ODP623 Life Threatening Diabetic Ketoacidosis as First Presentation of Tacrolimus-Induced Diabetes Mellitus.

Abstract

Abstract Background New-onset diabetes after transplantation (NODAT) is a serious complication after a solid organ transplant. NODAT occurs in 2% to 53% of all solid organ transplant recipients.1 Tacrolimus is an immunosuppressive agent associated with diabetogenic potential which predominantly is a result of suppression of insulin secretion from pancreatic beta cells. Diabetic ketoacidosis as the first presentation of new onset tacrolimus induced diabetes is rare. We report a case of diabetic ketoacidosis (DKA) in a patient without prior history of diabetes mellitus and receiving tacrolimus as part of immunosuppressive regime post-renal transplant. Clinical Case A 62-year-old female with past medical history of autosomal polycystic kidney disease status-post deceased donor renal transplant and hypertension presented with weakness and fatigue. She had undergone transplant 8 months prior to this presentation and her immunosuppressive regime consisted of mycophenolate mofetil and tacrolimus. The patient was encephalopathic on arrival with normal vitals. Laboratory evaluation was significant for blood glucose of 673, bicarbonate of <10, anion gap of 24, Beta-hydroxybutyrate >8 and a pH of 7.19 on arterial blood gas analysis thus confirming diagnosis of diabetic ketoacidosis (DKA). Tacrolimus level was elevated at 35.7. Intravenous fluids and insulin were initiated with resolution of symptoms and DKA. She was transitioned to a basal-bolus insulin regimen. Further labs revealed Hemoglobin A1C of 11.6% (no previous value), negative insulin antibodies and glutamic acid decarboxylase antibody, and a low C-peptide level at 0.47 (when blood glucose was 150mg/dl). Her tacrolimus dose was adjusted, and she was discharged on a basal-bolus insulin regimen. On follow up, the patient had lower insulin requirements with improvement in C-peptide level to 1.8, thus, indicating beta cell dysfunction in setting of supratherapeutic tacrolimus levels. Conclusion Tacrolimus remains the preferred immunosuppressive agent after kidney transplantation given lower incidence of acute rejections and better tolerance. However, due to its toxic effects on pancreatic beta cells it is imperative blood sugar levels should be routinely monitored in patients on tacrolimus. Appropriate monitoring can lead to timely diagnosis and successful outcomes. Further studies are required to investigate risks factors associated with tacrolimus induced DKA.