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首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Central pulse pressure and aortic stiffness determine renal hemodynamics: pathophysiological implication for microalbuminuria in hypertension.
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Central pulse pressure and aortic stiffness determine renal hemodynamics: pathophysiological implication for microalbuminuria in hypertension.

机译:中央脉压和主动脉僵硬程度决定了肾脏的血液动力学:高血压中微量白蛋白尿的病理生理意义。

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A significant link has been reported between aortic stiffening and renal microvascular damage, but the underlying mechanism remains poorly understood. We hypothesized that alterations in central and renal hemodynamics are responsible for this link. In 133 patients with hypertension, pressure waveforms were recorded on the radial, carotid, femoral, and dorsalis pedis arteries with applanation tonometry to estimate the aortic pressures and aortic (carotid-femoral) and peripheral (carotid-radial and femoral-dorsalis pedis) pulse wave velocities. Flow-velocity waveforms were recorded on the renal segmental arteries with duplex ultrasound to calculate the resistive index (RI) as [1 - (end-diastolic velocity/peak systolic velocity)] and on the femoral arteries to calculate the reverse/forward flow index and diastolic/systolic forward-flow ratio. Albuminuria was defined as urinary albumin/creatinine ratio >/=30 mg/g of creatinine. The renal RI (mean: 0.65+/-0.07) was strongly correlated (P<0.001) with the aortic pulse pressure (r=0.62), incident pressure wave (r=0.55), augmented pressure (r=0.49), and aortic pulse wave velocity (r=0.51), although not with the mean arterial pressure or peripheral pulse wave velocities. The correlations remained highly significant after consideration of confounders including age, cholesterol, hemoglobin A(1c), and glomerular filtration rate. The renal RI was inversely correlated with the femoral reverse and diastolic forward flow indices. Both aortic pulse pressure and renal RI correlated with the urinary albumin/creatinine ratio independent of confounders. Each 0.1 increase in renal RI was associated with a 5.4-fold increase in the adjusted relative risk of albuminuria. In conclusion, increased aortic pulse pressure causes renal microvascular damage through altered renal hemodynamics resulting from increased peripheral resistance and/or increased flow pulsation.
机译:据报道,主动脉硬化与肾脏微血管损害之间存在重要联系,但其潜在机制仍知之甚少。我们假设中枢和肾脏血流动力学的改变是造成这种联系的原因。在133例高血压患者中,采用压平眼压计记录pressure,颈,股和足背动脉的压力波形,以评估主动脉压力以及主动脉(颈-股动脉)和周围(颈-radi动脉和股-背-足)脉搏波速。用双工超声在肾节段动脉上记录流速波形,以将电阻指数(RI)计算为[1-(舒张末期速度/峰值收缩速度)],并在股动脉上计算出反向/正向流动指数和舒张/收缩前向流量比。蛋白尿定义为尿白蛋白/肌酐比率> / = 30 mg / g肌酐。肾RI(平均值:0.65 +/- 0.07)与主动脉搏动压力(r = 0.62),入射压力波(r = 0.55),增压压力(r = 0.49)和主动脉高度相关(P <0.001)脉搏波速度(r = 0.51),但不包括平均动脉压或周围脉搏波速度。在考虑年龄,胆固醇,血红蛋白A(1c)和肾小球滤过率等混杂因素后,相关性仍然非常重要。肾RI与股骨逆流和舒张前向流指数呈负相关。独立于混杂因素,主动脉脉压和肾RI均与尿白蛋白/肌酐比值相关。肾RI的每升高0.1倍,所调节的白蛋白尿相对危险度就升高5.4倍。总之,增加的主动脉搏动压力会由于周围阻力增加和/或血流搏动增加而导致肾血流动力学改变,从而引起肾脏微血管损害。

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