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肾病综合征中止血激活的分子标志物。

Molecular markers of hemostasis activation in nephrotic syndrome.

作者信息

Sagripanti A, Cupisti A, Ferdeghini M, Pinori E, Barsotti G

机构信息

Institute of Medical Clinic, University of Pisa, Italy.

出版信息

Nephron. 1989;51(1):25-8. doi: 10.1159/000185236.

Abstract

Fibrinopeptide A (FPA), a sensitive index of in vivo thrombin activity, beta-thromboglobulin (beta TG) and platelet factor 4 (PF4), specific markers of platelet intravascular activation, have been measured in plasma by radioimmunoassays in 23 patients with nephrotic syndrome and in 32 normal subjects. FPA concentration was 2.40 +/- 1.42 ng/ml (mean +/- SD) in nephrotic patients and 1.16 +/- 0.58 ng/ml in normal controls (p less than 0.001); beta TG concentration was 57.9 +/- 33.2 ng/ml in nephrotic patients and 25.7 +/- 7.4 ng/ml in controls (p less than 0.001); PF4 level was not different from controls. These data indicate in vivo blood hypercoagulability and platelet hyperfunction in nephrotic syndrome. Moreover, we have documented a slow in vitro FPA generation pattern (delta FPA): 0.97 +/- 0.51 ng/ml/10 min; this suggests that thrombin activity is predominantly local.

摘要

纤维蛋白肽A(FPA)是体内凝血酶活性的敏感指标,β-血小板球蛋白(βTG)和血小板第4因子(PF4)是血小板血管内活化的特异性标志物,我们采用放射免疫分析法对23例肾病综合征患者和32例正常受试者的血浆进行了检测。肾病患者的FPA浓度为2.40±1.42 ng/ml(均值±标准差),正常对照组为1.16±0.58 ng/ml(p<0.001);肾病患者的βTG浓度为57.9±33.2 ng/ml,对照组为25.7±7.4 ng/ml(p<0.001);PF4水平与对照组无差异。这些数据表明肾病综合征患者体内存在血液高凝状态和血小板功能亢进。此外,我们记录了体外FPA生成模式缓慢(ΔFPA):0.97±0.51 ng/ml/10分钟;这表明凝血酶活性主要在局部。

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