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静脉铁剂与促红细胞生成素:治疗慢性肾脏病贫血的朋友还是敌人?

Intravenous iron versus erythropoiesis-stimulating agents: friends or foes in treating chronic kidney disease anemia?

作者信息

Kalantar-Zadeh Kamyar, Streja Elani, Miller Jessica E, Nissenson Allen R

机构信息

Harold Simmons Center for Kidney Disease Research and Epidemiology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA 90502, USA.

出版信息

Adv Chronic Kidney Dis. 2009 Mar;16(2):143-51. doi: 10.1053/j.ackd.2008.12.008.

DOI:10.1053/j.ackd.2008.12.008
PMID:19233073
Abstract

Patients with chronic kidney disease (CKD), especially those requiring maintenance hemodialysis treatments, may lose up to 3 g of iron each year because of frequent blood losses. Higher doses of erythropoiesis-stimulating agents (ESAs) may worsen iron depletion and lead to an increased platelet count (thrombocytosis), ESA hyporesponsiveness, and hemoglobin variability. Hence, ESA therapy requires concurrent iron supplementation. Traditional iron markers such as serum ferritin and transferrin saturation ratio (TSAT) (ie, serum iron divided by total iron-binding capacity [TIBC]), may be confounded by non-iron-related conditions. Whereas serum ferritin <200 ng/mL suggests iron deficiency in CKD patients, ferritin levels between 200 and 1,200 ng/mL may be related to inflammation, latent infections, malignancies, or liver disease. Protein-energy wasting may lower TIBC, leading to a TSAT within the normal range, even when iron deficiency is present. Iron and anemia indices have different mortality predictabilities, in that high serum ferritin but low iron, TIBC, and TSAT levels are associated with increased mortality, whereas hemoglobin exhibits a U-shaped risk for death. The increased mortality associated with targeting hemoglobin above 13 g/dL may result from iron depletion-associated thrombocytosis. Intravenous (IV) iron administration may not only decrease hemoglobin variability and ESA hyporesponsiveness, it may also reduce the greater mortality associated with the much higher ESA doses that have been used in some patients when targeting higher hemoglobin levels.

摘要

慢性肾脏病(CKD)患者,尤其是那些需要维持性血液透析治疗的患者,由于频繁失血,每年可能会流失多达3克铁。更高剂量的促红细胞生成素(ESA)可能会使铁缺乏恶化,并导致血小板计数增加(血小板增多症)、ESA反应低下和血红蛋白变异性增加。因此,ESA治疗需要同时补充铁剂。传统的铁指标,如血清铁蛋白和转铁蛋白饱和度(TSAT)(即血清铁除以总铁结合力[TIBC]),可能会受到非铁相关疾病的干扰。虽然血清铁蛋白<200 ng/mL提示CKD患者存在缺铁,但铁蛋白水平在200至1200 ng/mL之间可能与炎症、潜伏感染、恶性肿瘤或肝脏疾病有关。蛋白质-能量消耗可能会降低TIBC,即使存在缺铁,也会导致TSAT处于正常范围内。铁和贫血指标具有不同的死亡率预测能力,即高血清铁蛋白但低铁、TIBC和TSAT水平与死亡率增加相关,而血红蛋白呈现出U形死亡风险。将血红蛋白目标值设定在13 g/dL以上时死亡率增加可能是由于铁缺乏相关的血小板增多症。静脉注射铁剂不仅可以降低血红蛋白变异性和ESA反应低下,还可以降低一些患者在将血红蛋白水平设定得更高时使用更高剂量ESA所带来的更高死亡率。

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