1. ¹Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel
2. ²Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
3. ³Department of Internal Medicine, Hadassah Hospital, Mt Scopus and Hebrew University Medical School, Jerusalem, Israel

Correspondence: H Degani, Department of Biological Regulation, Weizmann Institute of Science, Rehovot 76100, Israel. E-mail: hadassa.degani@weizmann.ac.il

Received 12 July 2005; Revised 13 September 2005; Accepted 5 October 2005; Published online 18 January 2006.

Abstract

The clinical detection of evolving acute tubular necrosis (ATN) and differentiating it from other causes of renal failure are currently limited. The maintenance of the corticomedullary sodium gradient, an indicator of normal kidney function, is presumably lost early in the course of ATN. Herein, sodium magnetic resonance imaging (²³Na MRI) was applied to study the early alteration in renal sodium distribution in rat kidneys 6 h after the induction of ATN. Three-dimensional gradient echo sodium images were recorded at 4.7 T with high spatial resolution. ATN was produced by the administration of radiologic contrast medium, combined with inhibition of nitric oxide and prostaglandin synthesis. The sodium images revealed that the sham-controlled kidney exhibited a linear increase in sodium concentration along the corticomedullary axis of 302 mmol/l/mm, resulting in an inner medulla to cortex sodium ratio of 4.30.3 (n=5). In the ATN kidney, however, the cortico-outer medullary sodium gradient was reduced by 21% (P<0.01, n=7) and the inner medulla to cortex sodium ratio was decreased by 40% (P<0.001, n=7). Small, though significant, increments in plasma creatinine at this time inversely correlated with the decline in the corticomedullary sodium gradient. Histological findings demonstrated outer medullary ATN involving 4% of medullary thick ascending limbs. Hence, ²³Na MRI non-invasively quantified changes in the corticomedullary sodium gradient in the ATN kidney when morphologic tubular injury was still focal and very limited. MRI detection of corticomedullary sodium gradient abnormalities may serve to identify evolving ATN at its early phases.