Effect of salt load on the intrarenal angiotensin activity and receptor-mediated prorenin system in kidney fibrosis

虽然肾内肾素血管紧张素系统(RAS)的激活参与了肾纤维化的进展，但盐负荷抑制循环RAS是如何加重肾脏纤维化的尚不清楚。本研究表明，高盐摄入增加了集合管和连接小管肾素受体顶端膜性转变，导致前肾素和肾素蛋白结合增加，而不伴随肾素mRNA的表达，继而非蛋白水解性激活前肾素和血管紧张素II生成，导致高盐摄入慢性抗胸腺细胞浆液性肾炎肾纤维化加重。

Although activation of intrarenal renin angiotensin system (RAS) is involved in the progression of kidney fibrosis, it is unknown how salt load that suppresses circulating RAS aggravates kidney fibrosis. This study demonstrated that high salt intake increased the apical membranous transition of (pro)renin receptor in collecting ducts and connecting tubules, resulting in the increased binding of prorenin and renin proteins without concomitant renin mRNA expression, followed by non-proteolytic activation of prorenin and angiotensin II generation, with resultant worsening of renal fibrosis in chronic anti-thymocyte serum nephritis on high salt intake.