SummaryABO blood group incompatible renal transplantation, using desensitization procedures, is an effective strategy. Efforts have been made to reduce desensitization: these are usually applied to all patients indiscriminately. The Guy's Hospital ABO blood group incompatible desensitization regimen uses a tiered approach, tailoring strategy according to initial antibody titres. Sixty-two ABO blood group incompatible living donor transplant recipients were compared with 167 recipients of blood group compatible living donor renal transplants. There were no statistically significant differences in allograft survival rates at 1 or 3 years posttransplant, rejection in the first year post-transplant or renal function in the first 3 years post-transplant. There was a higher rate of death in ABO blood group incompatible transplant recipients -this could be associated with differences in age and HLA mismatch between the two groups. Four ABO blood group incompatible patients experienced antibody-mediated rejection (no episode was associated with a rise in ABO blood group antibodies). Of the patients who received no desensitization, or rituximab alone, none has experienced antibody mediated rejection or experienced allograft loss. Tailoring the use of desensitization in ABO blood group incompatible renal transplantation according to initial ABO blood group antibody titres led to comparable results to blood group compatible transplantation.

Mortality was high among patients admitted from the wards to ICU; many were inpatients for days or weeks before admission. The longer these patients were in hospital before ICU admission, the higher their mortality. Patients with delayed admission differed in some respects compared to those admitted earlier.

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SummaryRituximab is a chimeric anti-CD20 monoclonal antibody that leads to B cell depletion. It is not licensed for use in renal transplantation but is in widespread use in ABO blood group incompatible transplantation. It is an effective treatment for post-transplant lymphoproliferative disorder, and is also used in both HLA antibody incompatible renal transplantation and the treatment of acute rejection. Recent evidence suggests rituximab may prevent the development of chronic antibody mediated rejection. The mechanisms underlying its effects are likely to relate both to long-term effects on plasma cell development and to the impact on B cell modulation of T cell responses. Rituximab (in multiple doses or in combination with other monoclonal antibodies and/or other immunosuppressants) may lead to an increase in infectious complications, although the evidence is not clear. Rarely, the drug can cause a cytokine release syndrome, thrombocytopenia and neutropenia. It has been related to an increased risk of progressive multifocal leucoencephalopathy and, recently, deaths from cardiovascular causes. Trials examining the effects of rituximab in induction therapy for compatible renal transplantation and the treatment of chronic antibody mediated rejection are ongoing. These trials should aid greater understanding of the role of B-cells in the alloresponse to renal transplantation.

Surgical complications following SPK transplantation can cause significant morbidity and adversely affect pancreas graft survival, but do not affect long-term kidney or patient survival.

Pancreas graft loss due to venous thrombosis is the leading non-immunological cause for graft failure following kidney-pancreas transplantation. Thromboelastography (TEG)-directed anticoagulation protocol has shown that approximately one-third of the patients undergoing pancreas transplantation require therapeutic anticoagulation to prevent the occurrence of graft thrombosis. This article presents the argument for individualised anticoagulation in these patients based on their TEG tracings and suggests the use of TEG in patients undergoing pancreas transplantation.

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