Role In Anemia Research Articles

Cardiorenal Consideration as a Risk Factor for Heart Failure

Cardiovascular disease-related factors are responsible for about 50% of the mortality in patients with both chronic kidney disease and end-stage renal disease. Therefore, it is not surprising that 30%-50% of patients with congestive heart failure also have an impaired glomerular filtration rate. This signifies a co-dependence between the kidneys and the heart. The role of anemia, microalbuminuria, calcium, and phosphorus imbalance in this cardiorenal interdependence is discussed in this article.

Emerging Role of Anemia in Heart Failure

Current medical therapy of heart failure (HF) focuses primarily on blockade of the neurohormonal pathways. This approach appears to have reached a benefit plateau, despite the introduction of new and improved drugs. Therefore, new targets for pharmacologic intervention are now being actively sought, and anemia has emerged as a potential candidate. Anemia is a frequently occurring comorbidity in patients with HF. However, its true prevalence is difficult to determine because no uniform definition of anemia associated with HF currently exists. Therefore, reported prevalence data can vary significantly, ranging from 4% to 55%, depending on the study population and the applied definition of anemia. Data from recent observational studies and clinical trials suggest that a low hemoglobin concentration in patients with HF is associated with, and is an independent risk factor for, increased morbidity and mortality. In light of these findings, anemia is being discussed as a possible new treatment target in patients with HF. So far, however, only a few small studies have explored this possibility using erythropoiesis-stimulating proteins, which for many years have been successfully used in the treatment of anemia secondary to chronic kidney disease or cancer chemotherapy. Preliminary data from these initial HF studies have shown that increased hemoglobin concentrations in patients with anemia were associated with improvements in cardiac and renal function as well as exercise capacity and a reduced need for hospitalizations. Larger, controlled clinical trials are needed to clearly establish the benefits and safety aspects of anemia treatment on morbidity and possibly mortality in HF patients.

2024: The Role of Anemia in Local Control After Breast Conservation Therapy for Early Stage Breast Cancer

2024: The Role of Anemia in Local Control After Breast Conservation Therapy for Early Stage Breast Cancer

Role of Anemia in Progression of Chronic Kidney Disease

Anemia is a well-known consequence of chronic kidney disease (CKD), and its prevalence progressively increases when the estimated glomerular filtration rate decreases to less than 60 mL/min/1.73 m2. However, analyses of the consequences of anemia and of the mechanisms of progression of CKD suggest that anemia also could contribute to the deterioration of kidney function. This hypothesis is based mostly on experimental data that imply that hypoxia of tubular cells plays an important role in tubulointerstitial damage associated with CKD and, thus, in the progression of renal failure. It also is supported by the fact that red blood cells represent a major antioxidant component of blood and that oxidative stress appears to contribute to glomerulosclerosis and tubulointerstitial damage. In humans, post hoc analysis of the Reduction of End points in non insulin-dependent diabetes mellitus (NIDDM) with the Angiotensin II Antagonist Losartan study and analyses of smaller prospective cohorts of CKD patients have shown that anemia is an independent risk factor for progression of CKD. In addition, 3 small randomized studies have suggested that anemia correction could slow the progression of CKD. Thus, the existence of a relationship between anemia and progression of CKD is not only plausible biologically, but also is supported by observational studies and by small intervention studies. However, only a large, randomized, prospective trial will be able to establish if anemia correction can slow the progression of CKD effectively.

Anemia and cardiovascular disease in diabetic nephropathy

Cardiovascular disease (CVD) is the major cause of morbidity and mortality in people with diabetes and in those with chronic kidney disease (CKD). Diabetes, occurring in epidemic proportions in the United States and worldwide, is also the leading cause of CKD and kidney failure. Identification of modifiable risk factors for CVD in patients with diabetes and CKD is thus of paramount importance. Anemia is increasingly recognized as a potential CVD risk factor in patients with diabetic nephropathy, in whom it is generally more severe and occurs at an earlier stage of CKD. In this review, we discuss the epidemiologic evidence, pathophysiologic mechanisms, and the current research findings, highlighting the role of anemia as a potential modifiable risk factor for CVD in patients with diabetic nephropathy, a particularly vulnerable population for CVD.

