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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Copper deficiency is a rare but reversible cause of cytopenia that can mimic myelodysplastic syndrome (MDS). In hemodialysis patients, zinc supplementation is often prescribed to treat dysgeusia caused by zinc deficiency. However, excessive zinc intake can suppress copper absorption, resulting in copper depletion. Here, we report a case of severe anemia due to zinc-induced copper deficiency in a patient undergoing maintenance hemodialysis.
Case Presentation. A 76-year-old man on maintenance hemodialysis presented with dysgeusia and began oral zinc acetate therapy for zinc deficiency (37 µg/dL). At that time, his hemoglobin levels were stable around 11 g/dL with weekly erythropoiesis-stimulating agent (ESA) therapy. His anemia gradually worsened, and his hemoglobin levels dropped to 6.9 g/dL, accompanied by thrombocytopenia (54,000/µL). Bone marrow examination revealed findings consistent with low-risk MDS, and high-dose ESA therapy together with repeated red blood cell transfusions were initiated as supportive treatment. However, his anemia persisted despite these interventions, and intradialytic hypotension subsequently became problematic. He was admitted to our department for further evaluation. Laboratory tests revealed a markedly decreased serum copper level (<5 µg/dL), whereas serum zinc level was within the normal range (105 μg/dL). Zinc acetate was discontinued, and intravenous copper replacement was initiated. Two weeks later, his anemia and thrombocytopenia began to improve along with an increase in serum copper level, and his hemoglobin levels stabilized at 9–10 g/dL with oral zinc-copper co-supplementation.
In hemodialysis patients, even therapeutic-dose zinc supplementation can induce copper depletion. Regular monitoring of serum copper, together with serum zinc levels, is essential during zinc therapy to avoid hematologic complications.
This abstract was originally presented at the 55th Eastern Regional Meeting of the Japanese Society of Nephrology. We hereby declare that the re-submission of this abstract to WCN has been permitted by the organizers of the original meeting.
