Anemia, chronic renal disease and chronic heart failure: the cardiorenal anemia syndrome

Abstract

SUMMARY The mortality and morbidity of congestive heart failure (CHF) have improved slightly over the years but are still very high. Many patients with CHF are anemic, which raises the question, ‘Could uncontrolled anemia be a cause?’ The anemia is associated with more severe CHF and higher mortality, hospitalization and morbidity rates. The only way to prove that anemia is causing this worsening of CHF is to correct it. We review here some of the published papers about correction of anemia. Many, but not all, show a positive effect of erythropoietin or its derivatives when coadministered with oral or intravenous (IV) iron, with improvements in left and right ventricular systolic and diastolic function, dilation, hypertrophy, renal function, New York Heart Association class, exercise capacity, oxygen utilization, caloric intake, quality of life, and the activity of endothelial progenitor cells. A reduction in hospitalizations, diuretic dose, pulmonary artery pressure, plasma volume, heart rate, serum brain natriuretic peptide levels, the inflammatory marker interleukin 6, and soluble Fas ligand (a mediator of apoptosis) were also observed. Iron deficiency may also play an important role in this anemia because improvement in CHF has been seen with IV iron treatment alone. We call the interaction between chronic renal failure, CHF and anemia the cardiorenal anemia syndrome. Each of these three elements causes or exacerbates the others, and their correction can prevent the progression of both renal and heart failure. However, until ongoing large placebo-controlled studies on darbepoetin alpha or IV iron are completed, we will not know whether these treatments really influence the outcome of renal failure and CHF.