Novel views on new-onset diabetes after transplantation: development, prevention and treatment

OBJECTIVETo determine incidence and prevalence of diabetes mellitus (DM) after lung transplantation (LTx), identify risk factors for persistent DM after LTx, and determine its effect on survival. RESEARCH DESIGN AND METHODSThis was a prospective, longitudinal study comparing DM status before and after LTx using oral glucose tolerance tests (OGTTs). DM prevalence and changes in metabolic control over time were determined. Risk factors for persistent DM and survival differences by DM status were assessed. RESULTSBetween August 2010 and December 2012, 156 patients underwent LTx. DM prevalence after 3, 12, and 24 months was 47%, 44%, and 40%, respectively. A further 20%, 11%, and 7% had impaired glucose tolerance and/or impaired fasting glucose. Incidence of new-onset DM after transplant (NODAT) was 32%, 30%, and 24% after 3, 12, and 24 months. Nonfasting insulin levels and second phase insulin release fell 3 months after transplant (Tx) but returned to baseline by 2 years. The only risk factors for NODAT were 1-and 2-h glucose levels on pre-Tx OGTT (OR 1.73 [95% CI 1.19-2.50], P = 0.004, and 1.84 [1.22-2.77], P = 0.004, respectively). Survival was reduced in patients with DM at study end versus those without (estimated mean 979 days [95% CI 888-1,071] vs. 1,140 days [1,070-1,210], P = 0.023). CONCLUSIONSMost patients had dysglycemia during the first year after LTx, and 32% developed NODAT. Hyperglycemia was caused both by b-cell dysfunction and by insulin resistance. Only pre-Tx OGTT glucose levels predicted persistent NODAT. As DM was common and associated with reduced survival, early detection and management of DM in LTx recipients are warranted.Diabetes mellitus (DM) is a common complication of solid organ transplantation and is associated with increased morbidity and mortality (1). It is especially common after lung transplantation (LTx), firstly because LTx recipients (LTR) require highdose immunosuppression with glucocorticoids in combination with calcineurin inhibitors and secondly because a significant minority of patients have cystic fibrosis (CF), which results both in lung damage necessitating LTx and in destruction of insulin-producing b-cells in the pancreas.

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Objectives: This study investigated the effect of prediabetes in long-term deceased-donor renal transplant recipients regarding graft survival, graft function, and evolution of new-onset diabetes after transplant compared with a control group of graft recipients with normal glucose tolerance test results. Materials and Methods: This was a follow-up trial of 187 deceased-donor renal transplant recipients. Based on oral glucose tolerance test results, the cohort was divided into groups A and B, comprising individuals with normal glucose metabolism (n = 130, 69.9%) and individuals with prediabetes (n = 56, 30.1%). Data are shown as means ± standard errors. Results: Both groups showed similar total transplant survival (116.8 ± 5.4 vs 114.5 ± 7.4 mo; P = .742) and transplant survival measured since oral glucose tolerance test (58.5 ± 1.4 vs 59.5 ± 1.9 mo; P = .990, Mantel-Cox P = .943). Univariate and multivariate Cox regression analyses showed no association of prediabetes with graft loss. Transplant function changes were similar between cohorts (-3 ± 1 vs -5 ± 2 mL/min/1.73 m 2 body surface area, using the Chronic Kidney Disease Epidemiology Collaboration formula; P = .538). At 5-year follow-up, recipients with prediabetes had higher hemoglobin A1c than controls (5.99% ± 0.10% vs 5.67% ± 0.04%; P = .002). Prediabetes was associated with a 4.5-fold increased hazard of new-onset diabetes after transplant (P = .021). Conclusions: Prediabetes was associated with a 4.5-fold higher hazard ratio for new-onset diabetes after transplant but not with reduced graft function or survival.