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Iron status, inflammation and hepcidin in ESRD patients: The confounding role of intravenous iron therapy.

Jairam A, Das R, Aggarwal PK, Kohli HS, Gupta KL, Sakhuja V, Jha V - Indian J Nephrol (2010)

Bottom Line: These patients also showed more marked inflammatory activation, as shown by the significantly higher CRP, TNF-α, and IL-6 levels.High hepcidin levels could explain the functional iron deficiency.The cause of the relatively greater degree of inflammatory activation as well as the relationship with IV iron administration needs further studies.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

ABSTRACT
Uremia is a state of heightened inflammatory activation. This might have an impact on several parameters including anemia management. Inflammation interferes with iron utilization in chronic kidney disease through hepcidin. We studied the body iron stores, degree of inflammatory activation, and pro-hepcidin levels in newly diagnosed patients with end-stage renal disease (ESRD), and compared them with normal population. In addition to clinical examination and anthropometry, the levels of iron, ferritin, C-reactive protein, tumor necrosis factor alfa, interleukin-6, and prohepcidin were estimated. A total of 74 ESRD patients and 52 healthy controls were studied. The ESRD patients had a significantly lower estimated body fat percentage, muscle mass, and albumin; and higher transferrin saturation (TSAT) and raised serum ferritin. Inflammatory activation was evident in the ESRD group as shown by the significantly higher CRP, IL-6, and TNF-α levels. The pro-hepcidin levels were also increased in this group. Half of the ESRD patients had received parenteral iron before referral. Patients who had received intravenous iron showed higher iron, ferritin, and TSAT levels. These patients also showed more marked inflammatory activation, as shown by the significantly higher CRP, TNF-α, and IL-6 levels. We conclude that our ESRD patients showed marked inflammatory activation, which was more pronounced in patients who had received IV iron. High hepcidin levels could explain the functional iron deficiency. The cause of the relatively greater degree of inflammatory activation as well as the relationship with IV iron administration needs further studies.

No MeSH data available.


Related in: MedlinePlus

Box-and-whisker plots showing the serum iron (microgm/dl), transferrin saturation (TSAT, %), ferritin (ng/ml), albumin (g/dl), C-reactive protein (mg/l), TNF-a (pg/ml) IL-6 (pg/ml), and hepcidin (ng/ml) in ESRD patients (solid blue line) and healthy controls (dashed red line). Log-transformed data, with the solid horizontal line denoting the median along with the interquartile range
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Figure 0002: Box-and-whisker plots showing the serum iron (microgm/dl), transferrin saturation (TSAT, %), ferritin (ng/ml), albumin (g/dl), C-reactive protein (mg/l), TNF-a (pg/ml) IL-6 (pg/ml), and hepcidin (ng/ml) in ESRD patients (solid blue line) and healthy controls (dashed red line). Log-transformed data, with the solid horizontal line denoting the median along with the interquartile range

Mentions: The anthropometric parameters, iron profile, and inflammatory markers of the two groups are shown in Table 2 and Figure 1. The ESRD patients had a significantly lower estimated body fat percentage and muscle mass, higher TSAT, and markedly raised serum ferritin levels. In the control population, iron deficiency was common (51%), whereas, iron overload was very rare (4%). Figure 2 shows the TSAT distribution among the ESRD subjects: about 20% had TSAT > 50% and 40% had TSAT< 25%. Half of the ESRD patients had received parenteral iron. Examination of the referral records showed that 47% had received an iron sucrose preparation, whereas, in the rest, the formulations were unknown or other forms of iron had been administered. Twenty-nine percent had received blood transfusions in the past (mean 2.2 units). Only 32 patients had received Epo, with most getting only a few doses or they took it intermittently.


Iron status, inflammation and hepcidin in ESRD patients: The confounding role of intravenous iron therapy.

Jairam A, Das R, Aggarwal PK, Kohli HS, Gupta KL, Sakhuja V, Jha V - Indian J Nephrol (2010)

Box-and-whisker plots showing the serum iron (microgm/dl), transferrin saturation (TSAT, %), ferritin (ng/ml), albumin (g/dl), C-reactive protein (mg/l), TNF-a (pg/ml) IL-6 (pg/ml), and hepcidin (ng/ml) in ESRD patients (solid blue line) and healthy controls (dashed red line). Log-transformed data, with the solid horizontal line denoting the median along with the interquartile range
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2966977&req=5

Figure 0002: Box-and-whisker plots showing the serum iron (microgm/dl), transferrin saturation (TSAT, %), ferritin (ng/ml), albumin (g/dl), C-reactive protein (mg/l), TNF-a (pg/ml) IL-6 (pg/ml), and hepcidin (ng/ml) in ESRD patients (solid blue line) and healthy controls (dashed red line). Log-transformed data, with the solid horizontal line denoting the median along with the interquartile range
Mentions: The anthropometric parameters, iron profile, and inflammatory markers of the two groups are shown in Table 2 and Figure 1. The ESRD patients had a significantly lower estimated body fat percentage and muscle mass, higher TSAT, and markedly raised serum ferritin levels. In the control population, iron deficiency was common (51%), whereas, iron overload was very rare (4%). Figure 2 shows the TSAT distribution among the ESRD subjects: about 20% had TSAT > 50% and 40% had TSAT< 25%. Half of the ESRD patients had received parenteral iron. Examination of the referral records showed that 47% had received an iron sucrose preparation, whereas, in the rest, the formulations were unknown or other forms of iron had been administered. Twenty-nine percent had received blood transfusions in the past (mean 2.2 units). Only 32 patients had received Epo, with most getting only a few doses or they took it intermittently.

Bottom Line: These patients also showed more marked inflammatory activation, as shown by the significantly higher CRP, TNF-α, and IL-6 levels.High hepcidin levels could explain the functional iron deficiency.The cause of the relatively greater degree of inflammatory activation as well as the relationship with IV iron administration needs further studies.

View Article: PubMed Central - PubMed

Affiliation: Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

ABSTRACT
Uremia is a state of heightened inflammatory activation. This might have an impact on several parameters including anemia management. Inflammation interferes with iron utilization in chronic kidney disease through hepcidin. We studied the body iron stores, degree of inflammatory activation, and pro-hepcidin levels in newly diagnosed patients with end-stage renal disease (ESRD), and compared them with normal population. In addition to clinical examination and anthropometry, the levels of iron, ferritin, C-reactive protein, tumor necrosis factor alfa, interleukin-6, and prohepcidin were estimated. A total of 74 ESRD patients and 52 healthy controls were studied. The ESRD patients had a significantly lower estimated body fat percentage, muscle mass, and albumin; and higher transferrin saturation (TSAT) and raised serum ferritin. Inflammatory activation was evident in the ESRD group as shown by the significantly higher CRP, IL-6, and TNF-α levels. The pro-hepcidin levels were also increased in this group. Half of the ESRD patients had received parenteral iron before referral. Patients who had received intravenous iron showed higher iron, ferritin, and TSAT levels. These patients also showed more marked inflammatory activation, as shown by the significantly higher CRP, TNF-α, and IL-6 levels. We conclude that our ESRD patients showed marked inflammatory activation, which was more pronounced in patients who had received IV iron. High hepcidin levels could explain the functional iron deficiency. The cause of the relatively greater degree of inflammatory activation as well as the relationship with IV iron administration needs further studies.

No MeSH data available.


Related in: MedlinePlus