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Effects of Immunoadsorption on Markers of Iron Metabolism: A Case Series
Noemi E Ginthör1, Tobias Niedrist2, Gerold Schwantzer3
1Clinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.
Immunoadsorption selectively eliminates circulating antibodies in antibody-mediated diseases. Iron deficiency is the most common cause of anemia; however, the potential role of immunoadsorption in contributing to iron depletion remains insufficiently established. This study quantified levels of eluted iron, ferritin, and transferrin in the regeneration solutions of peptide ligand adsorbers from 13 patients and in ABO antigen-specific non-regenerative adsorbers from five patients. Markers of anemia and iron status were assessed at baseline and monitored for up to 2 weeks. Analysis of regeneration solutions from regenerative adsorbers revealed considerable levels of eluted iron (5.46 ± 7.4 μg/dL in NaCl 0.9%; 1.46 ± 1.45 μg/dL in glycine, and 3.61 ± 6.07 μg/dL in PBS), ferritin (52.65 ± 96.14 ng/mL in NaCl 0.9%; 18.79 ± 46.44 ng/mL in glycine and 4.93 ± 14.79 ng/mL in PBS), and transferrin (0.168 ± 0.26 g/L in NaCl 0.9%; 0.594 ± 2.37 g/L in glycine, and 0.005 ± 0.02 g/L in PBS). In ABO adsorbers, 50.27 ± 22.66 μg/dL iron, 88.39 ± 33.21 ng/mL ferritin, and 1.165 ± 0.41 g/L transferrin were detected, implicating adsorbers to directly deplete iron-related proteins. Blood hemoglobin (-1.88 g/dL), erythrocyte count (-0.58 × 1012/L), hematocrit (-5.32%), and MCH (-0.53 pg), as well as iron (-10 μg/dL) and ferritin (-22.3 ng/mL) levels were decreased at the final visit. These findings demonstrate that immunoadsorption contributes to the depletion of iron-related proteins from plasma, with adsorbers playing a pivotal role in iron loss. This highlights the need for vigilant monitoring of iron parameters and potential mitigation strategies in immunoadsorption patients.
Immunoadsorption selectively eliminates circulating antibodies in antibody-mediated diseases. Iron deficiency is the most common cause of anemia; however, the potential role of immunoadsorption in contributing to iron depletion remains insufficiently established. This study quantified levels of eluted iron, ferritin, and transferrin in the regeneration solutions of peptide ligand adsorbers from 13 patients and in ABO antigen-specific non-regenerative adsorbers from five patients. Markers of anemia and iron status were assessed at baseline and monitored for up to 2 weeks. Analysis of regeneration solutions from regenerative adsorbers revealed considerable levels of eluted iron (5.46 ± 7.4 μg/dL in NaCl 0.9%; 1.46 ± 1.45 μg/dL in glycine, and 3.61 ± 6.07 μg/dL in PBS), ferritin (52.65 ± 96.14 ng/mL in NaCl 0.9%; 18.79 ± 46.44 ng/mL in glycine and 4.93 ± 14.79 ng/mL in PBS), and transferrin (0.168 ± 0.26 g/L in NaCl 0.9%; 0.594 ± 2.37 g/L in glycine, and 0.005 ± 0.02 g/L in PBS). In ABO adsorbers, 50.27 ± 22.66 μg/dL iron, 88.39 ± 33.21 ng/mL ferritin, and 1.165 ± 0.41 g/L transferrin were detected, implicating adsorbers to directly deplete iron-related proteins. Blood hemoglobin (-1.88 g/dL), erythrocyte count (-0.58 × 1012/L), hematocrit (-5.32%), and MCH (-0.53 pg), as well as iron (-10 μg/dL) and ferritin (-22.3 ng/mL) levels were decreased at the final visit. These findings demonstrate that immunoadsorption contributes to the depletion of iron-related proteins from plasma, with adsorbers playing a pivotal role in iron loss. This highlights the need for vigilant monitoring of iron parameters and potential mitigation strategies in immunoadsorption patients.
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