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Urinary markers of intrarenal renin-angiotensin system activity in vivo

机译:体内肾内肾素-血管紧张素系统活性的尿液标志物

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摘要

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.
机译:最近的兴趣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。在断定这些成分是独立的标记之前,我们需要排除它们在尿液中的存在,如白蛋白(一种相当大小的蛋白质),是由于(干扰)肾小球滤过引起的。这篇评论主要讨论了它们的过滤,重吸收和局部释放。考虑到人体研究中尿血管紧张素原与白蛋白之间的密切相关性,得出的结论是,在人体中,尿血管紧张素原是一种过滤屏障损伤标志物,具有与尿白蛋白相同的预测能力。相反,在动物中,可能会发生肾小管血管紧张素原释放,尽管肾小管特异性基因敲除研究不支持这种血管紧张素原的功能性作用。相对于白蛋白,尿中肾素水平高200倍以上,与白蛋白无关。这可能反映了肾素从泌尿道的释放,但也可能归因于已过滤的血浆来源的肾素原的激活和/或不完全的肾小管重吸收。

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