BioProject

In deceased donor kidney transplantation, acute kidney injury (AKI) prioir to surgery is a major determinant of delayed graft function (DGF), but AKI is histologically silent and difficult to assess. More...

In deceased donor kidney transplantation, acute kidney injury (AKI) prioir to surgery is a major determinant of delayed graft function (DGF), but AKI is histologically silent and difficult to assess. We hypothesized that a molecular measurement of AKI would add power to conventional risk assessments to predict the early poor allograft function at first week post transplantation. Overall design: We performed microarrays on implantation biopsies taken during reperfusion in 70 deceased donor kidneys from 53 donors. Early poor function was classified by two definitions on day 7 post-transplantation: serum creatinine greater than 265 umol/L (3 mg/dL) or the requirement for dialysis. Donor age and related risk scores (Irish, Schold, KDRI) associated with worse early function, as expected, but histologic features (glomerulosclerosis; pathology risk scores (Remuzzi, MAPI)) correlated with donor age but not with poor function. However, molecular AKI signal, previously defined in kidneys with early injury, was the best single predictor of poor allograft function. The combination of donor age and the AKI signal improved the prediction of poor function. In addition, asssessments of tissue quality particularly donor age, Banff ct, Irish and KDRI scores, showed negative correlative trend with late graft function, whereas the AKI signal did not. Thus donor age and the molecular AKI signal are the main predictors of early impaired function, but have little impact on survival. Less...