Does iron depletion induced by erythropoietin slow the progression of chronic kidney disease?
Division of Nephrology and Hypertension King/Drew Medical Center Los Angeles California USA Sir, Jungers et al. [1] propose that erythropoietin (Epo) administration improves hypoxia-mediated oxidative stress, thereby slowing the process of interstitial fibrosis and progression of chronic renal disease. I propose another potential mechanism by which Epo may reduce oxidative stress. Iron catalyzes the Haber-Weiss reaction and thereby promotes free radical generation and lipid peroxidation. In the setting of ongoing inflammatory and haemodynamic injury to the glomerulus, tubules and interstitium, the ambient iron concentration in the interstitium and mesangium would determine the production of reactive oxygen species. Epo stimulates erythropoiesis and incorporation of iron into haemoglobin, thereby inducing iron depletion. Iron depletion would reduce oxidative stress, inhibit sclerosis and fibrosis and thereby slow the progression of renal disease. In the study by Jungers et al. [1], pati
