Anemia Management in the Cardiorenal Patient: A Nephrological Perspective

Heart failure (HF) and chronic kidney disease (CKD) frequently coexist, sharing significant overlap in prevalence and pathophysiological mechanisms. This coexistence, termed cardiorenal syndrome (CRS), often leads to anemia, which exacerbates both HF and CKD, thereby increasing morbidity and death. Managing anemia in CRS is complex due to conflicting guidelines and the multifactorial nature of the condition. 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-glucose 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-glucose cotransporter 2 inhibitors and intravenous iron has shown consistent benefits in patients with CRS, normalization of hemoglobin with erythropoiesis-stimulating 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-glucose cotransporter 2 inhibitors, and considering erythropoiesis-stimulating agents if hemoglobin remains <10 g/dL. Further research is needed to optimize anemia management strategies in patients with CRS.