Yilmaz Gulay, Ustundag Sedat, Temizoz Osman, Sut Necdet, Demir Muzaffer, Ermis Veli, Sevinc Can, Ustundag Ayten
Clin Lab. 2015;61(8):1061-70. doi: 10.7754/clin.lab.2015.141236.
The cause of early-accelerated atherosclerosis development observed in Chronic Kidney Disease (CKD) is not fully understood. The determination of the relationship between the levels of fibroblast growth factor 23 (FGF-23) and the development of endothelial dysfunction, left ventricular hypertrophy, and myocardial infarction lends support to the possibility that FGF-23 plays a role in the development of atherosclerosis in CKD. Only a few studies, however, have been conducted that analyze the relationship between FGF-23 levels in the progression of CKD and the development of atherosclerosis, and these studies have generally been limited to those patients receiving dialysis therapy due to end stage renal disease (ESRD).
In the present study, carotid artery intima-media thicknesses (IMT) were measured ultrasonically as a marker of atherosclerosis in 91 patients with CKD stage 3 - 4 (61 female and 30 male, age between 19 - 65 years, glomerular filtration rate [GFR] 15 - 60 mL/min 1.73 m2, CKD was not related to diabetes mellitus, and without cardiovascular-cerebral disease) in contrast to 36 healthy volunteers (26 female and 10 male, age between 19 - 65 years, GFR > 90 mL/min 1.73 m2, and without any diagnoses of acute or chronic disease), and a possible role of FGF-23 on atherosclerosis was analyzed.
Patients were similar to controls with respect to age, gender, smoking status, body mass index, and plasma glucose and lipid profile. On the other hand, IMT measurements (p < 0.00001) and FGF-23 levels (p = 0.00012) were significantly higher in patients than controls. IMT was measured above the subclinical atherosclerosis limit of 0.750 mm in 54% of the patients. Multivariate regression analysis showed that patients' age, high sensitive c-reactive protein (hsCRP), and FGF-23 levels were independent predictors of IMT (p < 0.00001, r = 0.559). Independent of other variables, every 1 μmol/L increase in FGF-23 levels resulted in 0.444 mm increase of IMT measurements in patients with CKD.
Our findings suggest that monitoring serum FGF-23 may be useful as a non-invasive indicator of subclinical atherosclerosis in patients with chronic kidney disease.
慢性肾脏病（CKD）中观察到的早期动脉粥样硬化加速发展的原因尚未完全明确。成纤维细胞生长因子23（FGF - 23）水平与内皮功能障碍、左心室肥厚和心肌梗死发展之间关系的确定，支持了FGF - 23在CKD动脉粥样硬化发展中起作用的可能性。然而，仅有少数研究分析了CKD进展过程中FGF - 23水平与动脉粥样硬化发展之间的关系，且这些研究一般仅限于因终末期肾病（ESRD）接受透析治疗的患者。
在本研究中，对91例3 - 4期CKD患者（61例女性，30例男性，年龄19 - 65岁，肾小球滤过率[GFR] 15 - 60 mL/min/1.73 m²，CKD与糖尿病无关，且无心脑血管疾病）进行超声测量颈动脉内膜中层厚度（IMT）作为动脉粥样硬化的标志物，并与36例健康志愿者（26例女性，10例男性，年龄19 - 65岁，GFR > 90 mL/min/1.73 m²，且无任何急慢性疾病诊断）进行对比，分析FGF - 23对动脉粥样硬化的可能作用。
患者在年龄、性别、吸烟状况、体重指数以及血糖和血脂谱方面与对照组相似。另一方面，患者的IMT测量值（p < 0.00001）和FGF - 23水平（p = 0.00012）显著高于对照组。54%的患者IMT测量值高于0.750 mm的亚临床动脉粥样硬化阈值。多因素回归分析显示，患者的年龄、高敏C反应蛋白（hsCRP）和FGF - 23水平是IMT的独立预测因素（p < 0.00001，r = 0.559）。独立于其他变量，CKD患者中FGF - 23水平每升高1 μmol/L，IMT测量值增加0.444 mm。
我们的研究结果表明，监测血清FGF - 23可能作为慢性肾脏病患者亚临床动脉粥样硬化的一种非侵入性指标。
