Nephrotic syndrome and end-stage kidney disease accompanied by bicytopenia due to copper deficiency.

A 69-year-old man presented with proteinuria and hematuria. He had received total parenteral nutrition for massive small bowel resection. However, due to the iatrogenic lack of trace elements for the next four years, he developed severe copper-deficiency anemia and neutropenia. In addition, his proteinuria and kidney dysfunction worsened concurrently with the development of nephrotic syndrome and end-stage kidney disease. After receiving trace elements, the patient's anemia and neutropenia improved, and the anuria dramatically resolved. Copper-containing enzymes, including ceruloplasmin have an antioxidant activity. In patients with various types of glomerular injuries, the ceruloplasmin expression is known to be increased. Copper deficiency can worsen nephrotic syndrome by decreasing the ceruloplasmin activity, which protects the glomeruli.