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Iron metabolism in hemodialyzed patients - a story half told? | LitMetric

AI Article Synopsis

  • All living organisms have developed ways to regulate iron levels, but recent research highlights the role of labile plasma iron (LPI) in causing tissue iron overload and its ability to produce reactive oxygen species.
  • A study was conducted on hemodialyzed patients to examine non-transferrin bound iron (NTBI) and its correlation with various markers of iron status and inflammation.
  • Results indicated that higher LPI levels were associated with increased serum iron, ferritin, and inflammation markers, suggesting that disturbed iron metabolism, anemia, and liver function may contribute to elevated NTBI in these patients.

Article Abstract

Introduction: All living organisms have evolved sophisticated mechanisms to maintain appropriate iron levels in their cells and within their body. Recently our understanding of iron metabolism has dramatically increased. Overt labile plasma iron (LPI) represents a component of non-transferrin bound iron (NTBI) that is both redox active and chelatable, capable of permeating into organs and inducing tissue iron overload. The LPI measures the iron-specific capacity of a given sample to produce reactive oxygen species. We studied for the first time NTBI correlations with markers of iron status and inflammation in prevalent hemodialyzed patients.

Material And Methods: Complete blood count, urea, serum lipids, fasting glucose, creatinine, ferritin, serum iron, total iron binding capacity (TIBC) were studied by standard laboratory method. The NTBI was assessed commercially available kits from Aferrix Ltd in Tel Aviv, Israel. A test result of 0.6 units of LPI or more indicates a potential for iron-mediated production of reactive oxygen species in the sample.

Results: Patients with LPI units ≥ 0.6 had higher serum iron, erythropoiesis stimulating agents (ESA) dose, ferritin, high-sensitivity C-reactive protein (hsCRP), hepcidin and lower hemojuvelin. In hemodialyzed patients NTBI correlated with hsCRP (r = 0.37, p < 0.01), ferritin (r = 0.41, p < 0.001), IL-6 (r = 0.43, p < 0.001). In multivariate analysis predictors of NTBI were hemoglobin and alkaline phosphatase, explaining 58% of the variability.

Conclusions: Elevated NTBI in HD may be due to disturbed iron metabolism. Anemia and liver function might also contribute to the presence of NTBI in this population.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4296069PMC
http://dx.doi.org/10.5114/aoms.2014.47823DOI Listing

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