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Open Access | 10.1172/jci.insight.190018
1Center for Iron Disorders, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, United States of America
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1Center for Iron Disorders, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, United States of America
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1Center for Iron Disorders, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, United States of America
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1Center for Iron Disorders, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, United States of America
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Published August 7, 2025 - More info
Anemia is a common and disabling complication of chronic kidney disease (CKD). Current therapies can be burdensome, and full correction of anemia is limited by cardiovascular side effects. New approaches that may offer additional therapeutic options are needed. We explored the anti-anemic effects of erythroferrone, an erythroid hormone that induces iron mobilization by suppressing the master iron-regulatory hormone hepcidin. In a preclinical murine model of adenine-induced CKD, transgenic augmentation of erythroferrone mobilized iron, increased hemoglobin concentrations by approximately 2 g/dl, and modestly improved renal function without affecting systemic or renal inflammation, fibrosis, or markers of mineral metabolism. This study supports the concept that therapeutic augmentation of erythroferrone is a promising approach for alleviating CKD-associated anemia.