Patients with end-stage renal disease (ESRD) are at a markedly increased risk for cardiovascular complications compared with the general population. In addition to traditional cardiovascular risk factors such as diabetes mellitus, hypertension, hyperlipidaemia or cigarette smoking, a number of population-specific factors are implicated, such as anaemia, hyperhomocysteinaemia, hyperphosphataemia and vascular calcification, as well as inflammation and oxidative stress. Iron overload has been suggested to increase the cardiovascular risk in the general population. Iron supplementation is a widespread clinical practice in ESRD, especially in patients on maintenance haemodialysis (HD). Iron may therefore contribute to cardiovascular complications through effects on low-density lipoprotein oxidation and endothelial dysfunction. Although the effects of iron stores and iron therapy on cardiovascular risk are not well defined in HD patients, the 'iron hypothesis' deserves attention: serum ferritin is a marker of morbidity and mortality in HD patients, and the administration of high amounts of intravenous iron increases the risks of hospitalization and death. In contrast to intravenous iron therapy, intestinal iron absorption is regulated by body iron stores and is suppressed in the presence of infection and iron overload. Prospective studies are needed to clarify the influence of iron stores and iron therapy on overall and cardiovascular morbidity and mortality in ESRD patients.