Von Willebrand factor research on related factor of coagulation abnormalities in type 2 diabetic nephropathy
10.3760/cma.j.issn.1008-6315.2012.10.001
- VernacularTitle:2型糖尿病肾病凝血异常相关因素分析
- Author:
Yan XIE
;
Qiaoyun TANG
;
Haijian ZHENG
;
Wei ZHANG
;
Jinhong WANG
- Publication Type:Journal Article
- Keywords:
Diabetic nephropathy;
Protein C;
von Willebrand factor;
Plasma fibrinogen
- From:
Clinical Medicine of China
2012;28(10):1009-1012
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the early changes of the coagulation system in type 2 diabetic nephropathy.Methods Sixty-two cases of patients with type 2 diabetic nephropathy were divided into two groups:normal albuminuria group ( N-UAlb group,UACR ＜ 30 mg/g,32 cases ),microalbuminuria group ( MUAlb group,UACR:30～300 mg/g,30 cases).Thirty healthy persons constituted a control group (NC group).Fibrinogen( FIB ),antithrombin Ⅲ ( AT-Ⅲ ),protein C ( PC ),protein S ( PS ) were measured by coagulation analyzer,while yon willebrand factor (vWF) and platelet granule membrane protein 140 (GMP-140) were detected by ELISA assay,platelet count (PLT),mean platelet volume(MPV),platelet hematocrit (PCT),platelet distribution width(PDW) by hematology analyzer.Results The level of fibrinogen,GMP-140 and vWF in the M-UAlb group were (4.20 ± 1.53 ) g/L,( 30.03 ± 7.77 ) μg/L,and ( 315.53 ± 47.24 ) ％ respectively,vwhich were significantly higher than those in the N-UAlb group [ ( 3.21 ± 0.89 ) g/L,( 18.22 ± 5.08 ) μg,/L and ( 191.88 ± 57.25 ) ％ respectively ] and the NC group [ ( 2.75 ± 0.53 ) g/L,( 14.26 ± 2.29 ) μg/L and ( 138.12 ± 61.27 ) ％ respectively ] ( F =5.42,10.42,30.44,P ＜ 0.05 or 0.01 ).The fibrinogen,vWF,GMP-140 were positively correlated with UACR ( r =0.313,P ＜ 0.05 ; r =0.620,P ＜ 0.01 ; r =0.680,P ＜ 0.01 ) and PC was negatively correlated with UACR ( r =-0.255,P ＜ 0.05 ).Conclusion Hypercoagulable state in diabetic nephropathy is associated with the high fibrinogen,endothelial dysfunction and platelet activation,and these changes have already emerged in patients without albuminuria.This might mind us that we should strengthen anticoagulant therapy on patients when they are not progressing to albuminuria.
