Background. A pathophysiologic feature possibly involved in ischemic injury
in transplant kidneys is mitochondrial dysfunction caused by disintegratio
n of oxidative metabolic pathways. Because the ability to synthesize ATP by
respiratory activity determines the organ's capacity to recover from ische
mic injury, an assessment of respiratory activity may provide information r
elated to graft viability.
Methods. NADH fluorimetry can be used to monitor kidney cortex metabolism n
oninvasively. During perfusion with (an)-aerobic perfusate, NADH fluorescen
ce images were recorded. We evaluated the NADH oxidation kinetics of 20 rat
kidneys, which were divided over four experimental groups. For six minimal
ly damaged kidneys and six kidneys that had been stored for one hour at 37
degrees C, perfusion was followed by transplantation. We related the kineti
c parameters of these kidneys with their post-transplantation function and
histology. The transplant function was monitored by serum creatinine and ur
ea levels.
Results. Storage of transplant kidneys for one hour at 37 degrees C signifi
cantly reduced the post-transplantation function. Isolated perfusion of gra
fts, however, was not detrimental for renal function. The rate of NADH oxid
ation decreased with decreasing graft quality, and a good correlation betwe
en NADH oxidation kinetics and post-transplantation function was found.
Conclusions. A reduction of NADH oxidation rates as a consequence of warm i
schemia supports the view that mitochondrial respiratory activity is impair
ed by ischemic injury. The correlation between NADH oxidation kinetics in p
erfused grafts and their post-transplantation function indicates that NADH
fluorimetry may be useful in predicting the viability of preserved grafts p
rior to transplantation.