GRAFT ISCHEMIA CORRELATES WITH URINARY-EXCRETION OF THE PROXIMAL MARKER ENZYME FRUCTOSE-1,6-BISPHOSPHATASE IN HUMAN KIDNEY-TRANSPLANTATION

This study was undertaken to test the hypothesis that ischemia prior t o transplantation causes tubular damage without clinical evidence of g raft dysfunction. The urinary excretion of fructose-1,6-bisphosphatase (EC 3.1.3.11, FBPase), a cytosolic enzyme located exclusively in the proximal tubules, and the lysosomal enzyme N-acetyl-beta-D-glucosamini dase (EC 3.2.1.30) were measured daily between postoperative days I an d 4 in 25 renal cadaveric graft recipients who enjoyed an entirely unc omplicated first postoperative month. During the first 4 posttransplan t days urinary FBPase excretion was 0.9 +/- 0.5 U/g (0.1 +/- 0.06 U/mm ol) urinary creatinine [+/- SD; range 0.2-2.1 U/g(0.02-0.24 U/mmol)]. Cold ischemia time was 20.6 +/- 8.4 h (median 22 h, range: 3-32 h). Mu ltiple regression revealed a significant correlation between cold isch emia time and posttransplant urinary FBPase excretion (multiple R = 0. 65, p < 0.001). There were no confounding effects of recipient's age a nd gender, number of previous transplants, cyclosporin A levels, warm ischemia time, anastomosis time, donor age and gender. Urinary FBPase excretion was significantly lower in grafts stored for a shorter time than the median cold ischemia time of 22 hours (0.69 +/- 0.42 U/g, n = 13) as compared to those stored for a longer period of time (1.13 +/- 0.56 U/g; n = 12; p = 0.035). These results indicate that graft injur ies occur even in the absence of graft dysfunction and that the durati on of cold ischemia itself correlates with a degree of tubular cell da mage as defined by urinary FBPase excretion.