Iron supplementation has become an integral part of the management of patients receiving epoetin
therapy, and clinicians have found it necessary to learn how and when to use it to the best advantage. Three routes of administration for
iron are available: oral, intramuscular, and intravenous. Oral
iron has the advantage of being simple and cheap, but it is limited by side-effects, poor compliance, poor absorption, and low efficacy. Intravenous
iron is the best means of guaranteeing delivery of readily available
iron to the bone marrow, but it requires greater clinical supervision. The i.v.
iron preparations vary widely in their degradation kinetics, bioavailability, side-effect profiles, and maximum dose for single administration.
Iron dextran is hampered by a small but significant risk of
anaphylaxis, whereas all i.v.
iron preparations can induce "free
iron" reactions if the circulating plasma
transferrin is overloaded. Intravenous
iron may be given in advance of epoetin
therapy, as concomitant treatment to prevent the development of
iron deficiency, as treatment of absolute or functional
iron deficiency, or as adjuvant
therapy to enhance the response to epoetin in
iron-replete patients. Markers of
iron status that may indicate a need for i.v.
iron include a serum
ferritin of less than 100 microg/liter, a
transferrin saturation of less than 20%, and a percentage of hypochromic red cells more than 10%. Various regimens are available for giving i.v.
iron: low-dose administration of 20 to 60 mg every dialysis session in
hemodialysis patients, medium-dose administration of 100 to 400 mg, and high-dose administration of 500 to 1000 mg.
Iron sodium gluconate can only be given as a low-dose regimen because of toxicity, whereas the only preparation suitable for high-dose administration is
iron dextran. Although concerns have been raised regarding
iron overload and long-term toxicity with i.v.
iron therapy in terms of increased risk of
infections, cardiovascular disease, and
malignancy, there is little evidence to substantiate this in patients receiving epoetin. Care should be taken, however, to prevent the serum
ferritin rising above 800 to 1000 microg/liter and the
transferrin saturation above 50%. Provided this is done, the benefits of i.v.
iron almost certainly outweigh the risks in terms of optimizing the response to epoetin
therapy.