Erythropoietin and Its Cardiovascular Effects

Chapter

Abstract

Recombinant human erythropoietin (EPO) was approved in 1989 for treatment of anemia secondary to chronic kidney disease (CKD). EPO has been shown to have non-hematological effects on cardiac myocytes, angiogenesis, and endothelial cells. Several post-approval studies of erythropoietic stimulating agents (ESAs) examined patient outcomes related to target Hb level and most demonstrated increased adverse cardiovascular outcomes with a “normal” Hb target of >13 g/dL. It is not possible from the data published to determine the relative quantitative importance of the increased target Hb itself versus the amount of ESA used and/or iron treatment as playing a causative role in the risk of adverse cardiovascular outcomes from higher target Hb levels. As a result of these studies, the FDA recommends in its product information for ESAs that treatment be initiated only when the Hb level is <10 g/dL, the rate of Hb decline indicates the likelihood of the patient requiring a red blood cell (RBC) transfusion, and lowering the risk of alloimmunization and/or RBC transfusion risk is a goal. Interactions among various factors are responsible for an increased incidence of hypertension, left ventricular hypertrophy and vascular thrombosis in patients receiving ESA therapy. A novel approach to the treatment of EPO deficiency in anemic patients with CKD is the use of agents which stimulate endogenous EPO production in renal and non-renal tissues. Such a strategy might decrease adverse outcomes by allowing for a more continuous physiologic level of EPO to stimulate RBC production rather than the high intermittent blood levels of ESA that result from pharmacological administration of an exogenous ESA.

KEYWORDS

Anemia Erythropoietin Hemoglobin Transfusion Chronic kidney disease 

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Copyright information

© Springer International Publishing AG 2017

Authors and Affiliations

  1. 1.Division of NephrologyIndiana University School of MedicineIndianapolisUSA

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