Division of Pharmacology and Vascular Medicine, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands.
J Hypertens. 2011 Nov;29(11):2147-55. doi: 10.1097/HJH.0b013e32834bbcbf.
To study which renin-angiotensin-aldosterone system (RAAS) component best reflects renal RAAS activity.
We measured urinary and plasma renin, prorenin, angiotensinogen, aldosterone, albumin and creatinine in 101 diabetic and nondiabetic patients with or without hypertension. Plasma prorenin was elevated in diabetic patients. Urinary prorenin was undetectable. Urinary albumin and renin were higher in diabetic patients. Men had higher plasma renin/prorenin levels, and lower plasma angiotensinogen levels than women. Plasma creatinine and albumin were also higher in men. Urinary RAAS components showed no sexual dimorphism, whereas urinary creatinine and albumin were higher in men. Angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor blockers increased plasma renin and decreased plasma angiotensinogen, without altering plasma aldosterone. In contrast, in urine, these drugs decreased renin and aldosterone without affecting angiotensinogen. When analyzing all patients together, urinary angiotensinogen excretion closely mimicked that of albumin, whereas urinary angiotensinogen and albumin levels both were 0.05% or less of their concomitant plasma levels. This may reflect the identical glomerular filtration and tubular handling of both proteins, which have a comparable molecular weight. In contrast, urinary renin excretion did not correlate with urinary albumin excretion, and the urinary/plasma concentration ratio of renin was more than 200 times the ratio of albumin, despite its comparable molecular weight. Urinary aldosterone excretion closely followed urinary creatinine excretion.
The increased urinary renin levels in diabetes and the decreased urinary renin levels following RAAS blockade, occurring independently of changes in plasma renin, reflect the activated renal RAAS in diabetes and the success of RAAS blockade in the kidney, respectively. Urinary renin, therefore, more closely reflects renal RAAS activity than urinary angiotensinogen or aldosterone.
研究肾素-血管紧张素-醛固酮系统（RAAS）的哪个成分能最好地反映肾脏 RAAS 的活性。
我们测量了 101 例糖尿病和非糖尿病患者（伴或不伴高血压）的尿和血浆肾素、原肾素、血管紧张素原、醛固酮、白蛋白和肌酐。糖尿病患者的血浆原肾素升高。尿原肾素无法检测到。糖尿病患者的尿肾素和白蛋白较高。男性的血浆肾素/原肾素水平高于女性，而血浆血管紧张素原水平低于女性。男性的血浆肌酐和白蛋白也较高。尿 RAAS 成分没有性别二态性，而男性的尿肌酐和白蛋白较高。血管紧张素转换酶抑制剂和血管紧张素 II 型 1 型受体阻滞剂增加了血浆肾素，降低了血浆血管紧张素原，而不改变血浆醛固酮。相反，在尿液中，这些药物降低了肾素和醛固酮，而不影响血管紧张素原。当将所有患者一起分析时，尿血管紧张素原排泄与白蛋白排泄非常相似，而尿血管紧张素原和白蛋白水平均为其相应血浆水平的 0.05%或更低。这可能反映了这两种蛋白相同的肾小球滤过和肾小管处理，它们具有相似的分子量。相比之下，尿肾素排泄与尿白蛋白排泄不相关，尽管肾素的分子量与之相当，但尿肾素/血浆浓度比值大于白蛋白的 200 倍。尿醛固酮排泄紧随尿肌酐排泄。
糖尿病患者尿肾素水平升高，以及 RAAS 阻断后尿肾素水平降低，这与血浆肾素的变化无关，分别反映了糖尿病时肾脏 RAAS 的激活和 RAAS 在肾脏中的阻断成功。因此，尿肾素比尿血管紧张素原或醛固酮更能反映肾脏 RAAS 的活性。
