Relationship between urinary angiotensinogen and salt sensitivity of blood pressure in patients with IgA nephropathy.
Relationship between urinary angiotensinogen and salt sensitivity of blood pressure in patients with IgA nephropathy.
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DOI：
10.1161/hypertensionaha.110.166843
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发表时间：
2011-08
期刊：
影响因子：
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通讯作者：
Imanishi M
中科院分区：
文献类型：
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作者：
Konishi Y;Nishiyama A;Morikawa T;Kitabayashi C;Shibata M;Hamada M;Kishida M;Hitomi H;Kiyomoto H;Miyashita T;Mori N;Urushihara M;Kobori H;Imanishi M
我们先前已证明，随着肾损伤的进展，IgA肾病患者的血压变得对盐敏感。我们还表明，此类患者尿中血管紧张素原水平升高与肾组织血管紧张素原基因表达增强以及血管紧张素II水平密切相关。在此，我们研究了IgA肾病患者尿中血管紧张素原与血压盐敏感性之间的关系。41例IgA肾病患者随机先后食用普通盐饮食（氯化钠12 g/d）1周和低盐饮食（氯化钠5 g/d）1周。盐敏感性指数计算为通过连接每种饮食摄入期间获得的2个数据点所绘制的压力 - 尿钠排泄曲线斜率的倒数。食用普通盐饮食的患者尿中血管紧张素原与肌酐的比值显著高于食用低盐饮食的患者（分别为17.5μg/g[范围：7.3 - 35.6μg/g]对比7.9μg/g[范围：3.1 - 14.2μg/g]肌酐；P<0.001）。我们患者的钠敏感性指数与肾小球硬化评分呈正相关（r = 0.43；P = 0.008），与尿中血管紧张素原与肌酐比值的对数变化呈正相关（r = 0.37；P = 0.017），但与尿蛋白排泄变化无关（r = 0.18；P = 0.49）。相反，在梅尼埃病且肾功能正常的患者（n = 9）中，钠摄入量的变化并未改变尿中血管紧张素原与肌酐的比值。这些数据表明，盐诱导的肾内血管紧张素原不适当增加以及相关的肾损伤，促成了IgA肾病患者盐敏感性高血压的发展。
We demonstrated previously that the blood pressure of patients with IgA nephropathy becomes salt sensitive as renal damage progresses. We also showed that increased urinary angiotensinogen levels in such patients closely correlate with augmented renal tissue angiotensinogen gene expression and angiotensin II levels. Here, we investigated the relationship between urinary angiotensinogen and salt sensitivity of blood pressure in patients with IgA nephropathy. Forty-one patients with IgA nephropathy consumed an ordinary salt diet (12 g/d of NaCl) for 1 week and a low-salt diet (5 g/d of NaCl) for 1 week in random order. The salt-sensitivity index was calculated as the reciprocal of the slope of the pressure-natriuresis curve drawn by linking 2 data points obtained during consumption of each diet. The urinary angiotensinogen:creatinine ratio was significantly higher in patients who consumed the ordinary salt diet compared with the low-salt diet (17.5 μg/g [range: 7.3 to 35.6 μg/g] versus 7.9 μg/g [range: 3.1 to 14.2 μg/g] of creatinine, respectively; P<0.001). The sodium sensitivity index in our patients positively correlated with the glomerulosclerosis score (r=0.43; P=0.008) and changes in logarithmic urinary angiotensinogen:creatinine ratio (r=0.37; P=0.017) but not with changes in urinary protein excretion (r=0.18; P=0.49). In contrast, changes in sodium intake did not alter the urinary angiotensinogen:creatinine ratio in patients with Ménière disease and normal renal function (n=9). These data suggest that the inappropriate augmentation of intrarenal angiotensinogen induced by salt and associated renal damage contribute to the development of salt-sensitive hypertension in patients with IgA nephropathy.