Ohashi Naro, Isobe Shinsuke, Matsuyama Takashi, Ishigaki Sayaka, Suzuki Takahisa, Tsuji Takayuki, Otsuka Atsushi, Kato Akihiko, Miyake Hideaki, Yasuda Hideo
Internal Medicine 1, Hamamatsu University School of Medicine, Japan.
Urology, Hamamatsu University School of Medicine, Japan.
Intern Med. 2019 Mar 1;58(5):643-648. doi: 10.2169/internalmedicine.1756-18. Epub 2018 Oct 17.
Objective The intrarenal renin-angiotensin system (RAS) is activated in clinical settings, such as chronic kidney disease (CKD), as well as in CKD animal models, and kidney transplant donors have a greater risk of end-stage renal disease than healthy controls. However, whether or not the intrarenal RAS is activated immediately after kidney donation in kidney transplant donors is unclear, and the mechanism underlying intrarenal RAS activation is unknown. Methods We investigated 10 kidney transplant donors (4 men and 6 women, 58.6±9.0 years of age). Their blood pressure (BP), estimated glomerular filtration rate (eGFR), plasma angiotensinogen (AGT) and plasma angiotensin II (AngII) levels (which reflect circulating RAS activation), urinary albumin excretion, and urinary AGT excretion (which reflects intrarenal RAS activation) were evaluated before kidney donation (-1.2±0.40 days) and after kidney donation (7.5±1.7 days). Results The renal function after kidney donation was significantly lower than before donation. There were no significant differences in the BP during 24-h ambulatory BP monitoring, plasma AngII levels, or urinary albumin excretion after kidney donation. In contrast, the levels of plasma AGT and urinary AGT excretion were significantly increased after kidney donation. The urinary AGT excretion after kidney donation did not show a significant relationship with the systolic BP, plasma AGT, plasma AngII, or urinary albumin excretion. In addition, the percentage change in urinary AGT excretion after kidney donation was not associated with the percentage change in other clinical parameters. Conclusion The intrarenal RAS is activated in kidney transplant donors immediately after kidney donation, independent of the systemic BP and filtration of increased plasma AGT, due to augmented inflammation.
目的 肾内肾素-血管紧张素系统(RAS)在慢性肾脏病(CKD)等临床环境以及CKD动物模型中被激活,肾移植供体发生终末期肾病的风险高于健康对照。然而,肾移植供体在肾脏捐献后肾内RAS是否立即被激活尚不清楚,且肾内RAS激活的潜在机制也不明确。方法 我们研究了10名肾移植供体(4名男性和6名女性,年龄58.6±9.0岁)。在肾脏捐献前(-1.2±0.40天)和肾脏捐献后(7.5±1.7天)评估他们的血压(BP)、估计肾小球滤过率(eGFR)、血浆血管紧张素原(AGT)和血浆血管紧张素II(AngII)水平(反映循环RAS激活)、尿白蛋白排泄以及尿AGT排泄(反映肾内RAS激活)。结果 肾脏捐献后的肾功能显著低于捐献前。肾脏捐献后24小时动态血压监测中的BP、血浆AngII水平或尿白蛋白排泄无显著差异。相比之下,肾脏捐献后血浆AGT水平和尿AGT排泄显著增加。肾脏捐献后的尿AGT排泄与收缩压、血浆AGT、血浆AngII或尿白蛋白排泄无显著关系。此外,肾脏捐献后尿AGT排泄的百分比变化与其他临床参数的百分比变化无关。结论 肾移植供体在肾脏捐献后肾内RAS立即被激活,这与全身BP和血浆AGT增加的滤过无关,而是由于炎症增强所致。