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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

According to contemporary views, the endothelium is not only a barrier separating blood from surrounding tissues, but a dynamic, heterogeneous organ, which possesses many secretory, metabolic and immunologic functions. Endothelial cells produce mediators, which regulate blood flow, influence platelet adhesion and aggregation, coagulation and fibrinolysis and also immunological response. Endothelial dysfunction is defined as an imbalance between vascular relaxing and contracting factors, between procoagulant and anticoagulant mediators or growth-inhibiting and growth-promoting substances. The definition is often confined to dysfunction of the vessel wall tonus control. The endothelial dysfunction frequently proceeds structural changes in vessels, as e.g. atherosclerotic plaque formation, neointima formation and vessel wall remodelling. This dysfunction has been confirmed in systemic hypertension, atherosclerosis, cardiac syndrome X, heart failure, using various invasive and non-invasive techniques. There are pharmacologic and non-pharmacologic methods to modify endothelial functions. It is obligatory to reduce risk factors of atherosclerosis, which lead to endothelial cell damage, i.e. hypertension, hyperlipidemia, cigarette smoking, estrogen deficiency and elevated levels of homocysteine. The role of physical exercise, low-cholesterol diet, discontinuation of smoking is emphasised. Among drugs statins, angiotensin-converting enzyme inhibitors and hormone replacement therapy are considered particularly beneficial. The importance of angiotensin receptor antagonists, endothelin receptor antagonists, L-arginine, growth factors and calcium-channel blockers for the improvement of endothelial function is studied.
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PMID:[Vascular endothelium--function, disorders and clinical modification probes]. 1171 25

Type II diabetes and hypertension are two pathologies which are frequently associated in adults, especially in developed countries. All the more so when patients are also obese: obesity is today, and will be in the next future, a true epidemic in these countries. These three pathologies imply a risk for cardiovascular complications much higher than that due to an isolated arterial hypertension. This increased risk is probably due to many factors: hyperglycemia, a dismetabolic syndrome (hyperlipemia, hyperuricemia, thrombophilia, altered Na(+)-H+ membrane exchanges = syndrome X) and hyperinsulinemia which favor atherosclerosis and clinical events. Consequently non-pharmacological and aggressive pharmacological therapy is necessary. Even if the trials done in the last years are questionable and not totally convincing, all researchers agree that lowering blood pressure to normality is the best way to improve prognosis of these patients. Usually for this purpose we need a therapy with more than one drug. Among the antihypertensive drugs, ACE-inhibitors (and perhaps also angiotensin receptor blockers) are preferred, especially in those hypertensives with diabetes who have also microalbuminuria or a frank proteinuria.
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PMID:[Diabetes and arterial hypertension]. 1177 8

Steroid-resistant nephrotic syndrome of childhood poses a dilemma in attempting to balance toxicity of medications against long-term prognosis. This report presents our preliminary experience with the novel use of combined mycophenolate mofetil (MMF) and angiotensin blockade (AB) in the treatment of nine children and young adults with focal glomerulosclerosis (FSGS). All patients were steroid resistant and had failed conventional treatment regimens. Prior to the initiation of the MMF-AB protocol, the patients were pre-treated with weekly intravenous methylprednisolone (MP) (15 mg/kg per week) for 4-8 weeks. Angiotensin-converting-enzyme inhibitors and/or angiotensin receptor blockers were begun when intravascular volume was restored. MMF was given at a dose of 250-500 mg/m(2) per day. Proteinuria, as measured by urine protein/creatinine ratios (Up/c), decreased by 43% following MP ( P<0.05). After 6 months of MMF-AB protocol, the Up/c was 72% below baseline ( P<0.01). This level was maintained for a minimum of 24 months of observation. Similarly, hyperlipidemia, as measured by total cholesterol and triglycerides, improved significantly with treatment (536+/-163 to 265+/-70 mg/dl, 447+/-168 to 230+/-92 mg/dl, respectively, P<0.01). Our data support the use of MMF and AB for treatment of steroid-resistant FSGS when other conventional treatments have failed and/or induced toxicity.
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PMID:Novel therapy of focal glomerulosclerosis with mycophenolate and angiotensin blockade. 1281 52

