Analysis of OPTN/UNOS registry suggests the number of HLA matches and not mismatches is a stronger independent predictor of kidney transplant survival

The impact of donor/recipient age difference and HLA mismatch on graft outcome in pediatric kidney transplantation

“…While the importance of HLA matching has been postulated to be less important in the current era of more powerful immunosuppression, it has emerged again more recently as a potentially important factor influencing long‐term graft survival . Poor HLA matching is associated with the development of DSA and can lead to chronic antibody‐mediated rejection, the main cause of long‐term graft loss .…”

“…While the importance of HLA matching has been postulated to be less important in the current era of more powerful immunosuppression, it has emerged again more recently as a potentially important factor influencing long-term graft survival. 26 30,31 In pediatric recipients, increasing number of HLA mismatches has also been shown to be associated with poorer graft outcomes, along with a negative impact on subsequent kidney transplants. 32,33 In keeping with these studies, we found that, for each HLA mismatch between the donor and the recipient, there is approximately 20% increased risk of long-term graft loss.…”

Donor SIRP-α polymorphisms: widening the innate-to-adaptive continuum in allograft rejection

“…The authors identified the transcription factor nuclear factor of activated T cells 5 (NFAT5) as a potential mediator of the epithelial cell response to the high sodium environment, as previously demonstrated in other tissues. 2,3 Expression of NFAT5 was increased in human renal medullary versus cortical tissue, and knockdown of NFAT5 or inhibition of kinases required for its activation in the tubular epithelial cell line attenuated chemokine production in response to NaCl. 1 To confirm that the differential localization of CD14þ mononuclear phagocytes is dependent on the medullary sodium gradient in vivo, the authors treated mice with tolvaptan or demeclocycline to induce diabetes insipidus (DI).…”

“…The role of these innate immune cell first responders in clinical allograft rejection and survival is in part borne out by the survival difference between living and deceased donor allografts in renal transplantation as well as the persistent increased incidence of acute rejection in the presence of delayed graft function. 3 An increasing body of evidence from experimental models has demonstrated that innate immune cells can also recognize and react to cells from other members of the same species, and that this innate nonself recognition can contribute to hematopoietic and solid organ transplant injury and rejection. 4 In murine models of kidney, heart, and bone marrow plug transplantation in recipients lacking adaptive immune effector cells including T and B lymphocytes and natural killer cells (BRG mice), infiltrates of activated monocytes capable of promoting rejection by adoptively transferred T cells occurred in allogeneic but not in syngeneic transplants, suggesting nonself recognition by monocytes.…”

Evaluation of predictive models for delayed graft function of deceased kidney transplantation

“…DGF is a major obstacle for successful transplantation as it causes post-transplantation oliguria, increased allograft immunogenicity and risk of acute rejection episodes, and decreased long-term survival [ 8 ]. Due to the adverse influences of DGF on the transplantation outcome, significant efforts have been made to identify risk factors for DGF [ 7 , 9 – 11 ]. Identification of risk factors for DGF is helpful for early preventive management.…”