Cardiovascular disease is virtually a sine qua non of chronic kidney disease, as is poor quality of life. Dialysis patient for example, have cardiovascular death rates 10 - 20 times those of the general population. Recent estimates indicate that at least half of all patients starting dialysis therapy will have an admission for a major cardiovascular event within 5 years, of which cardiac failure is the most common. Both experimental and clinical studies suggest that the cardiovascular system in uremia is in a state of premature senescence, one which is poorly suited to the supraphysiological hemodynamic demands to which it is subjected. Most patients develop cardiomyopathy, which clearly predisposes to cardiac decompensation. Anemia and hypertension are the most obvious modifiable overload parameters in uremic patients. Several prospective observational studies have demonstrated anemia to be an independent risk factor for each step in the process leading from hemodynamic overload, through maladpative left ventricular enlargement to left ventricular failure and death. This process starts with declining renal function, long before end-stage renal disease, the traditional time at which intervention has started to be seriously considered. The case for normal hemoglobin in patients with chronic kidney disease is still greatly disputed. Observational studies, which examine left ventricular size, quality of life, functional status, hospitalization and survival, are overwhelmingly supportive. Intervention trials, to date, suggest clear benefits of a physiological approach to anemia management in terms of quality of life, and likely benefits in terms of left ventricular stress minimisation and associated remodelling. Whether these translate into a reduction in outcomes like cardiac failure or death remains an unanswered question.