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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To be appropriately labelled as a 'risk factor' any putative risk factor should increase the prediction power of standard statistical models based on 'traditional' (Framingham) risk factors. In end-stage renal disease (ESRD), Framingham risk factors do not fully explain the cardiovascular burden of these patients. Inflammation, hyperhomocysteinemia and anemia contribute to the high cardiovascular risk of ESRD, but knowledge is still incomplete. We suspected that asymmetric dimethylarginine (ADMA) is an important cardiovascular risk factor in dialysis patients. This substance inhibits nitric oxide synthase thus triggering a series of pathophysiological events leading to atherosclerosis. To test this hypothesis, we studied the relationship between ADMA and intima media thickness (IMT) in the carotid artery. ADMA was found to be strongly and independently related to IMT. More importantly we found that patients with relatively higher plasma ADMA had shorter survival and a higher rate of incident cardiovascular complications in comparison to those with a relatively lower plasma concentration. These data represent a sound basis for intervention studies aimed at modifying the plasma ADMA concentration in ESRD patients.
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PMID:Endothelial damage, asymmetric dimethylarginine and cardiovascular risk in end-stage renal disease. 1220 95

Homocysteine serum levels were measured in patients with end-stage renal disease in relation to severity of renal anemia and oxidative stress parameters such as 4-hydroxynonenal (HNE) and malondialdehyde (MDA). The predialytic homocysteine serum levels of the patients are five times as high as in healthy controls. It was found that homocysteine does not correlate to hemoglobin concentration and to oxidative stress, but rather to parameters of nutrition status such as albumine concentration and protein catabolic rate. The homocysteine accumulation represents a cardiovascular risk factor which is statistically independent of oxidative stress, but dependent on nutrition or energy status in patients with chronic renal failure.
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PMID:Homocysteine in chronic renal failure in relation to renal anemia and to oxidative stress parameters 4-hydroxynonenal and malondialdehyde. 1222 23

Cardiovascular injury has been shown to be the most critical factor affecting quality of life and mortality in patients suffering from chronic renal failure. Oxidative stress has been thought to be an important risk factor for cardiovascular disorders. As oxidative stress parameters with high cardiovascular risk factor 4-hydroxynonenal and other aldehydic lipid peroxidation products, F2-isoprostanes, homocysteine, and cholesterol oxidation products were measured in chronic renal failure patients. 4-Hydroxynonenal and some cholesterol oxidation products correlated well with the degree of renal anemia. F2-isoprostane levels were related to inflammation, whereas homocysteine was increased due to malnutrition. Further, cholesterol oxidation products correlated well with the consumption of lipophilic antioxidants such as alpha-tocopherol. There was an almost linear correlation between the left ventricular mass index and 4-hydroxynonenal. Both parameters furthermore showed an inverse relationship to hemoglobin concentration. The correction of renal anemia by means of erythropoietin therapy led to an efficient strengthening of the antioxidative defence system. The improvement of the antioxidative capacity is of complex nature comprising both enzymatic pathways and low molecular antioxidants. The correction of renal anemia with its well documented reduction of the cardiovascular risk can be regarded as an antioxidative therapy, demonstrating the clinical efficiency of antioxidative protection in patients with chronic renal failure.
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PMID:Oxidative stress in cardio renal anemia syndrome: correlations and therapeutic possibilities. 1294 May 31

The number of patients with end-stage renal disease is constantly growing. If patients at risk are identified early enough, currently available therapeutic options allow a potent primary and secondary prevention of progressive renal failure. If the underlying disease can not be eliminated, the mainstay of the therapy are supportive measures such as antihypertensive and, in case of an underlying diabetes mellitus, antidiabetic therapy, dietary restrictions as well as avoidance of additional nephrotoxic agents. Furthermore, even a mild renal insufficiency has been identified as a potent cardiovascular risk factor. The second major goal of supportive therapy therefore is a reduction of the markedly increased cardiovascular morbidity of these patients. This can be achieved through treatment of various consequences of renal failure, such as hyperparathyroidism, renal anemia etc. Supportive therapy thus represents a highly complex and interdisciplinary treatment, which should prompt an early inclusion of a nephrologist into the therapeutic strategy.
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PMID:[Therapy and prophylaxis of renal failure]. 1463 78

