Risk factors for progression of coronary artery calcification in patients with chronic kidney disease: The CRIC study.

Risk factors for progression of coronary artery calcification in patients with chronic kidney disease: The CRIC study.
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DOI:
10.1016/j.atherosclerosis.2018.02.009
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发表时间:
2018-04
期刊:
影响因子:
5.3
通讯作者:
CRIC Study Investigators
CRIC Study Investigators
中科院分区:
医学2区
文献类型:
--
作者:
Bundy JD;Chen J;Yang W;Budoff M;Go AS;Grunwald JE;Kallem RR;Post WS;Reilly MP;Ricardo AC;Rosas SE;Zhang X;He J;CRIC Study Investigators

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冠状动脉钙化(CAC)在慢性肾脏病(CKD)患者中很常见,可预测心血管疾病(CVD)的风险。我们研究了CKD患者中新的危险因素与CAC进展的关系。在慢性肾功能不全队列(CRIC)研究的1,123例CKD患者中,在基线和随访访视时使用电子束计算机断层扫描或多探测器计算机断层扫描测量CAC(以Agatston单位计)。在平均3.3年的随访中,109例(25.1%)基线时无CAC的参与者发生了CAC事件,124例(18.0%)基线时有CAC的参与者发生了CAC进展,定义为每年增加≥100个Agatston单位。在对已确定的动脉粥样硬化危险因素进行校正后,一些新的危险因素与随访期间CAC的变化相关。与1 SD更高水平的风险因素相关的平方根转换CAC评分变化为-0.20(95%置信区间,−0.31至−0.10; p <0.001)估计肾小球滤过率,0.14(0.02 - 0.25; p=0.02)24小时尿白蛋白,0.25(0.15至0.34; p <0.001)对于半胱氨酸蛋白酶抑制剂C,-0.17(−0.27至−0.07; p <0.001)血清钙,0.14(0.03 - 0.24; p=0.009)血清磷酸盐,0.24(0.14至0.33; p <0.001)对于成纤维细胞生长因子-23,0.13总甲状旁腺激素为0.04 ~ 0.23; p=0.007,白细胞介素-6为0.17(0.07 ~ 0.27; p <0.001),肿瘤坏死因子-α为0.12(0.02 ~ 0.22; p=0.02)。肾功能下降、钙和磷代谢紊乱以及炎症,独立于已确定的CVD风险因素,可能使CKD患者的CAC进展。
Coronary artery calcification (CAC) is common among patients with chronic kidney disease (CKD) and predicts the risk for cardiovascular disease (CVD). We examined the associations of novel risk factors with CAC progression among patients with CKD. Among 1,123 CKD patients in the Chronic Renal Insufficiency Cohort (CRIC) Study, CAC was measured in Agatston units at baseline and a follow-up visit using electron beam computed tomography or multidetector computed tomography. Over an average 3.3-year follow-up, 109 (25.1%) participants without CAC at baseline had incident CAC and 124 (18.0%) participants with CAC at baseline had CAC progression, defined as an annual increase of ≥100 Agatston units. After adjustment for established atherosclerotic risk factors, several novel risk factors were associated with changes in CAC over follow-up. Changes in square root transformed CAC score associated with 1 SD greater level of risk factors were −0.20 (95% confidence interval, −0.31 to −0.10; p <0.001) for estimated glomerular filtration rate, 0.14 (0.02 to 0.25; p=0.02) for 24-hour urine albumin, 0.25 (0.15 to 0.34; p <0.001) for cystatin C, −0.17 (−0.27 to −0.07; p <0.001) for serum calcium, 0.14 (0.03 to 0.24; p=0.009) for serum phosphate, 0.24 (0.14 to 0.33; p <0.001) for fibroblast growth factor-23, 0.13 (0.04 to 0.23; p=0.007) for total parathyroid hormone, 0.17 (0.07 to 0.27; p <0.001) for interleukin-6, and 0.12 (0.02 to 0.22; p=0.02) for tumor necrosis factor-α. Reduced kidney function, calcium and phosphate metabolism disorders, and inflammation, independent of established CVD risk factors, may progress CAC among CKD patients.
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