With increasing cardiovascular safety hazards associated with erythropoiesis-stimulating agent (ESA) use, an emerging approach to anemia management in CKD is the use of agents to stimulate endogenous erythropoietin (EPO) production.1 In normoxia, the persistence of hypoxia-inducible factor prolyl hydroxylase (HIF-PH) results in degradation of HIF and hence reduced EPO production. In hypoxia, HIF-PH activity is reduced, allowing HIF to accumulate and increasing EPO production and release into the bloodstream.