Agarwal Rajiv, Rizkala Adel R, Bastani Bahar, Kaskas Marwan O, Leehey David J, Besarab Anatole
Indiana University School of Medicine, Richard L. Roudebush VA Medical Center, Indianapolis, IN 46202, USA.
Am J Nephrol. 2006;26(5):445-54. doi: 10.1159/000096174. Epub 2006 Oct 11.
It is unknown whether intravenous iron or oral iron repletion alone can correct anemia associated with chronic kidney disease (CKD). We conducted a randomized multicenter controlled trial in adult anemic, iron-deficient non-dialysis CKD (ND-CKD) patients (>or=stage 3) not receiving erythropoiesis-stimulating agents (ESAs).
The participants were randomized to receive either a sodium ferric gluconate complex (intravenous iron) 250 mg i.v. weekly x 4 or ferrous sulfate (oral iron) 325 mg t.i.d. x 42 days. Hemoglobin (Hgb), ferritin and transferrin saturation (TSAT) were measured serially, and the Kidney Disease Quality of Life (KDQoL) questionnaire was administered on days 1 and 43. The primary outcome variable was change from baseline (CFB) to endpoint in Hgb values.
Seventy-five patients were analyzed (intravenous iron n = 36, oral iron n = 39). CFB in Hgb was similar in the two groups (intravenous iron 0.4 g/dl vs. oral iron 0.2 g/dl, p = n.s.). However, the increase in Hgb was only significant with intravenous iron (p < 0.01). In comparison to oral iron, intravenous iron achieved greater improvements in ferritin (232.0 +/- 160.8 vs. 55.9 +/- 236.2 ng/ml, p < 0.001) and TSAT (8.3 +/- 7.5 vs. 2.9 +/- 8.8%, p = 0.007). Intravenous iron caused greater improvements in KDQoL scores than oral iron (p < 0.05). The most common side effect reported with intravenous iron was hypotension, while constipation was more common with oral iron.
Oral and intravenous iron similarly increase Hgb in anemic iron-depleted ND-CKD patients not receiving ESAs. Although in comparison to oral iron, intravenous iron may result in a more rapid repletion of iron stores and greater improvement in quality of life, it exposes the patients to a greater risk of adverse effects and increases inconvenience and cost.
单独使用静脉铁剂或口服铁剂是否能纠正与慢性肾脏病（CKD）相关的贫血尚不清楚。我们对未接受促红细胞生成素（ESA）治疗的成年贫血、缺铁性非透析CKD（ND-CKD）患者（≥3期）进行了一项随机多中心对照试验。
参与者被随机分为接受葡萄糖酸铁钠复合物（静脉铁剂）250mg静脉注射，每周1次，共4次，或硫酸亚铁（口服铁剂）325mg，每日3次，共42天。连续测量血红蛋白（Hgb）、铁蛋白和转铁蛋白饱和度（TSAT），并在第1天和第43天进行肾脏病生活质量（KDQoL）问卷调查。主要结局变量是Hgb值从基线（CFB）到终点的变化。
分析了75例患者（静脉铁剂组n = 36，口服铁剂组n = 39）。两组Hgb的CFB相似（静脉铁剂组0.4g/dl，口服铁剂组0.2g/dl，p =无统计学意义）。然而，仅静脉铁剂使Hgb升高具有显著性（p < 0.01）。与口服铁剂相比，静脉铁剂使铁蛋白（232.0±160.8对55.9±236.2ng/ml，p < 0.001）和TSAT（8.3±7.5对2.9±8.8%，p = 0.007）有更大改善。静脉铁剂比口服铁剂使KDQoL评分有更大改善（p < 0.05）。静脉铁剂最常见报告的副作用是低血压，而口服铁剂便秘更常见。
口服和静脉铁剂在未接受ESA治疗的贫血缺铁性ND-CKD患者中同样能升高Hgb。虽然与口服铁剂相比，静脉铁剂可能使铁储备补充更快，生活质量改善更大，但它使患者面临更大的不良反应风险，并增加不便和费用。
