Cardiovascular disease is the leading cause of increased mortality in patients with renal failure and vigorous attention to cardiovascular risk factors is therefore required to improve patient outcome. The availability of recombinant human Epo has focused the interest on the role of chronic anaemia in the pathogenesis of cardiovascular disease. Severalfold evidence indicates that anaemia can contribute to cardiac volume overload and together with overhydration, fistula flow and the pressure overload secondary to arterial hypertension, it may play a significant role in the development of cardiac hypertrophy. As in the general population left ventricular hypertrophy is a severe adverse risk factor in renal patients. In addition, in the presence of ischaemic heart disease anaemia may further worsen cardiac oxygen supply. This dual effect of anaemia probably explains why epidemiological studies have shown that a 1 g/dl decrease in haemoglobin levels is an independent, statistically significant risk factor for the development of cardiac morbidity and mortality. Follow-up examinations have demonstrated that partial correction of anaemia with recombinant Epo can improve cardiac oxygen supply and partially reverse pathological changes in left ventricular geometry. However, although partial anaemia correction regularly reduces left ventricular volume, the effects on wall thickness are far less significant. Moreover, in patients with advanced cardiac disease it has recently not been possible to demonstrate that a normalization of haemoglobin levels provides further benefit. It is not unlikely therefore that the development of severe anaemia has to be prevented by early implementation of Epo therapy in order to achieve the maximum benefit with respect to the cardiovascular system.