New onset diabetes after kidney transplantation in autosomal dominant polycystic kidney disease: a retrospective cohort study.

BACKGROUND: New onset diabetes after transplantation (NODAT) is a common adverse outcome of organ transplantation that increases the risk of cardiovascular disease, infection and graft rejection. In kidney transplantation, apart from traditional risk factors, autosomal dominant polycystic kidney disease (ADPKD) has also been reported by several authors as a predisposing factor to the development of NODAT, but any rationale for an association between ADPKD and NODAT is unclear. We examined the cumulative incidence of NODAT in or own transplant population comparing ADPKD patients with non-ADPKD controls. METHODS: A retrospective cohort study to determine the cumulative incidence of patients developing NODAT (defined by World Health Organization-based criteria and/or use of hypoglycaemic medication) was conducted in 79 patients with ADPKD (79 transplants) and 423 non-ADPKD controls (426 transplants) selected from 613 sequential transplant recipients over 8 years. Patients with pre-existing diabetes as a primary disease or comorbidity and/or with minimal follow up or early graft loss/death were excluded. RESULTS: Of the 502 patients (505 transplants) studied, 86 (17.0%) developed NODAT. There was no significant difference in the cumulative incidence of NODAT in the ADPKD (16.5%; CI 13.6-20.7%) compared with the non-ADPKD (17.1%; CI 8.3-24.6%) control group. Of the 13 patients in the ADPKD group with NODAT, three required treatment with insulin with or without oral hypoglycaemic agents. Among the 73 NODAT patients in the non-ADPKD group, eight received insulin with or without oral hypoglycaemics. Furthermore, of the patients that did develop NODAT, there was no difference in the time to its development in patients with and without ADPKD. CONCLUSION: There was no evidence of an increased incidence of NODAT in ADPKD kidney transplant recipients.

Blood group incompatibility in kidney transplantation: definitely time to re-examine!

We report a successful kidney transplant (A1 donor to an O recipient), with antibody removal pre- and post-transplant, and pre-transplant administration of anti-CD20 monoclonal antibody (rituximab), intravenous immunoglobulin, and conventional transplant immunosuppression. The transplant, which was performed without splenectomy, is the first such transplant in Australia. At 20 months, the patient's creatinine level was 110-130 micromol/L, with no evidence of rejection and no complications. ABO-incompatible transplantation should increase "live donor" kidney transplantation, reduce waiting times, and improve patient outcomes.