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Anemia in CRS is influenced by factors such as inadequate erythropoietin production, iron deficiency, reduced red blood cell life span, and chronic inflammation, which inhibit iron absorption and mobilization. This interplay of mechanisms worsens anemia, further aggravating HF and CKD. Anemia significantly impacts the prognosis of both HF and CKD, and recent trials have shown that hemoglobin increases, particularly with sodium\u2013glucose cotransporter 2 inhibitors, can improve outcomes in patients with HF and CKD. Iron deficiency is also prevalent in both patients with HF and patients with CKD and is associated with poorer exercise capacity and a higher mortality rate. Guidelines for diagnosing and treating iron deficiency differ between HF and CKD. Furthermore, treatment of anemia in CRS is controversial: While sodium\u2013glucose cotransporter 2 inhibitors and intravenous iron has shown consistent benefits in patients with CRS, normalization of hemoglobin with erythropoiesis\u2010stimulating agents improves symptoms and quality of life but have not consistently demonstrated cardiovascular benefits. There are no definitive guidelines for anemia management in CRS. Treatment should address HF, CKD, and anemia concurrently. A proposed algorithm includes correcting iron deficiency, initiating sodium\u2013glucose cotransporter 2 inhibitors, and considering erythropoiesis\u2010stimulating agents if hemoglobin remains &lt;10\u2009g\/dL. 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