Bharath Atthe, Presenter: Nothing to Disclose

Andriy Babsky PhD, Abstract Co-Author: Nothing to Disclose

Navin Bansal PhD, Abstract Co-Author: Nothing to Disclose

To apply 23Na MRI to examine the early alteration in renal sodium distribution in the rat kidney with acute tubular necrosis (ATN) caused by ischemia-reperfusion injury model.

All 23Na and 1H MRI experiments were performed on a Varian 9.4-Tesla, 31-cm horizontal bore system. In-magnet ischemia was induced for 0 (control), 10, 20, 30 or 50 minutes on Wistar rats (n=5 for each group) by a snare taut placed around the vascular pedicle of the left kidney. 23Na images were collected every 10 minute during baseline, ischemia and 60 min reperfusion periods. T2-weighted 1H images were obtained for drawing regions of interest (ROI) around the medulla and cortex. The relaxation time measurements (T1 and T2) were conducted on separate cohort of animals during 50 min ischemia and 60 min reperfusion (n=3 for each measurement).

There was a slight decrease in the medulla to cortex sodium gradient after 10 and 20 min of ischemia but the gradient recovered completely on reperfusion. The corticomeduallary sodium gradient decreased from 1.64 ± 0.03 to 1.406 ± 0.41 after 30 min of ischemia and from 1.58 ± 0.03 to 1.226 ± 0.07 after 50 min of ischemia. On 1 hr of reperfusion the ratio continued to decrease and plateaued at 1.34 ± 0.1 for 30 min ischemia group and 1.213 ± 0.05 for 50 min ischemia group. The steep decrease in the corticomeduallary sodium gradient during ischemia with no recovery after reperfusion, especially in the 50 min ischemia group, suggests irreversible tubular dysfunction of the kidney. 23Na relaxation times in the medulla and cortex did not differ significantly. The relaxation times slightly decreased in both the kidney regions after ischemia but recovered back on reperfusion. However, the changes in relaxation times did not alter the 23Na MRI SI dramatically.  

23Na MRI clearly demonstrated the loss of corticomeduallary sodium gradient during early evolving ATN caused by ischemia. The sodium reabsorption function of the kidney appears to be irreversibly damaged after 50 min of ischemia.  

23Na MRI has great potential in the 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.  

Atthe, B, Babsky, A, Bansal, N, Sodium Magnetic Resonance Imaging of Evolving Acute Tubular Necrosis Using Ischemia-Reperfusion Injury Model in a Rat.  Radiological Society of North America 2008 Scientific Assembly and Annual Meeting, February 18 - February 20, 2008 ,Chicago IL. http://archive.rsna.org/2008/6017045.html