de Vries B et al. (2006) Redox-active iron released during machine perfusion predicts viability of ischemically injured deceased donor kidneys. Am J Transplant 6: 2686–2693

A shortage of organs for transplantation has increased interest in the use of kidneys from non-heart-beating (NHB) donors; however, up to one-fifth of these grafts fail in the immediate post-transplantation period as a result of warm ischemic damage incurred before or during harvest and preservation. Redox-active iron (RAI), which catalyzes the generation of highly reactive oxygen species, contributes to renal ischemia–reperfusion injury in mice. Now, de Vries et al. report that ischemically injured NHB donor kidneys release RAI to the perfusion fluid during preservation. Further, pretransplantation RAI concentration reflects graft viability, a finding that—if validated in other centers—could optimize selection of marginal kidneys for transplantation.

The authors analyzed RAI concentration in perfusate samples collected from 231 deceased donor kidneys (205 from NHB and 26 from heart-beating brain-dead donors) during hypothermic machine pulsatile perfusion. Significantly more RAI was released into perfusate by ischemically injured NHB donor kidneys than by heart-beating donor kidneys not subject to warm ischemia (3.9 ± 1.1 vs 2.8 ± 1.0 µmol/l; P = 0.001). The increase in RAI occurred during the first hour of perfusion; therefore, warm ischemia, rather than cold ischemia during hypothermic machine perfusion, seems to be the underlying cause.

RAI concentration independently predicted post-transplantation graft function, with a 1 µmol/l increase raising the odds of primary nonfunction nearly 1.7-fold (P = 0.01). The addition of RAI concentration to prognostic models based on other donor and graft characteristics enabled graft function to be predicted with greater sensitivity and specificity, particularly in uncontrolled NHB category 2 donors.