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Abstract: SA-PO807

Serum Concentration of Non-Transferrin Bound Iron in Hemodialysis Patients Is Increased after Oral Iron Administration

Session Information

Category: Dialysis

  • 605 Dialysis: Anemia and Iron Metabolism


  • Saito, Noriko, Shinraku-en hospital, Niigata, Japan
  • Saito, Kazuhide, Niigata University, Niigata, Japan
  • Morioka, Tetsuo, Shinraku-en Hospital, Niigata, Japan
  • Shimada, Hisaki, Shinraku-en hospital, Niigata, Japan
  • Ikarashi, Kozo, Shinraku-en Hospital, Niigata, Japan
  • Tsubata, Yutaka, Shinrakuen hospital, Niigata city, Japan
  • Sasagawa, Taiji, Shinraku-en Hospital, Niigata, Japan
  • Ikuta, Katsuya, Asahikawa Medical University, Asahikawa, Japan
  • Kohgo, Yutaka, International University of Health and Welfare, Nasushiobara, Japan
  • Miyazaki, Shigeru, Shinraku-en Hospital, Niigata, Japan

Non-transferrin bound iron (NTBI), which appears in serum in iron overload, is thought to cause organ damage through free radical production. We reported NTBI was increased after intravenous iron administration (IVIA) in hemodialysis (HD) patients (ASN2016), on the other hand, their kinetics after oral iron administration(OIA) is unknown. Aim of this study is to assess the kinetics of NTBI concentration after OIA in HD patients.


16 HD patients without any iron load within 4 weeks, whose Hb<12g/dl, ferritin<100ng/ml and CRP<1.0mg/dl, were enrolled. They received oral ferrous sulfate 105mg at the start of HD session. We evaluated the following markers before and at 1,2,3,4 and 48 hours(hr) after OIA : NTBI, Hepcidin-25(HPC), high sensitive CRP(hsCRP), 8-oxo-2'-dehydroguanosin, serum iron, transferrin saturation(TSAT), transferrin(Tf), ferritin ,soluble Tf receptor and standard hematological parameters. NTBI was measured by recently described reliable method(Clin Chim Acta437:129-135, 2014). 4 HD patients without OIA were also enrolled as control.


1. Fe before OIA was 30(24-49)μg/dl and significantly increased to 45(27-57)μg/dl at 1hr and reached the peak level of 272(104-320)μg/dl at 4hr and then decreased to 52(34-81)μg/dl at 48hr (Medians(interquartile range)).
2. TSAT before OIA was 12(7-17)%, significantly increased to 24(17-39)% at 2hr, reached the peak level of 70(34-80)% at 4hr and decreased to 17(14-26)% at 48hr.
3. NTBI before OIA was 0.02(0-0.10) μM and significantly increased to 0.15(0.03-0.56)μM at 4hr and decreased to 0.02(0-0.07) at 48hr.
4. NTBI at 4hr after OIA correlated with TSAT at 4hr(r=0.894,p<0.001).
5. The predictor of NTBI 4hr after OIA was percentage of hypochromic red cells( %HypoHe) before OIA by stepwise analysis (β=0.548, p=0.028, R2=0.3)
6. Ferritin before OIA was 16(15-29)ng/ml and significantly increased to 35(19-48)ng/ml at 48hr. HPC was unchanged during 48hr.
7. In control patients TSAT, NTBI and ferritin were not changed during 48hr.


TSAT and NTBI significantly increased at 2hr and 4hr after OIA, respectively and both peaked at 4hr. %HypoHe before OIA was negative predictor of NTBI at 4hr. Clinical significance of NTBI increment after OIA should be further examined.


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