Abstract: SA-PO810
Iron Supplementation for Hemodialysis Patients: Less Oxidative Stress by Oral Ferric Citrate Hydrate as Compared to Intravenous Saccharated Ferric Oxide
Session Information
- Dialysis: Anemia and Iron Metabolism
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Dialysis
- 605 Dialysis: Anemia and Iron Metabolism
Authors
- Nakayama, Masaaki, Tohoku University, Tohoku University Hospital, Sendai City, Japan
- Tani, Yoshihiro, Fukushima Medical University, Fukushima, Japan
- Zhu, Wan-Jun, Tohoku University, Tohoku University Hospital, Sendai City, Japan
- Yokoyama, Keitaro, Division of Nephrology and Hypertension, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan
- Fukagawa, Masafumi, Tokai University School of Medicine, Isehara, KANAGAWA, Japan
- Akiba, Takashi, Sekikawa Hospital, Tokyo, Japan
- Wolf, Myles S., Duke University , Durham, North Carolina, United States
- Hirakata, Hideki N., Fukuoka Renal Clinic, Fukuoka City, Japan
Background
Orally dosed ferric citrate hydrate (FC) corrects renal anemia in patients on hemodialysis (HD), suggesting a need for exploration of the biological differences in effects of iron supplementation using different routes of administration. To address this issue, the present study compared oral FC with intravenous saccharated ferric oxide (FO) in stable HD patients.
Methods
Six patients received 3 consecutive protocols in the first HD session of the week in a fasting state: nothing given, as control (C); oral load of FC (480 mg iron), and 5 minutes of intravenous FO (40 mg iron). Iron dynamics and biological impact on redox-inflammation status during the study (6 hours) were examined.
Results
Significant increases in serum iron and transferrin saturation (TSAT) were seen with both FC and FO. Regarding total iron-binding capacity, no changes were found in FC, whereas significant increases were seen in FO, despite the lower serum iron levels in FO, suggesting appearance of nontransferrin-binding iron (NTBI). This is suggested by the significant changes of NTBI/serum Iron ratio (%) in FO, but not in FC (Fig). Compared to C, increases were seen in serum myeloperoxidase (oxidative marker) with accompanying significant decreases in thioredoxin (anti-oxidant) in FO, whereas no changes were found in FC. While ratio of intact- to c-terminal FGF23 at 4 hours after starting HD were significantly higher with FO, as compared with C or FC.
Conclusion
Oral FC differs from intravenous FO in areas such as transferrin-binding capacity, NTBI generation, induction of oxidative stress, and FGF23 metabolism. Oral FC may have benefits in terms of iron supplementation for anemia associated with chronic kidney disease.
Funding
- Commercial Support –