Division of Pharmacology and Vascular Medicine, Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands.
Curr Hypertens Rep. 2013 Apr;15(2):81-8. doi: 10.1007/s11906-012-0326-z.
Recent interest focuses on urinary renin and angiotensinogen as markers of renal renin-angiotensin system activity. Before concluding that these components are independent markers, we need to exclude that their presence in urine, like that of albumin (a protein of comparable size), is due to (disturbed) glomerular filtration. This review critically discusses their filtration, reabsorption and local release. Given the close correlation between urinary angiotensinogen and albumin in human studies, it concludes that, in humans, urinary angiotensinogen is a filtration barrier damage marker with the same predictive power as urinary albumin. In contrast, in animals, tubular angiotensinogen release may occur, although tubulus-specific knockout studies do not support a functional role for such angiotensinogen. Urinary renin levels, relative to albumin, are >200-fold higher and unrelated to albumin. This may reflect release of renin from the urinary tract, but could also be attributed to activation of filtered, plasma-derived prorenin and/or incomplete tubular reabsorption.
最近的研究热点集中在尿肾素和血管紧张素原作为肾素-血管紧张素系统活性的标志物。在得出这些成分是独立的标志物的结论之前，我们需要排除它们在尿液中的存在（如白蛋白，一种大小相当的蛋白质）是由于（受损）肾小球滤过所致。这篇综述批判性地讨论了它们的滤过、重吸收和局部释放。鉴于人类研究中尿血管紧张素原与白蛋白之间的密切相关性，该综述得出结论，在人类中，尿血管紧张素原是滤过屏障损伤的标志物，其预测能力与尿白蛋白相同。相比之下，在动物中，可能会发生肾小管血管紧张素原的释放，尽管肾小管特异性敲除研究并不支持这种血管紧张素原的功能作用。与白蛋白相比，尿肾素水平相对较高，与白蛋白无关。这可能反映了肾素从泌尿道的释放，但也可能归因于滤过的、血浆衍生的前肾素的激活和/或不完全的肾小管重吸收。