Although the presence of anaemia after renal transplantation is well known, specific data on the prevalence and risk factors are scarce. Results from the recent TRansplant European Survey on Anemia Management (TRESAM) survey, conducted in 4263 recipients of a renal transplant from 72 centres in Europe, revealed that 38.6% of patients were anaemic [haemoglobin (Hb) concentrations < or =13 g/dl for male patients and < or =12 g/dl for female patients]. Of these patients, 11.6% had moderate anaemia (Hb concentrations >11 and < or =12 g/dl for male patients and >10 and < or =11 g/dl for female patients), while 8.5% had severe anaemia (Hb concentrations < or =11 g/dl for male patients and < or =10 g/dl for female patients). A strong association existed between Hb concentration and renal graft function. Of the patients with a serum creatinine level >2 mg/dl (which indicates impaired kidney function), 60.1% were anaemic, compared with 29.0% of those with a serum creatinine level < or =2 mg/dl (P<0.01). Other risk factors for anaemia include therapy with angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists, the use of azathioprine or mycophenolate mofetil, kidneys from older donors and recent infections. Furthermore, only 18.8% of patients with severe anaemia were treated with erythropoietic therapy. The findings from the TRESAM survey are in agreement with the results from another recently published study that included 128 renal transplant patients from two centres in the USA, who were followed for 5 years after transplantation. It was found that 30% of patients were anaemic at some point after transplantation. The prevalence increased with time after transplantation, with 26% of patients being anaemic 5 years' post-transplant. A multivariate logistic regression model identified three risk factors for post-transplant anaemia: serum total CO(2), blood urea nitrogen and creatinine. There is an unexpectedly high incidence of anaemia in patients with a functioning renal transplant: around one-third of these patients are anaemic. Most of the evidence suggests that impaired erythropoietin production by the renal allograft is the most important pathogenic factor of post-transplant anaemia. Whether this high incidence of anaemia may be an additional cardiovascular risk factor in renal transplant patients remains to be proven. However, there does not appear to be any reason why anaemic renal transplant recipients should not be treated like any other patients with renal anaemia.
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PMID:Anaemia after renal transplantation. 1528 61

Anemia, a potentially correctable cardiovascular risk factor, continues to be a major problem in kidney-transplant patients. Erythropoietin levels increase rapidly after successful kidney transplantation, and by 3 months, most patients achieve hemoglobin levels greater than 12 g/dL. Anemia may be caused by problems commonly seen in the general population such as iron deficiency or gastrointestinal blood loss, by immunosuppressive medications, or by more rare abnormalities such as hemolytic uremic syndrome or parvovirus B19-induced aplastic anemia. Iron deficiency is common at the time of transplantation and beyond and frequently contributes to anemia. Markers of iron deficiency (ferritin or transferrin saturation) are frequently inconclusive because of the presence of inflammation and infection. Immunosuppressive medications, such as azathioprine and mycophenolate mofetil (MMF), are a common cause of mild bone-marrow suppression and, thus, anemia. Sirolimus can cause more severe bone-marrow suppression, although this effect can lessen over time. The transplant patient with chronic kidney disease (CKD) frequently develops anemia, yet agents such as epoetin-alpha and darbepoetin are greatly underutilized. Evaluation of anemia should be undertaken when hemoglobin fails to normalize by 3 months after transplantation. Later after transplantation, especially in the setting of chronic allograft dysfunction, evaluation should take place when the hemoglobin falls to less than 11 g/dL in premenopausal females or to less than 12 g/dL in males and postmenopausal females.
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PMID:Anemia in the kidney-transplant patient. 1641 65

Cardiovascular disease is highly prevalent at all stages of chronic kidney disease (CKD) and is the leading cause of morbidity and mortality. Individuals with CKD commonly have multiple risk factors for the development of cardiovascular disease, including both traditional and nontraditional risk factors. Anemia is a nontraditional cardiovascular risk factor found in CKD that contributes to the development and progression of structural abnormalities of the heart, namely left ventricular hypertrophy and dilation. In addition, a deficiency of erythropoietin per se also may have important pathophysiologic consequences. In this review we summarize the evidence from observational studies showing an association between anemia and adverse cardiac outcomes at all stages of CKD. In addition, we provide an overview of the evidence accumulating from randomized controlled trials conducted in both nondialysis and dialysis CKD populations evaluating the effect of anemia correction on cardiac outcomes such as changes in left ventricular hypertrophy.
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PMID:Anemia and the heart in chronic kidney disease. 1694 67

