Résumé
New onset diabetes after transplant [NODAT] is common after solid organ transplantation and is associated with factors such as pre-transplant obesity and weight gain. We report an unusual case of severe insulin resistance [IR] leading to the development of NODAT four years after a technically successful simultaneous combined pancreaskidney transplant [SPKT] in a patient with long-standing Type 1 Diabetes [TIDM] complicated by end-stage diabetic nephropathy. Our subject became insulin-independent following his SPKT, but his significant weight gain following a short course of steroids for a biopsy-proven episode of mild pancreatic rejection at one year worsened his IR. His oral glucose tolerance at three years indicated preserved glucose tolerance but showed elevated c-peptide. Homeostasis Model Assessment [HOMA] indicated significant IR and a compensatory increase in beta-cell function. Symptomatic hyperglycemia requiring insulin developed at four years. Repeat metabolic testing confirmed glucose intolerance but demonstrated ongoing c-peptide production, albeit at lower levels. HOMA suggested ongoing IR but a loss of beta-cell function. Renal function had been excellent throughout. This genetically distinct pancreatic allograft maintained normal glucose tolerance in the face of marked insulin resistance for more than three years. Insulin resistance was sufficient to induce a progressive decline in insulin secretion leading to frank, though non-ketotic diabetes