Background: Non-transferrin bound iron (NTBI) has been found to be raised in end stage renal disease (ESRD) patients on hemodialysis (HD) receiving intravenous (IV) iron. Such NTBI is proposed to cause oxidative damage to biomolecules. Method: NTBI, both ferrous (Fe+2) and ferric (Fe +3) forms, serum ferritin, protein thiols and lipid hydroperoxides were estimated by spectrophotometric and electrochemiluminescence immunoassay methods in patients with chronic renal failure (CRF), patients with ESRD on HD not receiving IV iron, and in normal controls. Results: NTBI (Fe+2) in HD patients not receiving IV iron was higher than in normal controls. NTBI (Fe+3) was significantly higher in HD patients not on IV iron therapy than in CRF and normal controls. There was no significant increase in NTBI in CRF patients when compared to normal controls. Serum ferritin was higher in HD patients compared to CRF and normal controls. There was a significant increase in lipid hydroperoxides and protein thiols in HD patients and CRF patients when compared to normal controls. The NTBI did not correlate with serum ferritin and oxidative markers. Conclusion: The source of NTBI in hemodialysis is not only IV iron therapy but also the hemodialysis procedure per se. It may be due to microhemolysis during hemodialysis. The NTBI is however found to be catalytically inactive.
All Science Journal Classification (ASJC) codes
- Clinical Biochemistry
- Biochemistry, medical