2006). ESAs are able to protect against initial kidney damage caused by ischemic insult or induced by glomerulopathy by alleviating apoptotic activity or oxidative stress (Johnson et al. 2006; Canadillas et al. 2010). Katavetin et al. demonstrated that EPO induced heme oxygenase (HO)‐1 to attenuate oxidative stress, which might be associated with slowing CKD progression in Dahl‐salt sensitive rats (Katavetin et al. 2007). This evidence concerns the gene EPO and chronic kidney disease.