MR Research Centre, Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Magn Reson Med. 2018 Aug;80(2):696-702. doi: 10.1002/mrm.27050. Epub 2017 Dec 28.
To investigate the correlation between renal ischemia and C-urea T relaxation rate in an acute kidney injury (AKI) rat model.
Six rats subjected to unilateral renal ischemia were investigated. Creatinine clearance, urine output, plasma creatinine as well as blood-urea nitrogen (BUN) values were acquired before and after the procedure. H T2* mapping was acquired using blood oxygenation level dependent (BOLD) MRI and hyperpolarized C-urea T mapping was acquired using a 2D golden-angle radial approach. Kidney perfusion was estimated using noncontrast flow alternating inversion recovery arterial spin labeling.
All rats showed clinical signs of AKI with increased plasma creatinine and increased BUN. Whole kidney C-urea T significantly decreased 26% (P = 0.001) 24 h after reperfusion. A significantly different (3.7 times steeper; P = 0.008) osmolality gradient was observed in the contralateral kidney (P = 0.008; R = 0.86) compared with the postischemic kidney (P = 0.0004, R =0.97). Whole kidney T2* signal (P = 0.14) and T2* gradient (P = 0.26) was similar between the two kidneys. Oxygen availability dependency on C-urea T was investigated by means of the correlation between the BOLD and T signals; a statistically significant difference (P = 0.03) was found in the contralateral kidney (P = 0.0001; R = 0.95), but not in the postischemic kidney (P = 0.31; R = 0.25).
We demonstrate that hyperpolarized [ C, N ]urea T relaxation correlates with renal oxygen tension ( T2*) in the healthy contralateral kidney, but not in the postischemic kidney. The whole kidney T relaxation difference between the postischemic and contralateral kidney may originate from altered blood volume in the postischemic kidney. Magn Reson Med 80:696-702, 2018. © 2017 International Society for Magnetic Resonance in Medicine.
在急性肾损伤(AKI)大鼠模型中,研究肾缺血与 C-尿素 T 弛豫率的相关性。
对 6 只单侧肾缺血大鼠进行了研究。在手术前后获得了肌酐清除率、尿量、血浆肌酐和血尿素氮(BUN)值。采用血氧水平依赖(BOLD)MRI 获得 H T2*映射,采用二维黄金角径向方法获得高极化 C-尿素 T 映射。采用非对比性血流反转恢复动脉自旋标记法估计肾灌注。
所有大鼠均出现 AKI 的临床症状,表现为血浆肌酐升高和 BUN 升高。再灌注后 24 小时,全肾 C-尿素 T 显著降低 26%(P=0.001)。与缺血后肾脏相比,对侧肾脏的渗透压梯度明显不同(3.7 倍陡峭;P=0.008;R=0.86)(P=0.008;R=0.97)。双侧肾脏的全肾 T2信号(P=0.14)和 T2梯度(P=0.26)相似。通过 BOLD 和 T 信号之间的相关性研究 C-尿素 T 的氧可用性依赖性,在对侧肾脏发现统计学上的显著差异(P=0.03)(P=0.0001;R=0.95),但在缺血后肾脏无显著差异(P=0.31;R=0.25)。
我们证明高极化[C,N]尿素 T 弛豫与健康对侧肾脏中的肾氧张力(T2*)相关,但与缺血后肾脏无关。缺血后和对侧肾脏之间的全肾 T 弛豫差异可能源于缺血后肾脏的血容量改变。磁共振医学 80:696-702,2018。©2017 国际磁共振学会。