**8. Summary**

The significant improvement in the short-term graft survival has not transformed into a much better long-term graft survival. CAN is an important cause of graft loss and it represents a complex process culminating immunological and non-immunological injuries. The occurrences of overt acute rejections, either cellular, humoral or both, in the early stage driven by allo-immunity can have an important bearing on the long term immunological milieu that prevails and hence influences the graft survival. Sub-clinical rejection and/ or chronic rejection from inadequate immunosuppression are frequently undiagnosed and untreated. Persistent DSA or de novo development of DSA after kidney transplant is increasingly recognized as an independent and detrimental factor for transplant glomerulopathy. Other than allo-reactivity, there are emerging data suggesting that the preexisting or de novo developing autoimmunity, mediated by either auto-antibodies and/or autoreactive T cells, may also cause post-transplant allograft injury (Dinavahi et al., 2011; Porcheray et al., 2010; Vendrame et al.,2010). Therefore, to appropriately identify and address the actual disease process, knowledge of the ongoing pathogenesis is needed in order to improve the long-term graft survival. From allo-immunological standpoint, it may include optimizing HLA match, avoiding sensitization, timely detecting and treating AR episodes, and maintaining adequate levels of immunosuppression to prevent the development of DSA, sub clinical rejection and chronic rejection of allografts.
