Atthe Bharath K, Babsky Andriy M, Hopewell Paige N, Phillips Carrie L, Molitoris Bruce A, Bansal Navin
Department of Radiology, Indiana University-Purdue University at Indianapolis, Indianapolis, Indiana 46202-5181, USA.
Am J Physiol Renal Physiol. 2009 Nov;297(5):F1288-98. doi: 10.1152/ajprenal.00388.2009. Epub 2009 Sep 2.
Reabsorption of water and other molecules is dependent on the corticomedullary sodium concentration gradient in the kidney. During the early course of acute tubular necrosis (ATN), this gradient is altered. Therefore, 23Na magnetic resonance imaging (MRI) was used to study the alterations in renal sodium distribution in the rat kidney during ischemia and reperfusion (IR) injury, which induces ATN. In-magnet ischemia was induced for 0 (control), 10, 20, 30 or 50 min in Wistar rats. 23Na images were collected every 10 min during baseline, ischemia, and 60-min reperfusion periods. T1 and T2 relaxation times were measured by both 23Na-MRI and -MRS on a separate cohort of animals during ischemia and reperfusion for correction of relaxation-related tissue sodium concentration (TSC). A marked decrease was observed in the medulla and cortex 23Na-MRI signal intensity (SI) during the early evolution of ATN caused by IR injury, with the sodium reabsorption function of the kidney being irreversibly damaged after 50 min of ischemia. Sodium relaxation time characteristics were similar in the medulla and cortex of normal kidney, but significantly decreased with IR. The changes in relaxation times in both compartments were identical; thus the medulla-to-cortex sodium SI ratio represents the TSC ratio of both compartments. The extent of IR damage observed with histological examination correlated with the 23Na-MRI data. 23Na-MRI has great potential for noninvasive, clinical diagnosis of evolving ATN in the setup of acute renal failure and in differentiating ATN from other causes of renal failure where tubular function is maintained.
水和其他分子的重吸收取决于肾脏中的皮质髓质钠浓度梯度。在急性肾小管坏死（ATN）的早期过程中，这种梯度会发生改变。因此，利用23Na磁共振成像（MRI）来研究大鼠肾脏在缺血再灌注（IR）损伤（可诱发ATN）过程中肾钠分布的变化。对Wistar大鼠进行0（对照）、10、20、30或50分钟的磁内缺血诱导。在基线、缺血和60分钟再灌注期间，每10分钟采集一次23Na图像。在另一组动物的缺血和再灌注期间，通过23Na-MRI和-MRS测量T1和T2弛豫时间，以校正与弛豫相关的组织钠浓度（TSC）。在由IR损伤引起的ATN早期演变过程中，观察到髓质和皮质的23Na-MRI信号强度（SI）显著降低，缺血50分钟后肾脏的钠重吸收功能受到不可逆损害。正常肾脏的髓质和皮质钠弛豫时间特征相似，但IR后显著降低。两个区域的弛豫时间变化相同；因此，髓质与皮质钠SI比值代表两个区域的TSC比值。组织学检查观察到的IR损伤程度与23Na-MRI数据相关。23Na-MRI在急性肾衰竭情况下对正在发展的ATN进行无创临床诊断以及将ATN与肾小管功能保持正常的其他肾衰竭原因进行鉴别方面具有巨大潜力。
