Hippokratia 2011; 15 (Suppl 2): 9-14
D. Farmakis, G. Filippatos
The term “cardiorenal anemia syndrome” (CRAS) was introduced to describe the frequent coexistence of heart failure (HF), renal dysfunction and anemia as well as the close pathogenetic relationship between them. Up to two thirds of patients with acute heart failure (HF) and nearly one third of those with chronic HF have at least moderate renal dysfunction. Anemia, on the other hand, is detected in 10-60% of HF patients, depending on definitions and HF severity. Data on the coexistence of anemia and kidney disease in HF is quite variable and a prevalence of 3-22% is reported by various studies. Both renal dysfunction and anemia are independent predictors of adverse prognosis in HF and seem to have an additive effect on patients’ survival. Anemia pathogenesis in CRAS is multifactorial and among other factors includes reduced synthesis of and/or resistance to erythropoietin and iron deficiency. As a result, erythropoiesis stimulating agents (ESA) and iron supplementation have both emerged as potential therapeutic modalities for CRAS. Although the first small clinical trials on ESA were promising, the subsequent large-scale testing of those agents resulted in controversial findings. Recent studies on the use of iron therapy in HF patients with iron deficiency have shown beneficial effects regarding patients’ symptoms, functional status and quality of life, which seem to occur irrespectively of the presence of anemia. However, there are several issues that need to be clarified, including whether the correction of iron deficiency is followed by better long-term prognosis, what patients benefit the most and therefore need to be treated or what therapeutic targets should be pursued.