Abstract
Iron deficiency is commonly observed in chronic kidney disease. Blood loss and iron consumption under erythropiesis activating agents (ESA) induce absolute deficiency whereas defect of iron intestinal absorption and storage release account for functional deficiency. High hepcidin plasma levels are probably induced by inflammatory process and can explain functional deficiency. However, hepcidin is negatively correlated with ESA needs and hepcidin expression is influenced by other factors as degree of renal insufficiency, iron pool, treatments (iron IV and ESA). IV iron is the common therapeutic approach of iron deficiency and only normalized iron marrow supply cannot account for his efficiency. New IV iron products allow us to conceive new therapeutic schemes. Hepcidin inhibition is another therapeutic alternative.
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