Effects of Phosphate Binders in Moderate CKD
Effects of Phosphate Binders in Moderate CKD
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DOI：
10.1681/asn.2012030223
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发表时间：
2012-08-01
影响因子：
13.6
通讯作者：
Chertow, Glenn M.
中科院分区：
文献类型：
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作者：
Block, Geoffrey A.;Wheeler, David C.;Chertow, Glenn M.
考虑到较高水平的磷与死亡率之间的关联，一些人建议在 CKD 人群中使用磷酸盐结合剂，但其在该人群中的安全性和有效性尚不清楚。在这里，我们的目的是确定磷酸盐结合剂对中度至晚期 CKD 患者矿物质代谢和血管钙化参数的影响。我们将 148 名估计 GFR=20-45 ml/min/1.73 m(2) 的患者随机分配至醋酸钙、碳酸镧、碳酸司维拉姆或安慰剂组。主要终点是平均血清磷从基线到第 3、6 和 9 个月平均值的变化。血清磷从活性治疗组和安慰剂组的基线平均值 4.2 mg/dl 下降至活性治疗组的 3.9 mg/dl 和安慰剂组的 4.1 mg/dl (P=0.03)。磷酸盐结合剂（而非安慰剂）可使 24 小时尿磷平均降低 22%。血清完整甲状旁腺激素中位数在积极治疗中保持稳定，在安慰剂中增加（P=0.002）。积极治疗并未显着影响血浆C端成纤维细胞生长因子23水平。然而，积极治疗确实显着增加了冠状动脉和腹主动脉的钙化（冠状动脉：中位增加 18.1% 与 0.6%，P=0.05；腹主动脉：中位增加 15.4% 与 3.4%，P=0.03）。总之，对于血清磷水平正常或接近正常的 CKD 患者，磷酸盐结合剂可显着降低血清和尿磷，并减轻继发性甲状旁腺功能亢进症的进展；然而，它们也会促进血管钙化的进展。磷酸盐结合剂治疗 CKD 的安全性和有效性仍不确定。
Some propose using phosphate binders in the CKD population given the association between higher levels of phosphorus and mortality, but their safety and efficacy in this population are not well understood. Here, we aimed to determine the effects of phosphate binders on parameters of mineral metabolism and vascular calcification among patients with moderate to advanced CKD. We randomly assigned 148 patients with estimated GFR=20-45 ml/min per 1.73 m(2) to calcium acetate, lanthanum carbonate, sevelamer carbonate, or placebo. The primary endpoint was change in mean serum phosphorus from baseline to the average of months 3, 6, and 9. Serum phosphorus decreased from a baseline mean of 4.2 mg/dl in both active and placebo arms to 3.9 mg/dl with active therapy and 4.1 mg/dl with placebo (P=0.03). Phosphate binders, but not placebo, decreased mean 24-hour urine phosphorus by 22%. Median serum intact parathyroid hormone remained stable with active therapy and increased with placebo (P=0.002). Active therapy did not significantly affect plasma C-terminal fibroblast growth factor 23 levels. Active therapy did, however, significantly increase calcification of the coronary arteries and abdominal aorta (coronary: median increases of 18.1% versus 0.6%, P=0.05; abdominal aorta: median increases of 15.4% versus 3.4%, P=0.03). In conclusion, phosphate binders significantly lower serum and urinary phosphorus and attenuate progression of secondary hyperparathyroidism among patients with CKD who have normal or near-normal levels of serum phosphorus; however, they also promote the progression of vascular calcification. The safety and efficacy of phosphate binders in CKD remain uncertain.