Abstract
Anemia is a common complication of chronic kidney disease (CKD) in children, and dysregulation of iron homeostasis plays a central role in its pathogenesis. Optimizing iron status is a prerequisite for effective treatment of anemia. Insufficient iron can lead to inappropriate escalation of the erythropoiesis-stimulating agent (ESA) dose, which is associated with adverse outcomes. Excess iron supplementation also has negative sequelae including free radical tissue damage and increased risk of systemic infection. Notwithstanding the importance of optimizing bioavailable iron for erythropoiesis for children with advanced CKD, achieving this remains challenging for pediatric nephrologists due to the historical lack of practical and robust measures of iron status. In recent years, novel techniques have come to the fore to facilitate accurate and practical assessment of iron balance. These measures are the focus of this review, with emphasis on their relevance to the pediatric CKD population.
Highlights
Anemia is a common complication of advanced chronic kidney disease (CKD), with prevalence exceeding 87% in children with CKD stages 4 and 5 [1, 2]
If sufficient iron is not available for erythropoiesis, this can lead to inappropriate escalation of erythropoiesis-stimulating agent (ESA) therapy, which is associated with adverse outcomes in both adults and children [5,6,7,8]
Achieving the optimal balance of bioavailable iron for erythropoiesis in children with advanced CKD is paramount in anemia management; it remains challenging for pediatric nephrologists
Summary
Anemia is a common complication of advanced chronic kidney disease (CKD), with prevalence exceeding 87% in children with CKD stages 4 and 5 [1, 2]. Novel techniques have come to the fore that can help to facilitate accurate and practical assessment of iron balance These measures are the focus of this review. Hepcidin dysregulation has been found to play a key role in the functional iron deficiency in CKD. The net effect of reduced renal clearance, and inflammatory upregulation, is chronic inappropriate elevation in hepcidin concentration resulting in suppression of both duodenal absorption of iron and its release from macrophages and hepatocytes. The combined effect of reduced iron absorption and release results in a net reduction in iron available for incorporation into emerging reticulocytes in the bone marrow, resulting in iron-restricted erythropoiesis This results in a suboptimal response to ESA, which can lead to inappropriate escalation of ESA doses if suitable assessment of bioavailable iron is not undertaken to inform iron supplementation
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