Monitoring kidney size to interpret <scp>MRI</scp>‐based assessment of renal oxygenation in acute pathophysiological scenarios

Abstract

Abstract Aim Tissue hypoxia is an early key feature of acute kidney injury. Assessment of renal oxygenation using magnetic resonance imaging (MRI) markers T 2 and T 2 * enables insights into renal pathophysiology. This assessment can be confounded by changes in the blood and tubular volume fractions, occurring upon pathological insults. These changes are mirrored by changes in kidney size (KS). Here, we used dynamic MRI to monitor KS for physiological interpretation of T 2 * and T 2 changes in acute pathophysiological scenarios. Methods KS was determined from T 2 *, T 2 mapping in rats. Six interventions that acutely alter renal tissue oxygenation were performed directly within the scanner, including interventions that change the blood and/or tubular volume. A biophysical model was used to estimate changes in O 2 saturation of hemoglobin from changes in T 2 * and KS. Results Upon aortic occlusion KS decreased; this correlated with a decrease in T 2 *, T 2 . Upon renal vein occlusion KS increased; this negatively correlated with a decrease in T 2 *, T 2 . Upon simultaneous occlusion of both vessels KS remained unchanged; there was no correlation with decreased T 2 *, T 2 . Hypoxemia induced mild reductions in KS and T 2 *, T 2 . Administration of an X‐ray contrast medium induced sustained KS increase, with an initial increase in T 2 *, T 2 followed by a decrease. Furosemide caused T 2 *, T 2 elevation and a minor increase in KS. Model calculations yielded physiologically plausible calibration ratios for T 2 *. Conclusion Monitoring KS allows physiological interpretation of acute renal oxygenation changes obtained by T 2 *, T 2 . KS monitoring should accompany MRI‐oximetry, for new insights into renal pathophysiology and swift translation into human studies.