摘要
目的观察慢性肾脏疾病(CKD)患者的尿酸、超敏C-反应蛋白(hs-CRP)、血管性血友病因子(vWF)、心脏结构与功能改变情况,探讨高尿酸在慢性肾衰竭发病中的机制。方法将68例CKD患者分为CKD合并高尿酸血症组(A组)及CKD组(B组),以20例健康体检者为对照组,清晨空腹抽血测定血尿酸、hs-CRP和vWF浓度,行心脏超声检查。结果各组患者尿酸与hs-CRP、vWF水平变化,A组与B组均高于对照组(P<0.05),A组高于B组(P<0.05);A组与B组的左心房内径、左心室舒张末期内径、左室舒张末期容量及收缩末期容量、短轴缩短率及射血分数与对照组相比差异均具有统计学意义(P<0.05)。A组与B组相比,A组的左心房内径、左心室舒张末期内径、左室舒张末期容量、收缩末期容量增加及射血分数、短轴缩短率降低显著多于B组(P<0.05),但两组室间隔厚度、左心室后壁厚度的差异无统计学意义。结论 CKD合并高尿酸血症的患者,尿酸与hs-CRP、vWF水平、心脏损伤情况呈正相关,说明尿酸在慢性肾脏疾病中发挥了不良作用,高尿酸血症是心脏结构和功能异常,特别是左心室壁肥厚,心肌顺应性降低,心室壁运动减弱的危险因素。
Objective To investigate the pathogenesis of hyperuricemia in chronic kidney disease (CKD) by observing plasma uric acid,high sensitivity C-reactive protein(hs-CRP),von willebrand factor(vWF),and alteration of cardiac structure and function in CKD patients.Methods 68 CKD patients and 20 health adults were included in the study.Patients were divided into 2 groups:group A with hyperuricemia and group B with normal uricemia.The concentrations of plasma uric acid,hs-CRP,and vWF as well as echocardiography were assessed in all groups.Results Concentrations of the examined biomarkers of both group A and group B were higher than those of the control group(P 0.05),and group A's were higher than group B's(P 0.05).There were significant changes in the left atrial diameter(LAD),left ventricular end-diastolic diameter (LVEDD),end-diastolic diameter(EDV),end systolic diameter(ESV),fractional shortening (FS),and ejection fraction(EF) in group A and B compared with the control group(P 0.05). Compared with group B,LAD,LVEDD,EDV,and ESV levels in group A increased significantly (P 0.05),while EF and FS decreased(P 0.05).Ventricular septal and left ventricular posterior wall remained unchanged.Conclusion In CKD patients with hyperuricemia,serum uric is directly correlated with hs-CRP,vWF,and injury of heart,which suggests that hyperuricemia may have harmful effects on CKD.Hyperuricemia may be a risky factor for cardiac structure and function alteration,especially for hypertrophy of left ventricular wall,the decrease of myocardial complialice and movement of ventricular wall.
出处
《兰州大学学报(医学版)》
CAS
2012年第1期57-60,共4页
Journal of Lanzhou University(Medical Sciences)
基金
兰州市科技计划项目(08-2-12)