Abstract
The metabolism of hepcidin is profoundly modified in chronic kidney disease (CKD). We investigated its relation to iron disorders, inflammation and hemoglobin (Hb) level in 199 non-dialyzed, non-transplanted patients with CKD stages 1–5. All had their glomerular filtration rate measured by 51Cr-EDTA renal clearance (mGFR), as well as measurements of iron markers including hepcidin and of erythropoietin (EPO). Hepcidin varied from 0.2 to 193 ng/mL. The median increased from 23.3 ng/mL [8.8–28.7] to 36.1 ng/mL [14.1–92.3] when mGFR decreased from ≥60 to <15 mL/min/1.73 m2 (p = 0.02). Patients with absolute iron deficiency (transferrin saturation (TSAT) <20% and ferritin <40 ng/mL) had the lowest hepcidin levels (5.0 ng/mL [0.7–11.7]), and those with a normal iron profile (TSAT ≥20% and ferritin ≥40), the highest (34.5 ng/mL [23.7–51.6]). In multivariate analysis, absolute iron deficiency was associated with lower hepcidin values, and inflammation combined with a normal or functional iron profile with higher values, independent of other determinants of hepcidin concentration, including EPO, mGFR, and albuminemia. The hepcidin level, although it rose overall when mGFR declined, collapsed in patients with absolute iron deficiency. There was a significant interaction with iron status in the association between Hb and hepcidin. Except in absolute iron deficiency, hepcidin’s negative association with Hb level indicates that it is not down-regulated in CKD anemia.
Highlights
Hepcidin is a new iron marker, discovered in 2001 and studied especially in hemochromatosis
Hepcidin levels increased from 23.3 ng/mL IQR [8.8–28.7] to 36.1 ng/mL IQR [14.1– 92.3] when measurement of their GFR (mGFR) declined from .60 mL/min/1.73 m2 to, 15 mL/min/1.73 m2
Independent of mGFR, higher levels of body mass index, albuminemia, C-reactive protein (CRP), oral iron therapy and lower levels of proteinuria and EPO were significantly associated with higher hepcidin concentrations (Tables 2 and 3)
Summary
Hepcidin is a new iron marker, discovered in 2001 and studied especially in hemochromatosis. Prohepcidin has no impact on iron metabolism in either healthy individuals [1] or patients with chronic kidney disease (CKD) [2], [3]. The involvement of hepcidin in iron disorders was clarified with the development of methods to quantify hepcidin-25 [2], [4]. Hepcidin has been evaluated in absolute iron deficiency, where its concentration is low, and in patients with chronic disease-related anemia [5]. The subsequent development of more specific assays for hepcidin-25 has led to a redefinition of normal values from around 50 ng/mL for the first assays to less than 10 ng/mL for those recently validated by the FDA [6]. Hepcidin has not yet proved its usefulness in clinical practice
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