Per Mose Nielsen1, Abubakr Eldirdiri2, Lotte Bonde Bertelsen1, Haiyun Qi1, Hans Stødkilde Jørgensen1, Jan Henrik Ardenkjaer-larsen2, and Christoffer Laustsen1
Renal I/R-I is a
leading cause of AKI in several disease states; there is a current lack of
precise methods to directly assess cortical tubular injury. In the present
study, we investigated the in situ conversion
of fumarate to malate in a unilateral Ischemia/reperfusion model, which is
correlated with renal tubular necrosis. We saw a strong binary [1,4-13C2]malate
signal in the I/R-I kidney and a strong binary [1,4-13C2]fumarate
signal in the healthy CL kidney. This was correlated with histological
examinations indication renal tubular necrosis. As well as compartmentalized
fumarase activity specific for I/R-I.
