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

• Published in: Acta Physiologica 2023-02, Vol.237 (2), p.e13868-n/a
• Main Authors: Cantow, Kathleen, Gladytz, Thomas, Millward, Jason M., Waiczies, Sonia, Niendorf, Thoralf, Seeliger, Erdmann
• Format: Article
• Language: English
• Subjects: acute kidney injury; Acute Kidney Injury - diagnostic imaging; Acute Kidney Injury - pathology; Animals; Aorta; BOLD‐MRI; Contrast media; Furosemide; Furosemide - pharmacology; Hemoglobin; Humans; Hypoxemia; Hypoxia; Kidney; kidney size; Kidneys; Magnetic resonance imaging; Magnetic Resonance Imaging - methods; Occlusion; Oxygen; Oxygenation; Pathophysiology; Physiology; Rats; renal oxygenation
• ISSN: 1748-1708; 1748-1716
• DOI: 10.1111/apha.13868

Aim Tissue hypoxia is an early key feature of acute kidney injury. Assessment of renal oxygenation using magnetic resonance imaging (MRI) markers T2 and T2* 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 T2* and T2 changes in acute pathophysiological scenarios. Methods KS was determined from T2*, T2 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 O2 saturation of hemoglobin from changes in T2* and KS. Results Upon aortic occlusion KS decreased; this correlated with a decrease in T2*, T2. Upon renal vein occlusion KS increased; this negatively correlated with a decrease in T2*, T2. Upon simultaneous occlusion of both vessels KS remained unchanged; there was no correlation with decreased T2*, T2. Hypoxemia induced mild reductions in KS and T2*, T2. Administration of an X‐ray contrast medium induced sustained KS increase, with an initial increase in T2*, T2 followed by a decrease. Furosemide caused T2*, T2 elevation and a minor increase in KS. Model calculations yielded physiologically plausible calibration ratios for T2*. Conclusion Monitoring KS allows physiological interpretation of acute renal oxygenation changes obtained by T2*, T2. KS monitoring should accompany MRI‐oximetry, for new insights into renal pathophysiology and swift translation into human studies.