Search

Several scores have been devised for providing a prognosis of outcomes after kidney transplantation. This study is a comprehensive test of these scores in a cohort of deceased donors with kidneys of lower-than-average quality and procurement biopsies. In total, 15 scores were tested on a retrospective cohort consisting of 221 donors, 223 procurement biopsies, and 223 recipient records for performance on delayed graft function, graft function, or death-censored graft loss. The best-performing score for DGF was the purely clinical Chapal score (AUC 0.709), followed by the Irish score (AUC 0.684); for graft function, the Nyberg score; and for transplant loss, the Snoeijs score (AUC 0.630) and the Leuven scores (AUCs 0.637 and 0.620). The only score with an acceptable performance was the Chapal score. Its disadvantage is that knowledge of the cold ischemia time is required, which is not known at allocation. None of the other scores performed acceptably. The scores fared better in discarded kidneys than in transplanted kidneys. Our study shows an unmet need for practical prognostic scores useful at the time of a decision about discarding or accepting deceased donor kidneys of lower-than-average quality in the Eurotransplant consortium. [ABSTRACT FROM AUTHOR]

Monoclonal anti-CD25-antibodies are successfully applied in organ transplantation to reduce the incidence of acute graft rejection. However, targeting the CD25 molecule might not only affect activated T-cells but also regulatory T-cells (Tregs) constitutively expressing the CD4+CD25+CD127lowFoxP3+ phenotype. In this study, we investigated the influence of the anti-CD25-antibody Basiliximab on the frequency of Tregs early after kidney transplantation comparing individuals receiving/not receiving induction therapy ( n = 14 and n = 7). Following Basiliximab administration, a distinct loss of CD4+CD25high T-cells was observed lasting for at least 6 weeks. This was not accompanied by a disappearance of the entire CD4+CD25+FoxP3+ Tregs but rather a decreased expression density of CD25 on the latter. In addition, a transient rise in CD4+CD25−FoxP3+ T-cells was found which expressed the CD127low phenotype. Thus, a phenotypic shift of Tregs from the CD25+ to the CD25− compartment was suggested. This was supported by in vitro findings showing that the disappearance of CD4+CD25high cells in the presence of Basiliximab was due to down-regulation of CD25 expression meanwhile the suppressive function of these cells was maintained. In conclusion, Basiliximab therapy directly affects CD4+CD25+CD127lowFoxP3+ Tregs but does not seem to be associated with functional consequences. Thus, it is unlikely that Basiliximab treatment negatively influences strategies involving Tregs to promote tolerance after organ transplantation. [ABSTRACT FROM AUTHOR]

Donors >60 years are now frequently accepted for living kidney transplantation (LKT). We asked whether a donor age >60 years may result in a higher risk for donor and recipient. All adult LKT from May 1996 to June 2005 were included. Long-term outcome was analysed, and results were compared for donors >60 and ≤60 years. Thirty-five grafts were obtained from donors >60 (group A) and 158 from donors ≤60 years (group B). In group A 40% and in group B 37% of grafts came from unrelated donors ( P = 0.769). The mean hospital stay of donors was 8 days in group A and 7 days in group B ( P = 0.171). The complication rate was 11% in group A and 17% in group B ( P = 0.409). Following LKT primary graft function was observed in 97% in group A and 96% in group B. One- and 5-year graft survival was 97% and 90% in group A and 99% and 91% in group B. For the first 2 years, mean serum creatinine was significantly higher in recipients of group A. Thereafter, values were comparable for both groups. As excellent results are achievable using living donors >60 years, we suggest that age should no longer be considered as a contra-indication for living donation. [ABSTRACT FROM AUTHOR]

After renal transplantation, different immunological and non-immunological factors lead to long-term allograft deterioration. Acute rejection episodes are one risk factor for chronic renal allograft dysfunction (CRAD). Following the current Banff classification the histological grade in acute rejection episodes is of limited prognostic value, therefore, additional morphological surrogate markers would be helpful. We investigated the biopsies of 91 patients with early acute rejection episodes for the immunohistochemical expression of key molecules (perforin, granzyme B, TIA-1, CD40) in the T cell-mediated rejection process. Staining results were correlated to long-term allograft outcome. Patients with greater than 2% of granzyme B or greater than 25% of CD40-positive cells in the interstitial infiltrate showed significantly shorter allograft survival. Patients with a CD40-positive vascular rejection or greater than 2% of granzyme B-positive cells in the interstitial infiltrate were significantly correlated with an earlier onset of CRAD. Our findings provide potential morphological surrogate markers in biopsies with early acute rejection episodes after renal transplantation. These could become part of combined clinical and histological algorithms, allowing patient-specific risk estimation and customized therapy options to be made. [ABSTRACT FROM AUTHOR]

A letter to the editor commenting on a case study related to difficulties that were encountered during kidney transplantation of a patient with severe adenine phosphoribosyl transferase deficiency, is presented.