Role of intratubular pressure during the ischemic phase in acute kidney injury.
Role of intratubular pressure during the ischemic phase in acute kidney injury.
复制标题
DOI：
10.1152/ajprenal.00527.2016
复制
发表时间：
2017-06
期刊：
影响因子：
--
通讯作者：
Jin Wei;Jiang-ping Song;Shan Jiang;Gensheng Zhang;Donald Wheeler;Jie Zhang;Shaohui Wang;E. Lai;Lei Wang;J. Buggs;Ruisheng Liu
中科院分区：
文献类型：
--
作者：
Jin Wei;Jiang-ping Song;Shan Jiang;Gensheng Zhang;Donald Wheeler;Jie Zhang;Shaohui Wang;E. Lai;Lei Wang;J. Buggs;Ruisheng Liu
夹闭肾静脉或肾蒂引起的急性肾损伤（阿基）比夹闭肾动脉更严重，但其机制尚不清楚。在本研究中，我们验证了我们的假设，即缺血期近端肾小管压力（Pt）增加会加重肾损伤并促进阿基的发展。我们通过在37°C下分别夹住肾动脉、肾蒂或肾静脉18分钟来诱导阿基。用微穿刺法测量缺血期Pt。我们发现，较高的Pt与更严重的阿基相关。为了确定Pt在缺血阶段对阿基发展的作用，我们通过改变肾动脉压来调整Pt。我们通过双侧肾静脉阻断诱导阿基，并通过收缩主动脉和肠系膜动脉调节缺血期肾动脉压力来改变Pt。当我们将肾动脉压从85 ± 5降至65 ± 8 mmHg时，Pt从53.3 ± 2.7降至44.7 ± 2.0 mmHg。肾缺血后24 h血浆肌酐从2.48 ± 0.23降至1.91 ± 0.21 mg/dl。当我们将肾动脉压升高至103 ± 7 mmHg时，Pt升高至67.2 ± 5.1 mmHg。肾缺血后24 h血浆肌酐升高至3.17 ± 0.14mg·dl。KIM-1、NGAL和组织学的变化与血浆肌酐相似。总之，我们发现缺血期较高的Pt促进了阿基的发展，而较低的Pt保护肾损伤。Pt可能是治疗阿基的潜在靶点。
Acute kidney injury (AKI) induced by clamping of renal vein or pedicle is more severe than clamping of artery, but the mechanism has not been clarified. In the present study, we tested our hypothesis that increased proximal tubular pressure (Pt) during the ischemic phase exacerbates kidney injury and promotes the development of AKI. We induced AKI by bilateral clamping of renal arteries, pedicles, or veins for 18 min at 37°C, respectively. Pt during the ischemic phase was measured with micropuncture. We found that higher Pt was associated with more severe AKI. To determine the role of Pt during the ischemic phase on the development of AKI, we adjusted the Pt by altering renal artery pressure. We induced AKI by bilateral clamping of renal veins, and the Pt was changed by adjusting the renal artery pressure during the ischemic phase by constriction of aorta and mesenteric artery. When we decreased renal artery pressure from 85 ± 5 to 65 ± 8 mmHg, Pt decreased from 53.3 ± 2.7 to 44.7 ± 2.0 mmHg. Plasma creatinine decreased from 2.48 ± 0.23 to 1.91 ± 0.21 mg/dl at 24 h after renal ischemia. When we raised renal artery pressure to 103 ± 7 mmHg, Pt increased to 67.2 ± 5.1 mmHg. Plasma creatinine elevated to 3.17 ± 0.14 mg·dl·24 h after renal ischemia. Changes in KIM-1, NGAL, and histology were in the similar pattern as plasma creatinine. In summary, we found that higher Pt during the ischemic phase promoted the development of AKI, while lower Pt protected from kidney injury. Pt may be a potential target for treatment of AKI.