Under normal conditions, inflammatory status is regulated by a complex equilibrium between plasma and intracellular mediators. This equilibrium is broken in patients receiving dialysis, which can lead to chronic inflammation causing deleterious consequences on their organs and systems. During recent years, substances that can inhibit the effects of inflammation have been sought. The results of these investigations have produced controversial data on the effects of recombinant human erythropoietin (epoetin) and, in this review, the effects of epoetin on the inflammatory status of dialysis patients are discussed. Aspects discussed include biomarkers of inflammation, and the relationships between epoetin, growth factors, endothelial dysfunction, endothelial fibrinolytic capacity, endothelial damage and oxidative stress. Relationships between epoetin and inflammation in non-uraemic patients are also addressed, as are associations between the malnutrition-inflammation-atherosclerosis syndrome and endothelial dysfunction. It is concluded that although epoetin administration in non-uraemic rats has been shown to have an anti-inflammatory and cytoprotective effect, the mechanisms responsible for regulating inflammation in uraemia are very complex and partially contradictory. The changes in pro-thrombotic and pro-atherogenic factors in dialysis patients require further study to evaluate all the factors implicated in the atherogenic process.