Malyszko J, Głowińska I, Malyszko J S, Levin-Iaina N, Koc-Zorawska E, Mysliwiec M
Department of Nephrology and Transplantology, Medical University, Bialystok, Poland.
Transplant Proc. 2011 Oct;43(8):2973-5. doi: 10.1016/j.transproceed.2011.08.055.
All living organisms have evolved sophisticated mechanisms to maintain appropriate iron levels in their cells and within their body. Recently our understanding of iron metabolism has dramatically increased. Overt labile plasma iron (LPI) represents a component of non-transferrin-bound iron (NTBI) that is both redox active and chelatable, capable of permeating into organs and inducing tissue iron overload. LPI measures the iron-specific capacity of a given sample to produce reactive oxygen species. We studied NTBI correlations with markers of iron status and inflammation in prevalent kidney allograft recipients.
Complete blood count, urea, creatinine, serum lipids, fasting glucose, ferritin, serum iron, and total iron-binding capacity (TIBC) were studied by standard laboratory method in the hospital central laboratory. NTBI was assessed by FeROS eLPI kit by Aferrix Ltd (Tel Aviv, Israel). A test result of 0.6 U of LPI or more indicated a potential for iron-mediated production of reactive oxygen species in the sample.
In kidney transplant recipients NTBI was correlated with TIBC (r=.46, P<.001) and ferritin (r=.31, P<.05), with tendencies to correlate with C-reactive protein. Patients with LPI units≥0.6 showed higher serum iron (P<.05), TIBC (P<.05), ferritin (P<.001) and mean corpuscular volume. High ferritin values together with elevated NTBI content were observed among patients undergoing multiple transfusions before and/or after transplantation.
Elevated NTBI as well as ferritin levels in kidney transplant patients may be due to disturbed iron metabolism, since the human body has no possibility to remove an iron excess. NTBI could be responsible for excessive synthesis of reactive oxygen species. Therefore, it may be linked to complications such as atherosclerosis, which is frequently encountered among this population.
所有生物都进化出了复杂的机制来维持细胞和体内适当的铁水平。最近,我们对铁代谢的理解有了显著提高。明显的不稳定血浆铁(LPI)是非转铁蛋白结合铁(NTBI)的一个组成部分,它具有氧化还原活性且可螯合,能够渗透到器官中并导致组织铁过载。LPI测量给定样本产生活性氧的铁特异性能力。我们研究了NTBI与肾移植受者中铁状态和炎症标志物的相关性。
在医院中心实验室通过标准实验室方法研究全血细胞计数、尿素、肌酐、血脂、空腹血糖、铁蛋白、血清铁和总铁结合力(TIBC)。NTBI由以色列特拉维夫的Aferrix Ltd公司的FeROS eLPI试剂盒评估。LPI检测结果为0.6 U或更高表明样本中存在铁介导的活性氧产生的可能性。
在肾移植受者中,NTBI与TIBC(r = 0.46,P < 0.001)和铁蛋白(r = 0.31,P < 0.05)相关,与C反应蛋白有相关趋势。LPI单位≥0.6的患者血清铁(P < 0.05)、TIBC(P < 0.05)、铁蛋白(P < 0.001)和平均红细胞体积更高。在移植前和/或移植后接受多次输血的患者中观察到高铁蛋白值与升高的NTBI含量。
肾移植患者中NTBI和铁蛋白水平升高可能是由于铁代谢紊乱,因为人体无法清除过量的铁。NTBI可能是活性氧过度合成的原因。因此,它可能与该人群中常见的并发症如动脉粥样硬化有关。