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作 者:席岚[1]
机构地区:[1]陕西省宝鸡市妇幼保健院产科,宝鸡721000
出 处:《中国医药导刊》2013年第6期978-979,共2页Chinese Journal of Medicinal Guide
摘 要:目的:探讨子痫前期患者的血流动力学变化与肾功能损害的关系。方法:选择我院2008年8月~2012年5月待产分娩的子痫前期患者284例(子痫前期组),妊娠期高血压患者247例(妊高征组)及正常妊娠孕妇65例(正常组)为研究对象。检测所有孕妇的尿蛋白、血肌酐(Scr)、血尿素氮(BUN)、血尿酸(UA)和肾小球滤过率(GFR)并予比较。以90ml/min.1.73m2为临界值,GFR小于该值的57例患者记为子痫前期伴肾功能损害组(即A组),GFR大于或等于该值的227例患者记为子痫前期无肾功能损害组(即B组),对比两组的血流动力学参数:心率(HR)、心脏指数(CI)、心输出量(CO)、每搏指数(SI)、每搏量(SV)、周围血管阻力指数(SVRI)、周围血管阻力(SVR)、心肌加速度指数(ACI)、速度指数(SV)。结果:子痫前期组出现BUN、UA异常及肾功能损害的发生率显著高于妊高组和正常组(P<0.01);子痫前期患者Scr、BUN和UA较妊高组、正常组明显身高;而GFR显著降低;子痫前期伴肾功能损害组SBRI、SVR显著高于无肾功能损害组,而CI、CO、SI、SV、VI显著低于无肾功能损害组(P均<0.01)。结论:子痫前期可引起肾功能受损,其孕妇心输出量的降低和外周阻力的增大是发生肾功能受损的重要因素。Objective:To investigate the relationship between hemodynamic alterations and renal impairment in preeclamptic womern.Methods:284 women with preeclampsia(PE),247 women with pregnancy-induced hypertension(PIH),and 65 women with normal pregnancy(NP) who admitted in our hospital were enrolled in this study.The urinary protein excretion,serum creatinine(Scr),blood urea nitrogen(BUN),uric acid(UA),glomerular filtration rate(GFR) of each women were tested and compared.The PE group was subdivided into two groups with or without renal impairment(GFR90ml/min.1.73 m2,n=57 vs GFR≥90 ml/min/1.73.m2,n= 227).The hemodynamic parameters,namely,heart rate(HR),cardiac index(CI),cardiac output(CO),stroke index(SI),peripheral vascular resistance index(VI) were compared between the two subgroups.Results:The incidence of BUN,UA and GFR abnormality in the PE group were significantly higher than those in the other two groups(P〈0.01);The Scr,BUN and UA level in PE group were significantly higher than those in the other two groups(P〈0.01),while the GFR was markedly dropped(P〈0.01);SVRI and SVR in the renal-impairment PE group were remarkably higher than those in the other group(P〈0.01),while maternal SI,SV,CI and CO walues in the renal-impairment PE group were significantly lower than those in the other group(P〈0.01).Conclusion:Preeclampsia could lead to renal impairment,which is mainly caused by decreased cardiac output and increased peripheral vascular resistance.
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