588 The prognostic role of anemia in acute heart failure. Data from the Italian survey on acute heart failure

588 The prognostic role of anemia in acute heart failure. Data from the Italian survey on acute heart failure

Diastolic dysfunction is associated with anaemia in patients with Type II diabetes

Anaemia is common in patients with diabetes and associated with an increased risk of diabetic complications. Although the role of anaemia in heart failure is established, we hypothesize that anaemia also contributes to an increased risk of cardiac dysfunction in patients with Type II diabetes. In the present study, 228 consecutive adults with diabetes were investigated using transthoracic echocardiography. Echocardiographic parameters were correlated with the Hb (haemoglobin) level and adjusted for other risk factors for cardiac dysfunction using multivariate analysis. More than one in five patients (23%) had anaemia, which was an independent risk factor for cardiac dysfunction on echocardiography. Over one-third of all patients with evidence of abnormal cardiac function (diastolic and/or systolic dysfunction) on echocardiography had anaemia compared with <5% of patients with normal echocardiographic findings. Most patients with anaemia had cardiac dysfunction (94%), with the major abnormality being diastolic dysfunction associated with an increased left ventricular mass and impaired relaxation indices. A continuous association between diastolic function and Hb was also observed in patients without anaemia. In patients with a history of cardiovascular disease, systolic dysfunction was twice as common in patients with anaemia. Anaemia was also correlated with plasma markers of cardiac risk, including BNP (brain natriuretic peptide), CRP (C-reactive protein) and AVP (arginine vasopressin). Notably, the predictive utility of these markers was eliminated after adjusting for Hb. Consequently, the inexpensive measurement of Hb may be a useful tool to identify diabetic patients at increased risk of cardiac dysfunction.

Neonatal Anemia Associated with Southeast Asian Ovalocytosis

The purposes of this study were to evaluate the reliability of the previously described diagnostic criteria for Southeast Asian ovalocytosis (SAO) in adults in the diagnosis of SAO in newborns and to describe the role of SAO in newborn infants presenting with pallor and jaundice. The inclusion criteria in this retrospective descriptive study were that the patient be a newborn with pallor or jaundice and with ovalocytes in the peripheral blood smear (PBS). The exclusion criteria were newborn status with other causes of neonatal hemolysis or anemia. Controls were age-matched newborn infants who did not have SAO or other causes of neonatal anemia or hemolysis. Hematological data were assessed with a hematology analyzer. DNA analysis for SAO band 3 was done by polymerase chain reaction. Among 107 newborn infants with SAO, 30 infants were excluded from the study. The exclusions were premature infants, an infant with congenital syphilis, low-birth-weight infants, infants with ABO blood group incompatibility, infants with 3-thalassemia, infants with hemoglobin E heterozygote or homozygotes, glucose-6-phosphate dehydrogenase-deficient infants, and infants with fetomaternal hemorrhage. The DNA analysis for SAO band 3 was done in 56 newborns, and 54 had positive results for SAO band 3 gene deletion. Approximately one half of the 54 newborn infants with SAO had hyperbilirubinemia, and 3 had severe hyperbilirubinemia. The mean hemoglobin concentration, packed cell volume, and red blood cell (RBC) count in the infants with SAO in the first week of life were significantly lower than those in control infants. The mean absolute number of reticulocytes, mean corpuscular hemoglobin, and red cell volume distribution width in infants with SAO band 3 in the first week of life were significantly higher than those in control infants. The neonatal diagnosis of SAO can be made by examination of RBC morphology in the PBS with the presence of stomatocytes, theta cells, and > or = 25% ovalocytes. SAO plays a role in anemia and hyperbilirubinemia in newborn infants.

