Anemia is highly prevalent among chronic kidney disease (CKD) patients (1) and patients receiving renal replacement therapy. Since erythropoiesis-stimulating agent (ESA) therapy became routinely available in the late 1980s, anemia of CKD has been treated with various ESAs, such as erythropoietin (EPO) alfa (Procrit, Johnson & Johnson, New Brunswick, New Jersey, USA; Epogen, Amgen, Thousand Oaks, California, USA), erythropoietin beta (Neorecormon, Hoffmann-La Roche, Basel, Switzerland), and darbepoetin alfa (Aranesp, Amgen).Anemia of CKD is clearly associated with reduced quality of life (QOL) and an increase in risk of death and cardiovascular events (2-4); this observation led to the hypothesis that aggressive correction of anemia might lead to improved mortality and better cardiovascular and QOL outcomes. Over recent years, average hemoglobin levels and EPO doses have been increasing, and higher targeted levels of Hb have been recommended in clinical guidelines. The rationale for these gradual increases in dose and targets was supported by extensive retrospective evidence (2-5) and QOL data that suggested a benefit to higher Hb levels.
展开▼
