Abstract

New-onset diabetes after transplantation (NODAT) is a recognized metabolic complication following kidney transplantation, typically occurring within the first year post-transplant. While hyperglycemia is a common manifestation, presentation as diabetic ketoacidosis (DKA) is exceedingly rare. A 22-year-old male with a history of hypertension and hypothyroidism underwent living-related renal transplantation from his mother for endstage renal disease. Pre-transplant metabolic evaluation revealed normal fasting insulin and C-peptide levels with mildly elevated insulin resistance indices. Post-operatively, the patient received triple-drug immunosuppression with tacrolimus, mycophenolate mofetil, and prednisolone, maintaining euglycemia during early recovery. On day 110 post-transplant, he presented with altered sensorium, anuria, and severe hyperglycemia (random blood glucose 1183 mg/dL), fulfilling criteria for diabetic ketoacidosis with high anion gap metabolic acidosis and ketonuria. Laboratory evaluation revealed mild allograft dysfunction (serum creatinine 2.53 mg/dL) and severe anemia (hemoglobin 6.5 g/dL). Intensive management with intravenous insulin infusion, aggressive fluid therapy, and immunosuppressive dose optimization led to complete metabolic recovery, successful graft preservation, and transition to subcutaneous insulin therapy. This case highlights the potential for tacrolimus-based immunosuppression to precipitate severe hyperglycemic crises such as DKA in transplant recipients, even in young patients without conventional diabetes risk factors. Early recognition, prompt multidisciplinary management, and regular glycemic monitoring are vital to prevent graft loss and mortality, particularly within the first six months following transplantation.

Keywords

new-onset diabetes after transplantation, diabetic ketoacidosis, tacrolimus, kidney transplantation, immunosuppression, pancreatic beta-cell dysfunction