Anemia treatment in chronic kidney disease: shifting uncertainty

Pfeffer, Marc A.

doi:10.1007/s10741-008-9087-9

Cited by 6 publications

(4 citation statements)

References 32 publications

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“…In total, almost 4,000 patients have been entered into the current double-blind, placebo-controlled Trial to Reduce Cardiovascular Events with Aranesp (Amgen, Thousand Oaks, CA) Therapy study of darbepoetin in nondialyzed diabetic patients with renal insufficiency and an initial Hb level of 9 -11 g/dl [71]. The target Hb level in that trial is 13 g/dl.…”

Section: The Effect Of Treating Anemia On Chfmentioning

confidence: 99%

Iron Metabolism, Iron Deficiency, Thrombocytosis, and the Cardiorenal Anemia Syndrome

2009

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In treating moderate to severe anemia of chronic kidney disease (CKD), oral iron is effective only in a minority of nondialysis patients. Intravenous iron is more effective and can raise levels of hemoglobin even without the use of erythropoiesis-stimulating agents (ESAs). Unfortunately, the current assays of iron status that are presently widely available are not especially helpful in predicting response. In patients on dialysis, i.v. iron is effective over a wide range of serum ferritin from <100 ng/ml to 800 ng/ml. None of the three available randomized controlled trials comparing oral with i.v. iron showed evidence of nephrotoxicity caused by i.v. iron.Iron deficiency is a risk factor for thrombocytosis and should, wherever possible, be avoided. Optimal coadministration of iron may reduce the risk for ESA-driven cardiovascular events. Increased total body iron stores (imperfectly reflected by serum ferritin levels in CKD) do not appear to be related to such events or hospitalization in CKD; it is unclear what other risk factors and mechanisms need to be considered.In the appreciable proportion of patients with both renal and cardiac dysfunction, management is further complicated by a vicious circle (which can be characterized as cardiorenal anemia syndrome) in which CKD, heart failure, and anemia exacerbate each other. In such patients, correction of anemia appears to improve cardiac function and quality of life without a greater risk for adverse events. The Oncologist 2009;14(suppl 1):22-33

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Section: The Effect Of Treating Anemia On Chfmentioning

confidence: 99%

Iron Metabolism, Iron Deficiency, Thrombocytosis, and the Cardiorenal Anemia Syndrome

2009

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“…A total of almost 4,000 patients have been entered in the current double-blind placebo-controlled TREAT (Trial to Reduce Cardiovascular Events with Aranesp Therapy) study of DA in non-dialyzed diabetic patients with renal insufficiency and an initial Hb of 9–11 g/dl [96]. The target Hb in the trial is 13 g/dl.…”

Section: To What Level Should Hb Be Corrected?mentioning

confidence: 99%

The Anemia of Heart Failure

Silverberg¹,

Wexler²,

Palazzuoli³

et al. 2009

Acta Haematol

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Anemia is common in congestive heart failure (CHF) and is associated with an increased mortality and morbidity. The most likely causes of anemia are chronic kidney disease (CKD) and excessive cytokine production, both of which can cause depression of erythropoietin (EPO) production and bone marrow activity. The cytokines also induce iron deficiency by both reducing gastrointestinal iron absorption and iron release from iron stores located in the macrophages and hepatocytes. Iron deficiency can cause thrombocytosis which might also contribute to cardiovascular complications in both CHF and CKD and is partially reversible with iron treatment. Thus attempts to control this anemia will have to consider both the use of erythropoiesis-stimulating agents (ESA), such as EPO, as well as oral and, probably more importantly, intravenous (IV) iron. The many studies on anemia in CHF patients treated with ESA and oral or IV iron, and even with IV iron without ESA have up to now shown a quite consistent positive effect on hospitalization, fatigue, shortness of breath, quality of life, exercise capacity, and β-natriuretic peptide reduction, in the absence of increased cardiovascular damage related to the therapy. Adequately powered long-term placebo-controlled studies of ESA and/or IV iron are currently being carried out and their results are eagerly awaited.

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“…The prevalence of anemia in HF is reported to be over 40% in patients with advanced HF [3]. The causes of anemia in HF are only partially understood, although several mechanisms have been implicated [4], including treatment with ACE-inhibitors [5], a blunted erythropoietin (EPO) production due to renal dysfunction [6], congestion [7], and iron deficiency [8]. However, these causes only partially explain the severity of anemia and are difficult to target.…”

Section: Introductionmentioning

confidence: 99%

Heart failure-associated anemia: bone marrow dysfunction and response to erythropoietin

et al. 2010

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Heart failure (HF)-associated anemia is common and has a poor outcome. Because bone marrow (BM) dysfunction may contribute to HF-associated anemia, we first investigated mechanisms of BM dysfunction in an established model of HF, the transgenic REN2 rat, which is characterized by severe hypertrophy and ventricular dilatation and SD rats as controls. Secondly, we investigated whether stimulation of hematopoiesis with erythropoietin (EPO) could restore anemia and BM dysfunction. After sacrifice, erythropoietic precursors (BFU-E) were isolated from the BM and cultured for 10 days. BFU-E were quantified and transcript abundance of genes involved in erythropoiesis were assayed. Number of BFU-E were severely decreased in BM of REN2 rats compared to SD rats (50 ± 6.2 vs. 6.4 ± 1.7, p < 0.01). EPO treatment increased hematocrit in the SD-EPO group (after 6 weeks, 49 ± 1 vs. 58 ± 1%, p < 0.01); however, in the mildly anemic REN2 rats, there was no effect (43 ± 1 vs. 44 ± 1%). This was paralleled by a 67% decrease in BFU-E in BM of REN2 rats compared to SD (p < 0.01). EPO significantly improved BFU-E in both SD and REN2 but could not restore this to control levels in the REN2 rats. Expression of several genes involved in differentiation (LMO2), mobilization (SDF-1), and iron incorporation (transferrin receptor) of the BM were differentially expressed in REN2 rats compared to SD rats, and EPO did not normalize this. Altogether, these results suggest that BM dysfunction is an important contributor to HF-associated anemia and that EPO is not an effective agent to treat HF-associated anemia.Electronic supplementary materialThe online version of this article (doi:10.1007/s00109-010-0710-6) contains supplementary material, which is available to authorized users.

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Anemia treatment in chronic kidney disease: shifting uncertainty

Cited by 6 publications

References 32 publications

Iron Metabolism, Iron Deficiency, Thrombocytosis, and the Cardiorenal Anemia Syndrome

Iron Metabolism, Iron Deficiency, Thrombocytosis, and the Cardiorenal Anemia Syndrome

The Anemia of Heart Failure

Heart failure-associated anemia: bone marrow dysfunction and response to erythropoietin

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