Anemia in cardiorenal disease: From pathogenesis to treatment

Heart failure and chronic kidney disease frequently coexist, which often leads to dysfunctional state favoring the development of anemia, termed cardiorenal anemia syndrome. Emerging evidence indicated that anemia is associated with decreased quality of life and adverse clinical outcomes in cardiorenal patients. However, the underlying pathophysiology of the anemia in this population remains incompletely understood and evidence-based recommendations for the anemia management are lacking. In the present review, the pathophysiology of anemia in cardiorenal patients and the management of anemia are discussed. Accordingly, the reduction of endogenous erythropoietin (EPO), the dysregulation of ion metabolism and increased hepcidin levels, bone marrow unresponsiveness to EPO, inactivation of EPO receptors, nutritional deficiencies caused by gastrointestinal dysfunction, shortened red blood cell life span, and inhibition of hematopoietic activity caused by medication are some of the underlying mechanisms of anemia in patient with HF and CKD. Therapeutically, hypoxia-inducible factor-prolyl hydroxylase inhibitors appear to exhibit unique advantages in managing anemia in cardiorenal patients. Intravenous iron supplementation may effectively and safely treat anemia in cardiorenal patients. Sodium-glucose cotransporter 2 inhibitors are indicated in the cardiorenal patients because of their cardiorenal benefit and additionally offer mild increases in hemoglobin/hematocrit that can help to correct or delay progression of anemia in these patients, but not in advanced CKD. However, although erythropoiesis stimulating agents use may be still a common strategy in dialysis patients, the evidence regarding the use of ESAs in cardiorenal patients is limited. Notably, further research is needed to optimize anemia management strategies in cardiorenal patients.