Andreas Pohlmann1, Jan Hentschel1, Mandy Fechner2, Uwe Hoff2, Gordana Bubalo2, Karen Arakelyan1, 3, Kathleen Cantow3, Erdmann Seeliger3, Bert Flemming3, Lajos Marko4, Helmar Waiczies1, 5, Sonia Waiczies1, 5, Wolf Hagen Schunck4, Dominik N. Mueller4, 6, Duska Dragun2, Thoralf Niendorf1, 5
1Berlin Ultrahigh Field Facility (B.U.F.F.), Max-Delbrueck Center for Molecular Medicine, Berlin, Germany; 2Nephrology and Intensive Care Medicine, Center for Cardiovascular Research, Charit, Berlin, Germany; 3Institute of Physiology, Center for Cardiovascular Research, Charit, Berlin, Germany; 4Max Delbrck Center for Molecular Medicine, Berlin, Germany; 5Experimental and Clinical Research Center, a cooperation between the Charit Medical Faculty and the Max Delbrck Center for Molecular Medicine, Berlin, Germany; 6Nikolaus-Fiebiger-Center, Friedrich-Alexander-University, Erlangen-Nrnberg, Germany
Acute kidney injury (AKI) is commonly caused by renal hypoperfusion. This ischemia/reperfusion (I/R) injury is characterized by a mismatch of local tissue oxygen supply and demand. There is an unmet need to better understand the mechanisms of the initial phase of I/R injury in AKI. Mapping of T2*/T2, known to be sensitive to blood oxygenation, might elucidate spatio-temporal pathophysiological changes in the kidney. We demonstrate for the first time the feasibility of continuous, high temporal resolution parametric MRI monitoring of renal I/R in rats. Observations in the early reperfusion phase promise to offer new insights into the pathogenesis of AKI.