdominal obesity is associated with cardiovascular disease. This study aims to compare two measures of abdominal obesity [waist and wais-to-hip ratio (WHR)] in patients with DM2 to identify cardiovascular risk factors: ischemic cardiopathy, hypertension, dislipidemia, obesity and diabetic nephropathy. A multicentric study was performed in 820 patients with type 2 DM. Waist circumference strongly correlated with body mass index (BMI), for men (r= 0.814; P< 0.05) and women (r= 0.770; P< 0.05). On the other hand, WRH was weakly correlated (r= 0.263, P< 0.05 for men; r= 0.092, P< 0.05 for women). Only waist circumference correlated with systolic pressure (r= 0.211, P< 0.05 for men; r= 0,224, P< 0.05 for women). ROC curve analysis demonstrated the superiority of waist circumference measurement compared to WHR regarding obesity and hypertension for men and women, and dyslipidemia for men. In conclusion, waist circumference is better correlated with cardiovascular risk factor than WRH.
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PMID:[Waist measure and waist-to-hip ratio and identification of clinical conditions of cardiovascular risk: multicentric study in type 2 diabetes mellitus patients]. 1754 44

The course of diabetic nephropathy is affected by several factors that can be manipulated. In primary prevention, near normal metabolic control beginning at the time of the diagnosis of diabetes diminishes the risk of microalbuminuria to an extent depending on the HbA1c level attained. Hypertensive diabetics should be consistently treated with renin-angiotensin system (RAS)-blocking agents. In secondary prevention, a multifactorial therapy is able to stop or retard further progression. Its components are a sustained decrease of blood pressure in the normotensive range using RAS-blocking agents (normotensive patients should also be treated) as well as near normal metabolic control that takes into account the changing pharmacokinetic and pharmacodynamic properties of blood glucose-lowering drugs in renal insufficiency. Consideration of further factors (smoking, protein intake, anemia) and several general nephroprotective measures complete the treatment spectrum. Therapy for dyslipidemia and the administration of aspirin are important in view of the high cardiovascular morbidity. It is essential to monitor kidney function and the therapeutic components at short intervals.
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PMID:[Protection of renal function in diabetics]. 1757 24

Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease.
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PMID:Chronic kidney disease: effects on the cardiovascular system. 1760 56

Metabolic syndrome (MetSyndr), a constellation of abnormalities [obesity, glucose intolerance, insulin resistance (IR), dyslipidemia (low HDL-cholesterol, high LDL-cholesterol and triglycerides (TG)], and elevated blood pressure (BP)], increases the risk of cardiovascular (CV) disease and premature death. From 10% to 30% of the adult population in industrialized countries has MetSyndr, which effectively predicts the development of type 2 diabetes mellitus (T2D) and CV disease. Because of the complex etiology of MetSyndr, a multi-targeted, integrated therapeutic approach is required to simultaneously treat high BP, obesity, lipid disorders and T2D (if present), to fully protect CV, cerebrovascular and renal systems. If lifestyle modification (weight control, diet, exercise, smoking cessation, moderation of alcohol intake) is ineffective, pharmaco-theraphy should be added to treat simultaneously the lipid- and non-lipid CV risk factors. Patients with HTN and MetSyndr should be started on angiotensin-converting enzyme (ACE) inhibitors, unless contraindicated. The ACE inhibitors and angiotensin receptor blockers (ARBs) reduce the odds of developing new onset T2D and also decrease albuminuria. The ACE inhibitors provide cardioprotective and renoprotective benefits beyond their effect on BP; they also improve IR. The ARBs are renoprotective in addition to being cardioprotective. Long-acting calcium channel blockers are also recommended in hypertensive patients with MetSyndr; these drugs also improve IR. Thiazides (at low doses) and selected ss-blockers can be given to patients with HTN and MetSyndr. Celiprolol in combination with diuretics has a favorable effect on glucose tolerance and IR in patients with HTN and MetSyndr, and spironolactone added to ACE inhibitor or ARB therapy provides additional reno- and CV protective benefits in patients with diabetic nephropathy. Carvedilol, a ss-blocker with vasodilating properties, added to ACE inhibitor or ARB therapy, is effective in preventing worsening of microalbuminuria in patients with HTN and MetSyndr; it also improves IR and glycemic control. Most patients eventually require two or more antihypertensive drugs to reach BP goal. It is recommended that therapy in patients whose BP is more than 20/10 mm Hg above target at diagnosis be initiated with a combination of antihypertensive drugs, administered either as individual drugs or as fixed-dose formulations. Treatment with fixed-dose combinations, such as irbesartan + hydrochlorothiazide provides good BP control in more than two-thirds of hypertensive patients with MetSyndr. Lipid and BP targets are reached in a high percent of patients with HTN and CV disease treated with a combination of amlodipine + atorvastatin. In conclusion, hypertensive patients with the MetSyndr be treated aggressively for each component of the syndrome to provide CV, cerebrovascular and renal protection.
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PMID:Metabolic syndrome: treatment of hypertensive patients. 1766 15

