Iron deficiency may be a result of a decrease in iron supply or an increase in iron demand and utilization.

In patients with renal compromise, a decrease in iron supply may occur due to reduced dietary intake of iron, impaired iron absorption, or excessive blood loss. Frequent phlebotomy and dialysis combine for an estimated loss of 1.0 to 3.0 g of iron annually,3 and other conditions, such as gastrointestinal bleeding, can further compound this loss.4  Absolute iron deficiency occurs when iron stores are depleted or are too low to support normal hemoglobin or red blood cell (RBC) synthesis.2

Severe anemia associated with end-stage renal disease (ESRD) is mainly due to a deficiency in erythropoietin, a hormone produced by healthy kidneys. Replacement therapy with recombinant human erythropoietin (epoetin alfa), a stimulant of RBC formation, can correct this type of anemia in dialysis patients. However, epoetin alfa therapy increases the demand for iron. When iron stores cannot be mobilized quickly enough to be transported to the bone marrow where iron is needed for the production of new RBCs, a functional iron deficiency may result, despite an adequate iron supply.2 This functional iron deficiency can delay or diminish the response to epoetin alfa therapy. Iron supplementation is required to restore and maintain proper iron balance and to ensure optimal therapeutic response to epoetin alfa.