Early monitoring of acute tubular necrosis in the rat kidney by²³Na-MRI

Abstract

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.

Dual energy CT monitoring of the renal corticomedullary sodium gradient in swine

“…In our study, we showed that material decomposition for DECT can potentially be applied as a long sought noninvasive means to evaluate dynamic changes in the renal corticomedullary sodium gradient. Of note, the baseline medulla-to-cortex sodium ratios of the swine kidneys in our study were in agreement with previous report of sodium gradient in the rat kidneys using sodium MR imaging (19). …”

Low birth weight increases susceptibility to renal injury in a rat model of mild ischemia-reperfusion

“…Renal parameters were altered only in LBW rats exposed to mild bilateral renal ischemia marked by elevations in RVR and reductions in eRPF, RBF, and GFR. Acute tubular damage has been previously observed by others in a model of early monitoring of tubular necrosis in the rat, utilizing Na 23 magnetic resonance imaging after just 1 h of renal reperfusion period (6). In this study utilizing the mild I/R protocol, renal structural changes were observed in kidneys of LBW rats exposed to the mild I/R protocol and harvested at the end of the 2-h reperfusion period.…”

Delayed Administration of Pyroglutamate Helix B Surface Peptide (pHBSP), a Novel Nonerythropoietic Analog of Erythropoietin, Attenuates Acute Kidney Injury

“…Therefore, fractional excretion of sodium together with glomerular filtration rate is used to monitor tubular as well as glomerular function. Deterioration in both these markers is indicative of AKI and has been shown to change during the evolution of AKI (4). During the recovery phase of AKI, viable nephrons undergo hyperfiltration and hypertrophy that is linked to the synthesis of cytokines and growth factors to cause a systemic inflammatory response syndrome and extracellular matrix accumulation due to the induction of transforming growth factor-β (a key fibrogenic cytokine).…”