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In many patients with chronic renal insufficiency a depletion of stored and cellular iron (absolute iron deficiency), a blockade of iron in body stores (functional iron deficiency) or an iron overload can be shown. The factors leading to absolute iron deficiency are: 1) loss of iron as a result of blood loss by the gastrointestinal tract, taking blood specimens for laboratory tests and related to dialytic procedure; 2) enhanced use of iron during intensive erythropoiesis stimulated by recombinant human erythropoietin; 3) dietary iron deficiency or impaired iron uptake from the gastrointestinal tract; 4) other forms of gastrointestinal tract impairment; 5) pharmaceutical substances forming inabsorbable iron complexes and/or diluting the acidity of the gastric juice; 6) certain demographic factors. Functional iron deficiency develops during treatment with recombinant human erythropoietin and in the infectious state and during the inflammatory process. The use of recombinant human erythropoietin accelerates erythropoesis and by so increases iron requirement frequently far higher than the ability of iron stores to "transfer" iron to the bone marrow--this may be a result of ineffective mobilisation of iron stores and/or ineffective transport. In the infectious process the use of iron is impaired because of augmented cytokines production which leads to increase iron uptake and storage in the reticulo-endothelial system. Iron overload is caused by excessive iron intake, e.g. parenteral iron administration or repeated blood transfusions.