Early monitoring of acute tubular necrosis in the rat kidney by 23Na-MRI

Atthe BK, Babsky AM, Hopewell PN, Phillips CL, Molitoris BA, Bansal N. Early monitoring of acute tubular necrosis in the rat kidney by Na-23-MRI. Am J Physiol Renal Physiol 297: F1288-F1298, 2009. First published September 2, 2009; doi: 10.1152/ajprenal.00388.2009.-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, Na-23 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. Na-23 images were collected every 10 min during baseline, ischemia, and 60-min reperfusion periods. T-1 and T-2 relaxation times were measured by both Na-23-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 Na-23-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 Na-23-MRI data. Na-23-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.