When kidney disease of any aetiology results in substantial loss of nephrons, a common clinical syndrome, characterised by hypertension, proteinuria and a progressive decline in renal function, ensues. This observation suggests that common mechanisms may contribute to progressive renal injury and that therapeutic interventions that inhibit these common pathways may afford renal protection. Research to date has identified several mechanisms that may contribute to progressive renal injury including glomerular haemodynamic changes, multiple effects of angiotensin II and detrimental effects of excessive filtration of plasma proteins by injured glomeruli. Clinical trials over the past decade have identified several interventions that are effective in slowing the rate of progression of chronic kidney disease (CKD). The use of ACE inhibitors, angiotensin receptor antagonists or a combination of the two should be regarded as fundamental to any therapy for slowing the rate of CKD progression. Hypertension should be treated aggressively to achieve a blood pressure target of < 130/80 mm Hg. Reduction of proteinuria to < 0.5 g/day should be regarded as an independent therapeutic goal. Although inconclusive, there is some evidence to support moderate dietary protein restriction to 0.6 g/kg/day in appropriate patients. Hyperlipidaemia may contribute to CKD progression and should be treated to reduce cardiovascular risk and potentially improve renal protection. Smoking cessation should be encouraged and, where necessary, assisted. Among diabetic patients tight glycaemic control should be achieved (glycosylated haemoglobin < 7%). These interventions are simple and relatively inexpensive. If applied to all patients with CKD they will result in substantial slowing of renal function decline in many patients and thereby reduce the number who progress to end-stage renal disease and require renal replacement therapy.
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PMID:Slowing the progression of adult chronic kidney disease: therapeutic advances. 1545 27

An aggressive global approach to screening and to the management of the metabolic syndrome is recommended to slow the growth of the syndrome throughout the United States. Prevention should begin in childhood with healthy nutrition, daily physical activity, and annual measurement of weight, height, and blood pressure beginning at 3 years of age. Such screenings will identify cardiovascular risk factors early, allow the health care provider to define global cardiovascular risk with the COSEHC Cardiovascular Risk Assessment Tool, and allow treatment of each risk factor. Lifelong lifestyle modifications and pharmacologic therapy will be required in most patients. Antihypertensive therapy for these patients should begin with an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker unless a compelling indication for another drug is present. Metformin should be considered the first drug for glucose control in the patient with type 2 diabetes. A statin should be used initially for hyperlipidemia unless contraindicated. Combinations of antihypertensive, antiglycemic, and lipid-lowering agents will often be required.
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PMID:Addressing the global cardiovascular risk of hypertension, dyslipidemia, diabetes mellitus, and the metabolic syndrome in the southeastern United States, part II: treatment recommendations for management of the global cardiovascular risk of hypertension, dyslipidemia, diabetes mellitus, and the metabolic syndrome. 1595 71

The nephrotic syndrome is characterized by metabolic disorders leading to an increase in circulating lipoproteins levels. Hypertriglyceridemia and hypercholesterolemia in this case may depend on a reduction in triglyceride-rich lipoproteins catabolism and on an increase in hepatic synthesis of Apo B-containing lipoproteins. These alterations are the starting point of a self-maintaining mechanism, which can accelerate the progression of chronic renal failure. Indeed, hyperlipidemia can affect renal function, increase proteinuria and speed glomerulosclerosis, thus determining a higher risk of progression to dialysis. 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase is the rate-limiting enzyme in cholesterol synthesis from mevalonate and its inhibitors, or statins, can therefore interfere with the above-mentioned consequences of hyperlipidemia. Statins are already well known for their effectiveness on primary cardiovascular prevention, which cannot be explained only through their hypolipemic effect. As far as kidney diseases are concerned, statin therapy has been shown to prevent creatinine clearance decline and to slow renal function loss, particularly in case of proteinuria, and its favorable effect may depend only partially on the attenuation of hyperlipidemia. Statins may therefore confer tissue protection through lipid-independent mechanisms, which can be triggered by other mediators, such as angiotensin receptor blockers. Possible pathways for the protective action of statins, other than any hypocholesterolemic effect, are: cellular apoptosis/proliferation balance, inflammatory cytokines production, and signal transduction regulation. Statins also play a role in the regulation of the inflammatory and immune response, coagulation process, bone turnover, neovascularization, vascular tone, and arterial pressure. In this study, we would like to provide scientific evidences for the pleiotropic effects of statins, which could be the starting point for the development of new therapeutical strategies in different clinical areas.
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PMID:Statins in nephrotic syndrome: a new weapon against tissue injury. 1607 7

