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Abstract

A significant and increasing number of chronic kidney disease (CKD) patients are treated with online hemodiafiltration (OL-HDF), even in the absence of more conclusive survival data. OL-HDF affords several clinical benefits including control of anemia of CKD, a common affliction in dialysis patients. In efforts to understand the underlying mechanisms that contribute to the purported benefits of OL-HDF, we examined the potential role and impact of OL-HDF on key stages of anemia and its correction: erythropoiesis of bone marrow, circulating erythrocytes and on anemia therapy. We review evidence that indicates OL-HDF may modulate key processes of anemia and its therapy, including underlying conditions and responses of uremic toxicity and inflammation that aggravate anemia. Our assessment indicates that OL-HDF favorably impacts anemia by not only eliminating putative uremic inhibitors that suppress erythropoiesis, reducing red cell destruction and increasing iron availability, but also by mechanisms restricting underlying inflammation and endothelial dysfunction that are crucial to both CKD and anemia. Copyright © 2011 S. Karger AG, Basel.

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Most cited references 51

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Uremia.

Thomas Hostetter, Timothy W. Meyer (2007)

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P-cresylsulphate, the main in vivo metabolite of p-cresol, activates leucocyte free radical production.

Eva Schepers, Natalie Meert, Griet Glorieux … (2007)

Chronic renal insufficiency is associated with the retention of solutes normally excreted by healthy kidneys. P-cresol, a prototype protein-bound uraemic retention solute, has been shown to exert toxic effects in vitro. Recently, however, it has been demonstrated that p-cresol in the human body is conjugated, with p-cresylsulphate as the main metabolite. The present study evaluates the effect of p-cresylsulphate on the respiratory burst activity of leucocytes. P-cresylsulphate significantly increased the percentage of leucocytes displaying oxidative burst activity at baseline. Oxidative burst activity of stimulated leucocytes was however not affected. In contrast, p-cresol had no effect on the leucocytes at baseline, but inhibited leucocytes burst activity after stimulation. The present study demonstrates, for the first time, that p-cresylsulphate, the main in vivo metabolite of p-cresol, has a pro-inflammatory effect on unstimulated leucocytes. This effect could contribute to the propensity to vascular disease in the uraemic population.

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Molecular mechanisms of hepcidin regulation: implications for the anemia of CKD.

Jodie L. Babitt, Ruby C Y Lin (2010)

Anemia is prevalent in patients with chronic kidney disease (CKD) and is associated with lower quality of life and higher risk of adverse outcomes, including cardiovascular disease and death. Anemia management in patients with CKD currently revolves around the use of erythropoiesis-stimulating agents and supplemental iron. However, many patients do not respond adequately and/or require high doses of these medications. Furthermore, recent clinical trials have shown that targeting higher hemoglobin levels with conventional therapies leads to increased cardiovascular morbidity and mortality, particularly when higher doses of erythropoiesis-stimulating agents are used and in patients who are poorly responsive to therapy. One explanation for the poor response to conventional therapies in some patients is that these treatments do not fully address the underlying cause of the anemia. In many patients with CKD, as with patients with other chronic inflammatory diseases, poor absorption of dietary iron and the inability to use the body's iron stores contribute to the anemia. Recent research suggests that these abnormalities in iron balance may be caused by increased levels of the key iron regulatory hormone hepcidin. This article reviews the pathogenesis of anemia in CKD, the role and regulation of hepcidin in systemic iron homeostasis and the anemia of CKD, and the potential diagnostic and therapeutic implications of these findings. Copyright 2010 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

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PubMed ID:: 21811070

DOI:: 10.1159/000329573

Keywords: Anemia,etiology,metabolism,physiopathology,therapy,Bone Marrow,Chronic Disease,Endothelium, Vascular,Erythrocytes,Erythropoiesis,Humans,Inflammation,Iron,blood,Kidney Diseases,Renal Dialysis

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Impact of hemodialysis therapy on anemia of chronic kidney disease: the potential mechanisms.

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Karger: Nephrology

Most cited references 51

Uremia.

P-cresylsulphate, the main in vivo metabolite of p-cresol, activates leucocyte free radical production.

Molecular mechanisms of hepcidin regulation: implications for the anemia of CKD.

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