In adults, the kidneys produce as much as 90% of circulating erythropoietin (EPO).EPO is produced in the renal peritubular interstitial fibroblasts.Consequently, all types of chronic renal diseases interfere in EPO production, and in the advanced stage of renal disease, anaemia is universal.Besides the central role of EPO deficiency, there are secondary factors associated with anaemia among end-stage renal disease patients undergoing hemodialysis (HD),like loss of blood during HD sessions (blood is lost inside the haemodialyzers), shortened erythrocyte survival due to uremic milieu, and hyperparathyroidism.Current target for anaemia control in HD patients is the partial correction of anaemia, which means targeting haemoglobin between 10 and 11 g/dl and haematocrit between 33 and 36%.Attempts at total correction are associated with higher incidence of HD vascular-access thrombosis, myocardial infarction and death.The steps to achieve the previously mentioned targets are, first, to discard iron deficiency by both the serum ferritin and the percentage transferrin saturation.Serum ferritin and the percentage of transferrin saturation must be,respectively, 200-500 ng/ml and 25-40% before starting EPO administration (in order to reach these targets, it is usually necessary to replace iron).The second step is to start subcutaneous administration of EPO at a dose of 80 to 120 units/kg/week for all patients with haemoglobin/haematocrit counts below the targets.The third step is to repeat haemoglobin measures every 15 days at least in the first three months oftreatrnent, and then, when the target is reached,to perform monthly control.The fourth is to try to maintain haemoglobin/haematocrit targets with the lowest EPO dose.Finally, the fifth step, if there is no response to EPO, is to investigate the following occurrences: inflammation and infection, osteitis fibrosa cystica, aluminum intoxication, haemolysis and anti-EPO antibodies.There are reasons to be wary of EPO use.First are the well-related cases of EPO-induced pure red cell aplasia, probably associated with a change of EPO formulation (removal of serum albumin from the formulation and replacement with Tween 80).Second, and more complex, are the effects of EPO on cardiovascular system.EPO increases vascular wall reactivity.and red cell mass, triggering hyperkalemia and accelerated hypertension.Furthermore, attempts to reach complete correction of anaemia have been correlated to a better quality of life, although patients with complete correction (haematocrit=42%) had higher rates of death and myocardial infarction when compared to patients submitted to partial correction of anaemia (haemtocrit=30%).Based on personal study (Hemodialysis International 2011;15: 493-500),we rank patients risk of death by the EPO dose in use.