Role of anemia in survival of patients with elderly aggressive non-Hodgkin's lymphoma after chemotherapy

Baseline anemia is a relevant prognostic factor in the overall population of non-Hodgkin's lymphoma (NHL) patients, and studies focusing on elderly NHL are awaited. We conducted a pooled analysis of a cohort of comparable patients enrolled (1993 – 2001) in three multicenter clinical trials on use of a MACOP-B-like regimen (VNCOP-B) for front-line treatment of elderly aggressive NHL. Models of Cox's proportional hazards regression analysis of prognostic value of pre-/post-treatment hemoglobin values in terms of 5-year overall survival included age, sex, initial tumor staging and response to treatment. Of the 168 patients screened, 16 were excluded due to missing data or lack of 5-year follow-up. In addition to achievement of complete/partial remission (adjusted relative risk [RR], 0.215; p = 0.0001) and advanced stage (II-IV vs. I – II; adjusted RR, 1.55; p = 0.0023), post-treatment hemoglobin values were an independent predictor of survival (adjusted RR per 1-g/dL increment, 0.76; p = 0.0041). In the present analysis, pretreatment hemoglobin values were associated with only marginal risk reduction (adjusted RR per 1-g/dL increment, 0.985; p = 0.049). Post-treatment hemoglobin values appear to provide a strong independent predictor of 5-year survival in elderly aggressive NHL, supporting the potential role of anemia correction in this group of patients.

Anterior ischaemic optic neuropathy after coronary artery bypass graft: the role of anaemia in diabetics

To ascertain factors associated with anterior ischaemic optic neuropathy (AION) following coronary artery bypass graft (CABG) in a Lebanese population. A retrospective chart review of consecutive CABG performed over a 5-year period (1995-1999) in one medical centre. A comparison of clinical characteristics was carried out between AION cases and subjects free from AION. The variables analysed included history of diabetes as well as preoperative, intraoperative, or postoperative values of haematocrit, blood sugar, oxygen saturation, and arterial blood pressure. A total of 1,594 persons were included. Three subjects experienced acute visual loss from AION following CABG, all had diabetes mellitus, and two suffered from severe postoperative anaemia. Among diabetics (n=484), the risk of AION was significantly higher in subjects with postoperative haematocrit falling below 22 (28.6%) than the rest (0.21%) (P=0.001). Blood transfusion was given in two subjects with prompt visual recovery. Severe anaemia in patients undergoing CABG appears to be a risk factor for AION, especially in diabetics, and needs prompt correction to prevent or reverse the ischaemic ocular events.

The role of anemia in congestive heart failure and chronic kidney insufficiency: the cardio renal anemia syndrome.

Anemia is a major problem in patients with chronic kidney insufficiency. The development of recombinant human erythropoietin has enabled physicians to correct this anemia. Although anemia has not been considered to be a common or important contributor to congestive heart failure, anemia of any cause can lead to cardiac damage and eventually congestive heart failure. Our joint renal-cardiac heart failure team found that anemia was indeed very common in congestive heart failure and was associated with severe, medication-resistant cardiac failure. Correction of the anemia with erythropoietin and intravenous iron led to a marked improvement in patients' functional status and their cardiac function, and to a marked fall in the need for hospitalization and for high-dose diuretics; renal function usually improved or at least stabilized. Subsequent investigations by others have confirmed many of our observations. We call this interrelationship between congestive heart failure, chronic kidney insufficiency, and anemia the Cardio-Renal Anemia syndrome. Treatment of the anemia in congestive heart failure may prove vital in preventing progression of both the heart failure and the associated renal disease.

Cardiovascular diseases in kidney transplant recipients: the role of anemia

Cardiovascular diseases are among the leading causes of mortality and death associated graft loss in kidney transplant recipients. Recently, there has been an increased awareness of the potential role of nontraditional risk factors such as anemia in contributing to the increased burden of cardiovascular diseases in kidney transplant recipients. Studies that are primarily based on retrospective data analyses have shown an association between anemia and cardiovascular outcomes. These findings underscore the need for prospective studies to better understand these risks and to implement management strategies that would have a positive impact on patient and graft outcomes. On the basis of the available data, this article reviews the magnitude of cardiovascular diseases and anemia in kidney transplant recipients with a focus on the role of anemia on cardiovascular outcomes in these patients.

