Post-Transplant Diabetes Mellitus in Renal Allograft Recipients: A Matched-Pair Control Study

The incidence of post-transplant diabetes mellitus was evaluated retrospectively in 901 consecutive renal transplant recipients. Thirty-two (3.6%) patients developed diabetes mellitus requiring drug therapy. 18 of 32 became hyperglycaemic within 3 months of transplantation. Post-transplant diabetes mellitus occurred in 24 of 628 (3.8%) patients treated with conventional therapy consisting in azathioprine and prednisone, and in 8 of 273 (2.9%) patients receiving cyclosporin A (CsA) in addition (triple therapy). To identify predisposing factors 32 nondiabetic patients matched for age, sex, number of graft, immunosuppressive protocol, and graft function at onset of diabetes were used as case controls. Thirteen of 32 patients with diabetes mellitus and 5 of 32 control patients had abnormal glucose tolerance pretransplant (P<0.025). HLA-B8 was significantly more frequent in patients with post-transplant diabetes mellitus than in control patients (9 of 29 vs 2 of 31, (P<0.02). Twelve (38%) patients became diabetic during or immediately after anti-rejection therapy with intravenous pulse prednisone. Four diabetic patients experienced chronic pancreatitis pre-transplant. Family history of diabetes mellitus, bodyweight, number of rejection episodes, and immunosuppressive drug doses were similar in both groups. Actuarial patient and graft survival was not significantly different in diabetic patients and controls, although 10-year data tended to be better in controls. Thus, post-transplant diabetes mellitus was not a frequent complication in patients sometimes predisposed by an impaired glucose tolerance pre-transplant and was triggered by pulse prednisone therapy in 38

Post-Transplant Diabetes Mellitus in Renal Allograft Recipients: A Matched-Pair Control Study

The incidence of post-transplant diabetes mellitus was evaluated retrospectively in 901 consecutive renal transplant recipients. Thirty-two (3.6%) patients developed diabetes mellitus requiring drug therapy. 18 of 32 became hyperglycaemic within 3 months of transplantation. Post-transplant diabetes mellitus occurred in 24 of 628 (3.8%) patients treated with conventional therapy consisting in azathioprine and prednisone, and in 8 of 273 (2.9%) patients receiving cyclosporin A (CsA) in addition (triple therapy). To identify predisposing factors 32 nondiabetic patients matched for age, sex, number of graft, immunosuppressive protocol, and graft function at onset of diabetes were used as case controls. Thirteen of 32 patients with diabetes mellitus and 5 of 32 control patients had abnormal glucose tolerance pretransplant (P<0.025). HLA-B8 was significantly more frequent in patients with post-transplant diabetes mellitus than in control patients (9 of 29 vs 2 of 31, (P<0.02). Twelve (38%) patients became diabetic during or immediately after anti-rejection therapy with intravenous pulse prednisone. Four diabetic patients experienced chronic pancreatitis pre-transplant. Family history of diabetes mellitus, bodyweight, number of rejection episodes, and immunosuppressive drug doses were similar in both groups. Actuarial patient and graft survival was not significantly different in diabetic patients and controls, although 10-year data tended to be better in controls. Thus, post-transplant diabetes mellitus was not a frequent complication in patients sometimes predisposed by an impaired glucose tolerance pre-transplant and was triggered by pulse prednisone therapy in 38

Predictors of new onset diabetes after renal transplantation

The development of new onset diabetes after transplantation (NODAT) is associated with increased cardiovascular morbidity and mortality. This study aimed at identifying risk factors for the development of NODAT. We performed a retrospective review of 787 renal transplants performed between 1994 and 2004 at a single centre. NODAT was diagnosed in patients who had two random plasma glucose concentrations >11.1 mmol/L after the first month post-transplant or patients who required treatment for hyperglycaemia within the first month and continued treatment thereafter. The incidence of NODAT was 7.7%. The incidence of NODAT requiring either insulin or oral hypoglycaemic agents was 4.5%. Risk factors for the development of NODAT were older age (HR 1.04, 95% CI: 1.01-1.07, p < 0.01), heavier weight at time of transplantation (HR 1.04, 95% CI: 1.02-1.07, p < 0.01), higher mean pre-transplant random plasma glucose concentrations (HR 1.54, 95% CI: 1.14-2.08, p < 0.01), higher plasma glucose within the first seven d post-transplant (HR 1.27, 95% CI: 1.09-1.47, p < 0.01) and use of tacrolimus (HR 3.70, 95% CI: 1.61-8.46, p < 0.01). Ten yr actuarial patient survival was 67.1% in patients with NODAT compared with 81.9% for those without diabetes and 65.3% in patients known to have diabetes pre-transplant. There was no difference in graft survival. We have identified a high-risk group in which attempts should be made to reduce the incidence of NODAT by tailoring immunosuppression, lifestyle modification and selecting non-diabetogenic medications. Improvements in management of patients at higher risk of NODAT may help reduce the incidence of deaths with a functioning graft

Post-transplant diabetes mellitus: a case-control analysis of the risk factors

Aim of the present study was to assess, in a pair-matched analysis design, risk factors for post-transplant diabetes mellitus (PTDM) in renal transplant recipients (KTx). The incidence of PTDM was evaluated in 538 consecutive KTx in relation to their baseline immunosuppression. PTDM was defined according to the 2003 American Diabetes Association and World Health Organization experts committee definition. As risk factors for PTDM development were considered: age, family history of diabetes, body mass index (BMI), baseline immunosuppression, doses and blood levels of the immunosuppressive agents used. Baseline immunosuppression consisted of CSA, TAC and SRL + CNI. Thirty-two pair-matched controls were identified among the 538 KTx and included in the risk analysis. Significant risk factors for the development of PTDM were identified in the family history of diabetes (P < 0.02) and BMI (P < 0.05). Higher BMI and positive family history for diabetes mellitus were significant risk factors for the development of PTDM, regardless of the immunosuppressive agent used