Circulating α-Klotho is Related to Plasma Aldosterone and Its Follow-Up Change Predicts CKD Progression
Circulating α-Klotho is Related to Plasma Aldosterone and Its Follow-Up Change Predicts CKD Progression
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循环 α-Klotho 与血浆醛固酮相关，其后续变化可预测 CKD 进展
DOI：
10.1159/000490138
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发表时间：
2018-01-01
影响因子：
2.8
通讯作者：
Lai, Lingyun
中科院分区：
文献类型：
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作者：
Qian, Jing;Zhong, Jianyong;Lai, Lingyun
背景/目标：我们的目的是确定可溶性α-klotho水平是否是慢性肾病（CKD）进展的指标，以及α-klotho在进一步肾损伤过程中是否与醛固酮相互作用。方法：112例1-5期CKD成人入组我们的队列研究。所有患者均随访6年（2010年1月至2015年12月）。在基线和1.5年随访时测量血清可溶性α-klotho和醛固酮。主要结局是开始肾脏替代治疗（RRT），次要结局是心脑血管事件的发生。采用风险校正的考克斯比例风险回归模型分析患者的RRT和心脑血管事件的长期进展。校正包括年龄、性别、eGFR、平均动脉压、24小时蛋白排泄和1.5年随访时α-klotho水平较基线的变化。结果如下：基线循环α-klotho水平与基线估计肾小球滤过率（eGFR; r = 0.224，p = 0.017）呈正相关，但与年龄、钙、磷酸盐或甲状旁腺激素水平无关。在考克斯回归分析中，校正年龄、性别、eGFR、平均动脉压和24小时蛋白排泄后，1.5年随访时α-klotho水平较基线的变化（p = 0.002）与肾脏替代治疗（RRT）的启动独立相关。醛固酮水平与CKD分期呈正相关，与循环alpha-klotho水平呈负相关。结论：1.5年随访期间可溶性α-klotho浓度的变化是CKD进展的指标。与α-klotho减少相关的肾损害可能涉及血浆醛固酮的上调。未来的研究需要验证我们的研究结果，并调查潜在的机制，α-klotho和醛固酮可能导致肾损伤。(C)2018作者（S）由S发布。Karger AG，巴塞尔
Background/Aims: We aimed to determine if soluble alpha-klotho level was an indicator of chronic kidney disease (CKD) progression and whether alpha-klotho interacted with aldosterone during the course of further renal damage. Methods: 112 adults with stages 1-5 CKD were enrolled into our cohort study. All of the patients were followed up for 6 years (from January 2010 to December 2015). Serum soluble alpha-klotho and aldosterone were measured at baseline and at 1.5-years follow-up. The primary outcome was the initiation of renal replacement therapy (RRT) and the secondary outcome was the occurrence of cardio-cerebrovascular events. Longterm progression to RRT and cardio-cerebrovascular events in patients was analyzed with a risk-adjusted Cox proportional hazards regression model. Adjustment included age, gender, eGFR, mean arterial pressure, 24-h protein excretion and the change in alpha-klotho level from baseline at 1.5-years follow-up. Results: Baseline circulating alpha-klotho levels were positively associated with baseline estimated glomerular filtration rate (eGFR; r = 0.224, p = 0.017), but not age, calcium, phosphate, or parathyroid hormone levels. The change in alpha-klotho level from baseline at 1.5-years follow-up (p = 0.002) was independently associated with renal replace treatment (RRT) initiation after adjustment for age, gender, eGFR, mean arterial pressure, and 24-h protein excretion in Cox regression analysis. Aldosterone levels were positively associated with CKD stage, and were inversely correlated with circulating alpha-klotho levels. Conclusion: The change in concentration of soluble alpha-klotho during the 1.5-years follow-up was an indicator of CKD progression. Renal damage associated with a reduction of alpha-klotho may involve the upregulation of plasma aldosterone. Future studies are needed to validate our findings, and to investigate the underlying mechanism by which alpha-klotho and aldosterone may cause renal damage. (C) 2018 The Author(s) Published by S. Karger AG, Basel