Anemia in chronic heart failure: pathogenetic mechanisms

Anemia can be the cause of heart failure, but also its consequence. The pathogenesis of anemia in chronic heart failure (CHF) has yet to be fully elucidated, but is likely to be complex. Epidemiologic studies suggest that kidney dysfunction (by reducing the erythropoietic response to anemia), inflammation (by inducing erythropoietin resistance), decreased body mass index, old age, female gender, and poor clinical status may be important factors in the development of anemia in CHF. Intestinal malabsorption, chronic aspirin use, and proteinuria predisposes to iron deficiency. Proinflammatory cytokines are likely to play a significant role in anemia in CHF by generating the “anemia of chronic illness” that is a hallmark of inflammatory conditions. Few studies have investigated the mechanisms of anemia in CHF. There is a need for such studies.

Quality of life during chemotherapy : the role of anemia

Quality of life during chemotherapy : the role of anemia

Anemia of chronic disease: Past, present, and future: Management of comorbidities in kidney disease in the 21st century: Anemia and bone disease

ANEMIA AND CHRONIC KIDNEY DISEASE Anemia is common among patients with chronic kidney disease (CKD) and is a powerful risk factor for cardiovascular disease [1–9]. The risk for developing anemia is several times higher in those with CKD as compared to the general United States population [9], and recent evidence indicates that anemia develops earlier in CKD than previously thought, especially in diabetic nephropathy [5]. The cause of anemia in CKD is multifactorial, including erythropoietin deficiency, decreased responsiveness to erythropoietin, shortened red blood cell survival, iron deficiency, and chronic inflammation [10]. Observational studies indicate that anemia in CKD is associated with increased risk for coronary artery disease [11], hospitalization for cardiac disease [12], death from congestive heart failure (CHF) [2], and all-cause mortality [1, 12, 13]. Anemia is a modifiable risk factor in patients with CKD; however, several studies indicate that treatment of anemia in the predialysis and dialysis populations is suboptimal [6, 7, 14, 15]. Cardiac disease at onset of dialysis is common, including concentric and eccentric left ventricular hypertrophy (LVH) in 75%, coronary artery disease in 15%, overt systolic dysfunction in 15%, and dysrhythmia in 7% [3]. Erythropoietin deficiency plays a major role in anemia and treatment with exogenous erythropoietin can completely correct anemia in many with CKD. Treatment of anemia has been associated with improvement in quality of life in CKD patients before and after initiation of dialysis [16]. In addition, treatment of anemia improves hemoglobin level and quality of life and has been shown to reduce progression of LVH. However, clinical erythropoietin treatment to normalize hemoglobin in patients on dialysis has not demonstrated reduction in mortality or morbidity [17, 18]. Thus, treatment with erythropoietin to improve anemia has not been shown to definitively reduce cardiovascular mortality or improve cardiac function in those with preexisting cardiac disease. Little is known about the effects

Prospective trials on anemia of chronic disease: The Trial to Reduce Cardiovascular Events with Aranesp® Therapy (TREAT): Management of comorbidities in kidney disease in the 21st century: Anemia and bone disease

Chronic kidney disease (CKD) is emerging as a major public health problem in the United States. Between 1973 and 1999 there was a more than 30-fold increase in the number of patients enrolled in the Medicare funded end-stage renal disease (ESRD) program, from approximately 10,000 to 340,000 [1]. The annual incidence of ESRD has nearly doubled from 48,350 patients (190 per million) in 1991 to 89,252 (317 per million) in 1999. Estimates from the Third National Health and Nutrition Examination Survey (NHANES III), using the glomerular filtration rate (GFR) equation from the Modification of Diet in Renal Disease (MDRD) study [2, 3], showed that the prevalence of CKD, defined as a GFR 60 mL/min /1.73 m2, was approximately 8.3 million individuals, or 4.7% [4]. The MDRD Study indicated that 85% of patients with impaired kidney function (GFR 55 mL/min/1.73m2) have progressive losses of kidney function at a rate of 4 mL/min per year [5]. The progressive nature of CKD, and epidemiologic factors that include population aging, increasing prevalence of type II diabetes and hypertension, improved survival of patients on dialysis, and the acceptance of higher risk patients into ESRD programs, explain the ongoing and projected increases in the numbers of patients with ESRD. The increasing incidence and prevalence of ESRD and CKD is a global trend not just confined to the United States [6]. Although incidence rates for the United States and Japan are nearly two-fold higher than those of other industrialized nations, the rates of growth appear to be quite similar, best described by an exponential growth curve at the rate of 7.36% per year [7]. The impact of these numbers must be interpreted from

