T ransplant-associated hyperglycemia (TAH) encompasses the full range of new-onset, posttransplantation glycemic abnormalities, including the prediabetic states of impaired fasting glucose and impaired glucose tolerance, as well as new-onset diabetes after transplantation (NODAT). TAH is a common transplant-related complication that leads to higher rates of cardiovascular events, death, and allograft loss (1,2). Numerous risk factors predispose patients to TAH; some, such as the use of calcineurin inhibitors (CNIs), impair pancreatic insulin secretion, whereas others, such as obesity, impair insulin sensitivity (3). The study by Hornum et al. (1) in this issue of CJASN aimed to elucidate the relative contributions of defects in insulin secretion versus insulin resistance in the development of TAH. Their results highlight the importance of insulin resistance.Estimation of the cumulative incidence of TAH depends on the population studied and the surveillance method used. US registry data analysis suggests that 15% of kidney recipients develop clinically diagnosed NODAT by 1 year after transplantation (4). More sensitive methods, such as oral glucose tolerance testing, allow detection of impaired fasting glucose or impaired glucose tolerance that, similar to NODAT, are associated with adverse posttransplantation cardiovascular outcomes (4). Single-center reports using these methods indicate that, in addition to patients who are classified as having NO-DAT, the prediabetic states are present among 30 to 45% of kidney recipients at 1 year after transplantation (1,5,6). Evidence from meta-analyses and clinical trials confirms that TAH occurs in a substantial proportion of transplant recipients and should be a major cause for concern (7-9).The greater risk for death and cardiovascular complications observed in patients with NODAT is similar to that seen in patients with diabetes in the general population (4). For example, in a single-center study with detailed information about the metabolic profile of kidney transplant recipients, Cosio et al. (10) reported an adjusted hazard ratio for mortality of 1.80 (P Ͻ 0.01) associated with NODAT. Notably, the metabolic milieu of patients with TAH is characterized not just by abnormal glucose homeostasis but also by deterioration in the lipid profile, higher BP, and elevated inflammatory markers. Even after multivariable adjustment for lipids, BP, and inflammation, however, TAH remains an independent risk factor for cardiovascular events (2). A recent analysis of US registry data suggested that for many patients with TAH, mortality becomes an important competing outcome, to the extent that TAH makes it more likely that a patient will die before the allograft fails (11).An extensive literature on TAH has illuminated the many risk factors for development of TAH. Before transplantation, older age, obesity, hepatitis C infection, family history of type 2 diabetes, and metabolic syndrome increase the probability of subsequent glycemic abnormalities through insulin resistance (3). ...