Kalantar-Zadeh Kamyar, Kalantar-Zadeh Kourosh, Lee Grace H
Division of Nephrology and Hypertension, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 West Carson Street, Torrance, CA 90502, USA.
Clin J Am Soc Nephrol. 2006 Sep;1 Suppl 1:S9-18. doi: 10.2215/CJN.01390406.
Although the emergence of erythropoiesis-stimulating agents has revolutionized the anemia management of chronic kidney disease (CKD) in the past two decades, strategies to assess iron (Fe) status and to provide Fe supplementation have remained indistinct. The reported cases of hemochromatosis in dialysis patients from the pre-erythropoiesis-stimulating agent era along with the possible associations of Fe with infection and oxidative stress have fueled the "iron apprehension." To date, no reliable marker of Fe stores in CKD has been agreed on. Serum ferritin continues to be the focus of attention. Almost half of all maintenance hemodialysis patients have a serum ferritin >500 ng/ml. In this ferritin range, Fe supplementation currently is not encouraged, although most reported hemochromatosis cases had a serum ferritin >2000 ng/ml. The moderate-range hyperferritinemia (500 to 2000 ng/ml) seems to be due mostly to non-Fe-related conditions, including inflammation, malnutrition, liver disease, infection, and malignancy. Recent epidemiologic studies have shown that a low, rather than a high, serum Fe is associated with a poor survival in maintenance hemodialysis patients. In multivariate adjusted models that mitigate the confounding effect of malnutrition-inflammation, serum ferritin <1200 ng/ml and Fe saturation ratio in 30 to 50% range are associated with the greatest survival in maintenance hemodialysis patients. Although ferritin is a fascinating molecule, moderate hyperferritinemia is a misleading marker of Fe stores in patients with CKD. It may be time to revisit the utility of serum ferritin in CKD and ask ourselves whether its measurement has helped us or has caused more confusion and controversy.
尽管促红细胞生成素在过去二十年中彻底改变了慢性肾脏病（CKD）的贫血管理，但评估铁（Fe）状态和提供铁补充剂的策略仍不明确。促红细胞生成素时代之前报道的透析患者血色素沉着症病例，以及铁与感染和氧化应激的可能关联，加剧了人们对“铁的担忧”。迄今为止，尚未就CKD中铁储存的可靠标志物达成共识。血清铁蛋白仍然是关注的焦点。几乎一半的维持性血液透析患者血清铁蛋白>500 ng/ml。在这个铁蛋白范围内，目前不鼓励补充铁，尽管大多数报道的血色素沉着症病例血清铁蛋白>2000 ng/ml。中度范围的高铁蛋白血症（500至2000 ng/ml）似乎主要归因于非铁相关状况，包括炎症、营养不良、肝病、感染和恶性肿瘤。最近的流行病学研究表明，维持性血液透析患者血清铁水平低而非高与生存率低相关。在减轻营养不良-炎症混杂效应的多变量调整模型中，血清铁蛋白<1200 ng/ml和铁饱和度在30%至50%范围内与维持性血液透析患者的最大生存率相关。尽管铁蛋白是一个引人关注的分子，但中度高铁蛋白血症在CKD患者中是铁储存的一个误导性标志物。或许是时候重新审视血清铁蛋白在CKD中的效用，并问问我们自己，它（血清铁蛋白）的检测是帮助了我们，还是造成了更多的困惑和争议。
