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Unanticipated Favorable Effects of Correcting Iron Deficiency in Chronic Hemodialysis Patients
  1. Victor E. Pollak,
  2. Jonathan A. Lorch,
  3. Robert T. Means Jr
  1. From the Department of Medicine (V.E.P.), University of Colorado Health Sciences Center, Denver
  2. MIQS, Inc (V.E.P.), Boulder, Colo
  3. Department of Medicine (J.A.L.), Saint Luke's Hospital and Columbia University College of Physicians and Surgeons, New York
  4. Hematology/Oncology Division (R.T.M.), Medical University of South Carolina and the Ralph H. Johnson Veterans Administration Medical Center, Charleston, SC.
  1. Address correspondence to: Victor E. Pollak, MD, MIQS, Inc, 5621-D Arapahoe Avenue, Boulder, CO 80303. E-mail vpollak{at}
  2. Presented at the 32nd Annual Meeting of the American Society of Nephrology, Miami Beach, Florida, on November 5, 1999.


Background Correction of anemia in hemodialysis patients is seldom completely attained, and the response of parameters other than hemoglobin concentration to anemia correction has not been evaluated in detail.

Methods Laboratory parameters that suggest iron deficiency occurred in 10-15% of 206 recombinant human erythropoietin (rhEPO)-treated patients. Oral iron was given for 9 months and intravenous iron thereafter on a patient-specific basis when iron deficiency was evident. Eighty-seven hemodialysis patients with data for 12 months were followed for another 12 months. A computerized information system enabled data management and analysis.

Results With oral iron, serum ferritin decreased (P<0.001), indicating further iron depletion. With intravenous iron, hemoglobin increased, evidence of iron deficiency decreased, and less rhEPO was needed. Striking macrocytosis appeared. Serum albumin and serum creatinine/kg body weight (an index of muscle mass) increased, while blood pressure decreased. Data were reanalyzed in four mean corpuscular volume (MCV) quartiles and two ferritin subsets at study onset. Iron deficient erythropoiesis (low MCV, mean corpuscular hemoglobin [MCH], and transferrin saturation) was striking in quartile 1; low ferritin was prevalent in all quartiles. With intravenous iron, hemoglobin increased only in quartile 1, the quartile with the greatest decrease (52%) in rhEPO dose. MCV increased in all quartiles (P<0.001). Serum albumin increased in all MCV quartiles and both ferritin subsets, but significant creatinine/kg increase and blood pressure decrease occurred only in the low-ferritin subset.

Conclusions Macrocytosis occurred with intravenous iron replacement. The universal MCV increase suggests unrecognized, inadequately treated, folic acid deficiency unmasked by an adequate iron supply. There was also improved well being. Effects were most clearly evident in patients with deficient iron stores.

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