Abstract
Introduction: Zinc (Zn) protoporphyrin (ZPP) presents in red blood cells (RBC) in small amounts, but increases in iron deficiency or lead poisoning. Formation of heme - a component of hemoglobin - finished with insertion of an iron into the molecule of protoporphyrin. In iron deficiency, or inhibition of iron insertion (lead poisoning), zinc replaces iron to form ZPP, which cannot bind to oxygen. Plasma zinc is lower in patients with chronic kidney diseases (CKD), but it’s not yet clear whether it’s a real deficit or is due to redistribution. Aim: The aim of this study was to evaluate the effects of iron supplementation on zinc redistribution in the body tissues of non-dialyzed chronic kidney disease (CKD) patients. Material and Methods: Zn and Fe status of 38 non-dialyzed patients with iron-deficit anemia (17 males; 21 females);mean GFR - 43.3 mL/min(32.5 to 57.3 mL/min), was evaluated before and after 5 i.v. injections of 100 mg iron each. The following parameters were tested: RBC and plasma Zn, ZPP, ferritin (F), transferrin saturation (TFS), and total iron (Fe). Results: F and TFS increased from 86.5+/-61.2 ng/mL to 132.4+/-64.3 ng/mL and from 21.5+/-9.4% to 26.8+/-8.3% (P<0.05), respectively, after iron supplementation. Absolute iron deficiency (ferritin <100 g/L and TFS < 20%) was present in 44% of the patients and decreased to 25% after iron treatment. After supplementation, patients with low plasma zinc decreased from 49.5% to 30.8% (p N.S.). At start of the study 29 of the patients had high erythrocyte zinc. After iron treatment, erythrocyte zinc decreased significantly in 24 patients (p< 0.001), and only a weak lowering was observed in ZPP (p N.S.). Conclusions: The study suggests that iron deficiency may participate in the inadequate distribution of zinc in patients with CKD and iron supplementation may decrease the abnormal elevated erythrocyte zinc levels.
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