Trial reportInternational urology and nephrology2014
Effects of additional iron doses on hepcidin-25 level in hemodialysis patients without evident iron deficiency.
Trial report in International urology and nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
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7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSerum hepcidin-25 is not only a marker of iron stores, but also an acute phase reactant, and it could fluctuate in response to erythropoietic activity. STUDY
designProspective interventional, 3-months duration, investigating the influence of additional intravenous (IV) iron on hepcidin-25 in hemodialysis (HD) patients without obvious iron deficiency (ID). SETTINGS AND
participantsSingle HD unit, 41 patients. MEASUREMENTS: Hepcidin-25 (ELISA method), ferritin, transferrin, transferrin saturation (TSAT), C-reactive protein and serum albumin--at baseline and assessment; hemoglobin, iron and darbepoetin doses--monthly.
interventionAdditional IV iron doses were administered, driven by hemoglobin trend: iron dose increased by 25 % for each 0.5 g/dL hemoglobin drop for baseline ferritin of 200-800 ng/mL. Iron was discontinued for stable hemoglobin or >13 g/dL. Darbepoetin doses were adjusted for 11 g/dL target hemoglobin.
resultsAt baseline, 21 % of patients had "optimal" iron status; none had "absolute" or "functional" ID, while 15 % had iron "overload." Hepcidin levels were 112.8 (95 % CI 105.3-121.8) ng/mL. Hemoglobin was within the target range. After 75 % augmentation in iron doses, hepcidin-25 decreased by 70 %. Transferrin increased, and TSAT and ferritin decreased. Prevalence of "functional" ID rose to 24 % and of iron "overload" declined to 0 %. Reversal of iron-restricted erythropoiesis was further sustained by unchanging hemoglobin and decrease in darbepoetin doses and darbepoetin resistance index. Reasonable associations between assessment versus baseline ratios for hepcidin-25 and transferrin (inverse), TSAT and ferritin (direct) were found. Despite the increased inflammation, decrease in transferrin and increase in ferritin ratios were independent predictors of hepcidin variability (model of logistic regression r (2) 0.34; p < 0.0001). LIMITATIONS: Low number of participants, less diabetic nephropathy/vascular diseases than general dialyzed population, uncontrolled design, use of hepcidin-25 ELISA assay.
conclusionsActivation of erythropoiesis by additional IV iron administration overcomes moderate inflammation in suppressing hepcidin-25. Thus, hepcidin-25 could be clinically useful to evaluate iron status in patients with renal anemia.
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