Increased alloreactivity and adverse outcomes in obese kidney transplant recipients are limited to those with diabetes mellitus

- Obese KTRs show a high incidence of pre-existing diabetes mellitus.
- Outcomes of obese diabetic KTRs are inferior to obese non-diabetic KTRs.
- Obese non-diabetic KTRs show comparable outcomes with non-obese KTRs.
- Obese diabetic KTRs show higher frequencies of preformed donor-reactive T-cells.

Previous studies on patient and allograft outcomes of obese kidney transplant recipients (KTRs) remain controversial. To what extent obesity-related comorbidities contribute to adverse outcomes, however, hasn't been addressed.We studied all KTRs from 2005 to 2012. 29 (4%), 317 (48%), 217 (33%), 76 (12%), and 21 KTRs (4%) were identified as underweight, normal-weight, overweight, obese, and morbid obese, respectively. 33 of 97 obese KTRs (34%) had pre-existent diabetes. Samples were collected before transplantation and at + 1, + 2, + 3 months posttransplantation. Donor-reactive T-cells were measured using an interferon-γ Elispot assay.Obese KTRs showed an increased incidence pre-existent diabetes (p < 0.001), but no differences for hypertension and coronary artery disease (p > 0.05). Among obese KTRs, those with pre-existent diabetes showed inferior patient and allograft survival, worse allograft function, delayed graft function, and prolonged hospitalization (p < 0.05). Interestingly, no differences were observed between obese non-diabetic, normal-weight diabetic, and normal-weight non-diabetic KTRs (p > 0.05). Obese diabetic KTRs showed higher frequencies of donor-reactive T-cells pretransplantation (p < 0.05).Our results suggest that the increased risk of mortality, allograft loss, delayed graft function, and prolonged hospitalization in obese KTRs is limited to those with diabetes. A state of obesity-related inflammation plus hyperglycemia may trigger increased alloreactivity and should call for adequate immunosuppression.