Conclusion:  This registry analysis suggests that IL-2Ra induction may be associated with

a reduction HIF inhibitor in rejection risk in cyclosporine-treated intermediate immunological risk recipients, but not in low-risk renal transplant recipients. Renal allograft outcomes have been improving over the last 10 years, perhaps related to improved immunosuppression and reduced acute rejection rates.1 Acute rejection, an important determinant of graft survival, occurs commonly in the early post-transplant period, but the incidence has decreased significantly over recent years.2 Antibodies designed to inactivate interleukin-2 receptor antibody (IL-2Ra) on T cells such as basiliximab are often used as induction therapy in immunosuppressive protocols to reduce the risk of acute rejection or to delay the introduction of calcineurin inhibitor (CNI) in those at high risk of delayed graft function.3,4 The effectiveness of IL-2Ra in reducing the risk of acute rejection is well established in deceased- and live-donor kidney transplantation.5,6 Unlike T-cell depletive therapies, IL-2Ra

is not associated with increased infection- or cancer-related morbidity and mortality.7–9 The use of IL-2Ra has been steadily increasing in Australia such that IL-2Ra induction therapy was used for >50% of new renal transplant recipients in Australia by 2005.10,11 Although the efficacy of IL-2Ra in reducing the risk of rejection is well established in renal transplant recipients, the effectiveness of this agent in renal transplant Hydroxychloroquine manufacturer recipients with differing immunological risk remains unclear.10,12,13 The aim of the present

study is to evaluate the efficacy of IL-2Ra induction on allograft outcomes including acute rejection, glomerular filtration rate (GFR), graft and patient Immune system survival in renal transplant recipients of low and intermediate immunological risk, and when stratified by initial immunosuppression. Using the Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry, all live- and deceased-donor renal transplant recipients in Australia from 1995 to 2005 were included in this study. Follow up was censored at 31 December 2006. Recipients were arbitrarily divided into low immunological risk (primary grafts with ≤2 human leucocyte antigen (HLA)-mismatches and panel-reactive antibody (PRA) < 10%) or intermediate immunological risk recipients (i.e. subsequent grafts or >2 HLA-mismatches or PRA > 25%). Multiple-organ graft recipients, recipients’ age less than 16 at time of transplant and recipients initiated on corticosteroids or CNI-free immunosuppressive regimens were excluded from the study. In addition, recipients who had received induction monoclonal or polyclonal T-cell depletive agents were also excluded.