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Iron metabolism in hemodialyzed patients - a story half told?

Malyszko J, Koc-Zorawska E, Levin-Iaina N, Slotki I, Matuszkiewicz-Rowinska J, Glowinska I, Malyszko JS - Arch Med Sci (2014)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: 2 Department of Nephrology, Medical University, Bialystok, Poland.

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.

No MeSH data available.


Related in: MedlinePlus

NTBI in HD population according to diabetic status
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Figure 0001: NTBI in HD population according to diabetic status

Mentions: Labile plasma iron ≥ 0.6 units was found in 19 out of 53 (36%) hemodialyzed patients. Median number of LPI units was 0.3 (mean 0.9), with a range of 0.0–11.0 units. Clinical and biochemical characteristics of hemodialyzed patients are given in Table I, while iron status and inflammatory markers are presented in Table II. Patients with LPI units ≥ 0.6 had higher serum iron, ESA dose, ferritin, hsCRP and hepcidin, and lower hemojuvelin (Table II). In hemodialyzed patients, NTBI correlated with presence of diabetes (r = 0.30, p < 0.05), hemoglobin (r = –0.31, p < 0.05), hsCRP (r = 0.36, p < 0.01), ferritin (r = 0.31, p < 0.05), alkaline phosphatase (r = 0.51, p < 0.01), alanine aminotransferase (r = 0.51, p < 0.01), aspartate aminotransferase (r = 0.43, p < 0.01), serum glucose (r = 0.27, p < 0.05), HDL (r = –0.29, p < 0.05), and IL-6 (r = 0.42, p < 0.001). In multivariate analysis predictors of NTBI were hemoglobin (β value –0.27, p = 0.0027) and alkaline phosphatase (β value 0.42, p = 0.004), explaining 58% of the variability. F = 98, p < 0.00046 and SE was 1.44. The 10 diabetic patients in our population had higher NTBI than nondiabetic patients (Figure 1). Moreover, 13 anemic patients (with anemia defined as hemoglobin below 10 g/dl) had higher NTBI relative to nonanemic patients (0.6; 0.4–1.2 eLPI units, vs. 0.2; 0.0–0.8 eLPI units, p < 0.05) as well as 13 HCV positive patients versus HCV negative ones (0.5; 0.3–1.0 eLPI units vs, 0.25; 0.0–0.7 eLPI units, p < 0.05).


Iron metabolism in hemodialyzed patients - a story half told?

Malyszko J, Koc-Zorawska E, Levin-Iaina N, Slotki I, Matuszkiewicz-Rowinska J, Glowinska I, Malyszko JS - Arch Med Sci (2014)

NTBI in HD population according to diabetic status
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4296069&req=5

Figure 0001: NTBI in HD population according to diabetic status
Mentions: Labile plasma iron ≥ 0.6 units was found in 19 out of 53 (36%) hemodialyzed patients. Median number of LPI units was 0.3 (mean 0.9), with a range of 0.0–11.0 units. Clinical and biochemical characteristics of hemodialyzed patients are given in Table I, while iron status and inflammatory markers are presented in Table II. Patients with LPI units ≥ 0.6 had higher serum iron, ESA dose, ferritin, hsCRP and hepcidin, and lower hemojuvelin (Table II). In hemodialyzed patients, NTBI correlated with presence of diabetes (r = 0.30, p < 0.05), hemoglobin (r = –0.31, p < 0.05), hsCRP (r = 0.36, p < 0.01), ferritin (r = 0.31, p < 0.05), alkaline phosphatase (r = 0.51, p < 0.01), alanine aminotransferase (r = 0.51, p < 0.01), aspartate aminotransferase (r = 0.43, p < 0.01), serum glucose (r = 0.27, p < 0.05), HDL (r = –0.29, p < 0.05), and IL-6 (r = 0.42, p < 0.001). In multivariate analysis predictors of NTBI were hemoglobin (β value –0.27, p = 0.0027) and alkaline phosphatase (β value 0.42, p = 0.004), explaining 58% of the variability. F = 98, p < 0.00046 and SE was 1.44. The 10 diabetic patients in our population had higher NTBI than nondiabetic patients (Figure 1). Moreover, 13 anemic patients (with anemia defined as hemoglobin below 10 g/dl) had higher NTBI relative to nonanemic patients (0.6; 0.4–1.2 eLPI units, vs. 0.2; 0.0–0.8 eLPI units, p < 0.05) as well as 13 HCV positive patients versus HCV negative ones (0.5; 0.3–1.0 eLPI units vs, 0.25; 0.0–0.7 eLPI units, p < 0.05).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: 2 Department of Nephrology, Medical University, Bialystok, Poland.

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.

No MeSH data available.


Related in: MedlinePlus