Review highlights iron deficiency anaemia management strategies in chronic kidney disease, suggesting improved approaches are necessary.
Iron deficiency anaemia (IDA) is one of the most prevalent and clinically significant complications of chronic kidney disease (CKD), contributing to increased morbidity, reduced quality of life, and accelerated disease progression. The pathogenesis of IDA in CKD is multifactorial, involving absolute or functional iron deficiency, inflammation-mediated disruptions in iron homeostasis, and diminished erythropoietin production by the diseased kidneys. Elevated hepcidin levels further exacerbate iron sequestration, impairing erythropoiesis. Effective management of IDA in CKD focuses on replenishing iron stores, optimizing haemoglobin levels, enhancing the efficacy of erythropoiesis-stimulating agents (ESAs), minimizing blood transfusions, and improving patient quality of life. Pharmacological interventions include oral and intravenous iron supplementation, ESAs, and novel agents such as hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs), ferric pyrophosphate citrate (FPC), and liposomal iron formulations. Emerging therapies targeting hepcidin pathways and erythroferrone analogs offer promising avenues to address treatment limitations, especially ESA resistance and inflammation-associated anaemia. Despite these advances, therapeutic challenges persist, underscoring the need for individualized, multidisciplinary approaches and continued research into innovative therapies for IDA in CKD.
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Sireesha et al. (2025) studied this question.
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