From the Evelyn F. McKnight Brain Institute (C.B.W., C.D., T.R., R.L.S.) and Departments of Neurology (C.B.W., C.D., M.S., T.R., R.L.S.), Public Health Sciences (C.B.W., R.L.S.), Human Genomics (R.L.S.), and Medicine (A.M., M.W.), Leonard M. Miller School of Medicine, and the Neuroscience Program (C.B.W., R.L.S.), University of Miami, FL; and Departments of Neurology (M.S.V.E.) and Medicine (S.S.), College of Physicians and Surgeons, and Department of Epidemiology (M.S.V.E.), Mailman School of Public Health, Columbia University, New York.
Neurology. 2014 May 13;82(19):1700-6. doi: 10.1212/WNL.0000000000000410. Epub 2014 Apr 4.
To examine fibroblast growth factor 23 (FGF23) as a risk factor for incident stroke in a racially/ethnically diverse population-based urban cohort.
Stroke-free Northern Manhattan Study participants with FGF23 measurements (n = 2,525) were followed for a mean of 12 (±5) years to detect incident strokes. We used Cox proportional hazards models to estimate the association of baseline FGF23 with incident total, ischemic, and hemorrhagic stroke.
Median FGF23 was 57 relative units (RU)/mL (interquartile range = 44-81 RU/mL). Each unit increase of natural log-transformed FGF23 conferred a 40% greater overall stroke risk after adjusting for estimated glomerular filtration rate and sociodemographic and vascular risk factors (hazard ratio = 1.4, 95% confidence interval 1.1-1.6, p = 0.004). Penalized spline analysis revealed a linear association with overall stroke risk at ≥90 RU/mL FGF23, compared with <90 RU/mL (hazard ratio = 1.5, 95% confidence interval = 1.2-2.1, p = 0.004). Greater FGF23 conferred a doubling of intracerebral hemorrhage (ICH) risk but no significant increased risk of ischemic stroke. The associations of elevated FGF23 levels with greater risks of overall stroke and ICH events were independent of phosphate and parathyroid hormone levels and were similar among participants without chronic kidney disease.
Elevated FGF23 was a risk factor for overall stroke and ICH events, in particular in a racially and ethnically diverse urban community, independent of chronic kidney disease.
在一个种族/民族多样化的基于人群的城市队列中，研究成纤维细胞生长因子 23（FGF23）是否是中风事件的危险因素。
无中风的北曼哈顿研究参与者进行了 FGF23 测量（n=2525），平均随访 12（±5）年以检测中风事件。我们使用 Cox 比例风险模型来估计基线 FGF23 与总中风、缺血性中风和出血性中风事件的相关性。
中位数 FGF23 为 57 相对单位（RU）/mL（四分位距=44-81 RU/mL）。调整估计肾小球滤过率以及社会人口学和血管危险因素后，自然对数转换的 FGF23 每增加一个单位，整体中风风险增加 40%（风险比=1.4，95%置信区间 1.1-1.6，p=0.004）。惩罚样条分析显示，与 FGF23<90 RU/mL 相比，FGF23≥90 RU/mL 与整体中风风险呈线性相关（风险比=1.5，95%置信区间=1.2-2.1，p=0.004）。较高的 FGF23 水平导致脑出血（ICH）风险增加一倍，但缺血性中风风险无显著增加。升高的 FGF23 水平与整体中风和 ICH 事件的更高风险相关，独立于磷酸盐和甲状旁腺激素水平，并且在无慢性肾脏病的参与者中相似。
升高的 FGF23 是整体中风和 ICH 事件的危险因素，尤其是在种族和民族多样化的城市社区中，独立于慢性肾脏病。