Diabetes mellitus confers a high risk of cardiovascular morbidity and mortality and requires aggressive management of all cardiovascular risk factors, including diabetic dyslipidemia. Although levels of low-density lipoprotein cholesterol are often normal or only slightly elevated in persons with diabetes, lipid-altering therapy with statins has been shown in large, randomized, controlled trials to decrease the risk of cardiovascular complications in this patient population. A target low-density lipoprotein cholesterol level of <70 mg/dL is now a therapeutic option in patients at very high risk for coronary heart disease, including patients with diabetes. Diabetes is also a leading cause of end-stage renal disease. In addition to their lipid-modifying effects, statins have been shown to slow the progression of diabetic nephropathy and potentially exert other renoprotective effects; these benefits, however, remain to be confirmed in clinical trials.
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PMID:High cardiovascular risk in patients with diabetes and the cardiometabolic syndrome: mandate for statin therapy. 1767 17

Diabetic nephropathy is a major cause of end-stage renal failure (ESRF) in patients with both type 1 and type 2 diabetes. Many factors such as genetic and non-genetic promoters, hypertension, hyperglycemia, accumulation of advanced glycation end products (AGEs), dyslipidemia, albuminuria and proteinuria influence the progression of this disease. It is important to determine pathogenesis and treatment of this disease. However, it is difficult to investigate since human diabetes is a heterogeneous and multifactorial disease. Therefore, most of these mechanisms have been investigated in animal experiments. KK/Ta mice have a clearly different genetic background in terms of body weight, blood glucose, impaired glucose tolerance (IGT), urinary albumin excretion and serum triglyceride than BALB/c mice. Renal lesions of KK/Ta mice closely resemble those in human early diabetic nephropathy. Thus, the KK/Ta mouse may serve as a suitable model for the study of type 2 diabetes and early diabetic nephropathy in humans. We reviewed genetic susceptibility using genome-wide linkage analysis and differential display polymerase chain reaction (DD-PCR) or Northern blot analysis, and treatment of diabetic nephropathy using angiotensin type 1 (AT1) receptor blockers (ARB) or thiazolidinediones (TZDs) in KK/Ta mice.
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PMID:Pathogenesis and treatment of type 2 diabetic nephropathy: lessons from the spontaneous KK/Ta mouse model. 1822 Jun 4

Accumulation of triosephosphates arising from high cytosolic glucose concentrations in hyperglycemia is one likely or potential trigger for biochemical dysfunction leading to the development of diabetic complications. This may be prevented by disposal of excess triosephosphates via the reductive pentosephosphate pathway. This pathway is impaired in experimental and clinical diabetes by mild thiamine deficiency. The expression and activity of the thiamine-dependent enzyme, transketolase--the pacemaking enzyme of the reductive pentosephosphate pathway, is consequently decreased. Correction of thiamine deficiency in experimental diabetes by high dose therapy with thiamine and the thiamine monophosphate prodrug, Benfotiamine, restores disposal of triosephosphates by the reductive pentosephosphate pathway in hyperglycemia. This prevented multiple mechanisms of biochemical dysfunction: activation of protein kinase C, activation of the hexosamine pathway, increased glycation and oxidative stress. Consequently, the development of incipient diabetic nephropathy, neuropathy and retinopathy were prevented. Both thiamine and Benfotiamine produced other remarkable effects in experimental diabetes: marked reversals of increased diuresis and glucosuria without change in glycemic status. High dose thiamine also corrected dyslipidemia in experimental diabetes--normalizing cholesterol and triglycerides. Dysfunction of beta-cells and impaired glucose tolerance in thiamine deficiency and suggestion of a link of impaired glucose tolerance with dietary thiamine indicates that thiamine therapy may have a future role in prevention of type 2 diabetes. More immediately, given the emerging multiple benefits of thiamine repletion, even mild thiamine deficiency in diabetes should be avoided and thiamine supplementation to high dose should be considered as adjunct nutritional therapy to prevent dyslipidemia and the development of vascular complications in clinical diabetes.
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PMID:The potential role of thiamine (vitamin B1) in diabetic complications. 1822 Jun 5


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