Prevalence and prognostic implication of anemia in decompensated chronic heart failure setting

Background: Several studies have demonstrated an association between anemia and prognosis in chronic heart failure (CHF). The role of anemia as an independent predictor of adverse outcomes needs to be confirmed in order to determine what treatment strategies, if any, are appropriate to treat anemia in this population. We examined the incidence, associated variable and short- and long-term prognosis in patients with decompensated heart failure and anemia. Methods: Between december/97 and March/00, three hundred and thirty patients were admitted because of decompensated HF. Anemia was defined by the presence of hematocrit less than 37% in women and less than 39% in men. Results: Anemia was diagnosed in 91 patients (29.1%), 24% in women vs. 32% in men (p = ns). Mean age in those with anemia (Group 1) was 62.9±14 compared with 65.5±15 in patients without anemia (Group 2)(p = ns). The following characteristics were different between Group 1 and Group 2: hypertension 33% vs 21% (p = 0.034) and chronic renal insufficiency (56 vs 27%, p = 0.002). In patients with and without anemia, NYHA functional class (2.24 vs. 2.33, p = ns) and ischemic etiology were similar (32% vs. 27%p = ns), and the prevalence of sinus rhythm was higher in subjects with anemia (34% vs 22%, p = 0.028). In groups 1 and 2, mean ejection fraction was 42.4±18 and 37.6±17% (p = 0.031), creatinine level was 1.8±1.6 vs. 1.3±0.4 mg/dL (p<0.001), and serum sodium level was 138±4.3 vs. 139.8±5.4 mEq/L (p = 0.03). Logistic regression analysis identified peripheral hypoperfusion (p<0.001,OR = 3.85) and natremia (p = 0.01,OR = 0.93) as independently associated with anemia. During hospitalization, the incidence of refractory heart failure was 8.8% in group 1 and 3.2% in group 2 (p = 0.043), and mortality rate was 2.9% vs 1% (p = ns), respectively. Twenty-four months cumulative survival was 40% in group 1 and 80% in group 2 (log rank test p = 0.041). Conclusion: Anemia was a frequent co-morbidity that afflicted one third of patients with decompensated heart failure, and it was related with other markers of disease severity. Short- as well as long-term prognosis were poor in subjects with anemia. Beside ongoing clinical trials researching the role of therapies for anemia in the treatment of patients with chronic heart failure, the effect of that therapies in decompensation setting should be evaluated

Anemia Is Associated With Worse Symptoms, Greater Impairment in Functional Capacity, and a Significant Increase in Mortality in Patients With Advanced Heart Failure

Anemia Is Associated With Worse Symptoms, Greater Impairment in Functional Capacity, and a Significant Increase in Mortality in Patients With Advanced Heart Failure

The optimal hemoglobin level in the cancer patient

URING the last 10 years, there has been growing interest in the role of anemia in cancer. This has prompted concerted efforts to more fully examine the impact of anemia on patient symptomatology, quality of life (QOL), and response to treatment, as well as to develop safer and more effective approaches for the treatment of

The optimal hemoglobin level in the cancer patient

URING the last 10 years, there has been growing interest in the role of anemia in cancer. This has prompted concerted efforts to more fully examine the impact of anemia on patient symptomatology, quality of life (QOL), and response to treatment, as well as to develop safer and more effective approaches for the treatment of