Cardiovascular disease occurs in ESRD patients at rates that are far higher than is seen in the general population, and cardiovascular deaths account for the majority of deaths among dialysis patients. Abnormal mineral metabolism is a novel cardiovascular risk factor among dialysis patients. Recently published results demonstrated that even with good control of BP and anemia, conventional hemodialysis is associated with significant left ventricular hypertrophy (LVH); however, daily hemodialysis was associated with a significant reduction in LV mass index (LVMI). Furthermore, it was shown that control of serum phosphorus correlates with the reduction in LVMI. These data suggest a novel mechanism for the deleterious effect of elevated serum phosphorus on cardiovascular outcomes among hemodialysis patients: LVH. Other investigators have noted an association of hyperphosphatemia and LVH; however, this study was the first to demonstrate that improvement in serum phosphorus is associated with reduction in LVM. In addition, it is shown that daily hemodialysis is an effective modality in improving serum phosphorus through significantly improved phosphorus removal. Elevated serum phosphorus leads to vascular calcification, which can lead to LVH by decreasing vascular compliance. However, our study showed an improvement in LVMI during a 12-mo period. Because vascular calcification is unlikely to remit over this time period, it is proposed that serum phosphorus has a reversible, cardiotoxic effect that leads to LVH that can be reversed successfully with good control of serum phosphorus.
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PMID:Left ventricular hypertrophy: is hyperphosphatemia among dialysis patients a risk factor? 1713 Feb 71

Anemia has received increasing attention as an independent cardiovascular risk factor in patients with chronic kidney disease (CKD); a number of studies have highlighted its clear relationship with CKD mortality, because its impact on cardiac function leads to the development of left ventricular hypertrophy. However, despite the association between higher hemoglobin levels and better outcomes, a number of clinical studies have failed to demonstrate that fully correcting anemia has a positive effect on morbidity and mortality in patients with CKD. The Cardiovascular Reduction Early Anemia Treatment Epoetin beta (CREATE) study was designed from the hypothesis that, as anemia develops early in the course of CKD and nearly at the same time as cardiovascular disease, its earlier correction may provide better protection against the development of cardiovascular abnormalities. This randomized, multicenter, open-label, parallel-group trial involved 603 patients who had moderate anemia (hemoglobin 11 to 12.5 g/dl) and stage 3 to 4 CKD (estimated GFR 15 to 35 ml/min) and were randomly assigned to attain complete or partial anemia correction. The final results are due to be published within a few months, but the preliminary analyses do not show that complete anemia correction leads to any cardiovascular advantage, although the cardiovascular event rate was half that expected, possibly as a result of patient selection, trial effect, and improved medical care. The baseline findings also indicated that the burden of cardiovascular disease already is very high even in relatively early stages of CKD.
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PMID:Anemia and cardiovascular risk: the lesson of the CREATE Trial. 1713 Feb 72

Cardiovascular disease (CVD) remains the most common cause of premature death in the chronic kidney disease (CKD) population. Individuals with CKD are at 10-20 times greater risk of cardiac death than controls without CKD, despite stratification for age, race, sex and diabetes. Heightened CVD mortality begins with mild kidney disease and rises further with more advanced kidney disease. Traditional risk factors account for up to 50% of cardiovascular disease in CKD, whilst renal specific markers, including anemia, disordered bone mineral metabolism and oxidative stress, also likely contribute to the total cardiovascular burden in CKD. Despite the increased mortality, there has been a dearth of interventional cardiovascular randomized controlled trials (RCTs) in the CKD population. Furthermore, many patients with kidney disease have been excluded from the majority of mainstream cardiovascular interventional trials. While recently published RCTs on traditional and non-traditional risk factors including dyslipidemia (PPP, 4D and ALERT, VA-HIT), cardiomyopathy (FOSIDIAL, telmisartan, carvedilol), anemia (US Normal Hematocrit, CHOIR and CREATE trials), hyperhomocystenemia (ASFAST, US folic acid trial, HOST), disordered bone mineral metabolism (Cunningham meta-analysis, DCOR), oxidative stress therapy (SPACE, HOPE and ATIC, N-acetylcysteine) and multidisciplinary multiple cardiovascular risk factor intervention clinics (LANDMARK) have added to the available pool of clinical data, level 1 clinical evidence remains significantly lacking. The negative findings in many of these trials highlight the potential dangers of extrapolating findings from non kidney disease patients to those with CKD. Further large, well-designed trials are urgently required to address this issue.
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PMID:Cardiovascular disease in patients with chronic kidney disease. A clinical review. 1791 25


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