Nephrotic syndrome is an important chronic disease in children, characterized by minimal change disease in the majority. Research on pathogenesis has emphasized the importance of T lymphocyte dysregulation and vascular permeability factors that might alter podocyte function and permselectivity. While mutations in genes that encode important podocyte proteins have also been identified, a hypothesis unifying available evidence on pathogenesis is yet to be proposed. Patients with nephrotic syndrome are at risk for life threatening infections and thromboembolic episodes. Long-term effects of persistent hyperlipidaemia and prolonged steroid therapy are increasingly recognized. Remission of proteinuria following corticosteroid therapy has greater prognostic value, in relation to long-term outcome, than the precise renal histology. Prospective studies show that prolonged duration of therapy for the initial episode results in sustained remission and reduced frequency of relapses. Treatment with levamisole, cyclophosphamide, cyclosporine and mycophenolate mofetil is beneficial in a variable proportion of patients with frequent relapses or steroid dependence. The management of steroid-resistant nephrotic syndrome is difficult; most patients failing to achieve remission show progressive renal damage. Calcineurin inhibitors (cyclosporine, tacrolimus) are capable of inducing remission in a significant proportion of patients, but at risk of nephrotoxicity. Reduction of proteinuria is also possible, in children, using angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers. Prospective trials are necessary to identify effective and safe therapies for patients with frequent relapses, steroid dependence and resistance.
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PMID:Nephrotic syndrome in children. 1610 86

Chronic allograft nephropathy (CAN) represents the cumulative and incremental damage to nephrons by time-dependent immunologic and nonimmunologic causes. Hyperlipidemia is one nonimmunologic mechanism that promotes injury and poor function in a renal transplant. The aim of our study was to determine the effect of lipid profiles on CAN among renal transplant recipients. We retrospectively evaluated 53 renal transplant recipients who were classified according to the presence of CAN: CAN+ = 28 (18 males, 10 females) constituted the study group, whereas those with stable graft function CAN- = 25 (14 males, 11 females) were the control group. Biochemical parameters included serum urea, creatinine, total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol, apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), lipoprotein (a), homocysteine, and high-sensitive CRP (hs CRP). Angiotensin-converting enzyme inhibitor (ACEI) and/or angiotensin receptor blocker (ARB) use was significantly greater among the CAN+ group compared with the controls (P = .02, P = .04). Also, higher serum creatinine levels were observed in the CAN+ group (1.49 vs 1.22 mg/dL, P = .002), whereas serum levels of total cholesterol, triglyceride, hs CRP, and albumin were similar in both groups. The levels of ApoA1, ApoB, and lipoprotein (a) were similar, whereas the LDL/HDL cholesterol ratio and homocysteine levels were significantly higher in the CAN+ group (P = .04, P = .04). In conclusion, the LDL/HDL ratio may have a positive impact on CAN and may be used as a parameter during patient follow-up.
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PMID:Lipid profile in chronic allograft nephropathy. 1654 52

Microalbuminuria is an established risk factor for renal disease, especially in the diabetic population. Recent studies have shown that microalbuminuria has also a highly relevant predictive value for cardiovascular morbidity and mortality. From normal to overt proteinuria levels, albuminuria shows a continuous marked increase in cardiovascular risk. This association is independent of other "classical" cardiovascular risk factors such as hypertension, hyperlipidemia or smoking. Furthermore it has a predictive value not only for patients with diabetic or renal disease, but also for hypertensive individuals or the general population. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been shown to display not only reno--but also cardioprotective effects. Their unique ability to lower albuminuria by 40% is related to a significant risk reduction in cardiovascular mortality. New clinical trials are needed to define "normal" albuminuria levels and how low we should go.
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PMID:[Microalbuminuria--a new cardiovascular risk factor?]. 1704 69


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