Copper deficiency anemia and nephrosis in zinc-toxicity: a case report

Zinc is a ubiquitous element that is essential for normal enzymatic function in multiple metabolic pathways. Chronic excessive zinc ingestion causes severe reversible anemia in humans. In animals, zinc toxicity leads to anemia as well as physiologic and morphologic damage to the pancreas, kidneys, and often, multisystem failure and death. In this case, a young female ingested approximately 2000 mg of zinc gluconate daily for 12 months. She subsequently developed anemia consistent with zinc-induced copper deficiency and severe nephrosis. After cessation of zinc ingestion, her anemia and nephrosis resolved. This case study underscores the importance of an accurate and thorough investigation of nutritional supplements during the history and physical examination. Given the promulgation of zinc for the treatment of skin disorders and the common cold, along with the commercialization of nutritional supplements, unimpeded by regulatory guidelines, it is imperative that primary care physicians be attuned to the potentially dangerous consequences of excessive zinc ingestion.