Absolute or relative erythropoietin deficiency is involved in the pathophysiology of CKD-associated anemia.
Although treatment with ESAs markedly improved patient-perceived quality of life and reduced the need for blood transfusions,16 the results from the Correction of Hemoglobin and Outcomes in Renal Insufficiency (CHOIR), Cardiovascular risk Reduction by Early Anemia Treatment with Epoetin b (CREATE), and TREAT trials all demonstrated an increased risk of CKD progression or cardiovascular events such as stroke, thrombosis, or death at nearly normal hemoglobin concentrations and higher ESA doses in patients with ND-CKD.
2–4 However, the many confounding factors that accompany CKD may have prevented clinicians from discerning the specific role anemia plays in the poor outcomes.