Abstract #1183828: The Role of Tacrolimus in DKA for Post-transplant Patients

Abstract

Post-transplant diabetes (PTDM) is a well-known complication of immunosuppressants post organ transplantation. Calcineurin inhibitors (CNI), steroids, and mycophenolate (MMF) are standard therapy, with tacrolimus (TAC) being the most common CNI. It is well recognized that TAC decreases insulin secretion and causes beta cell apoptosis causing an insulin deficient state. However, diabetic ketoacidosis (DKA) has not yet been widely reported in transplant patients. We describe 3 cases of DKA in post-transplant patients on TAC. 1: 51yo male with hypertension, presented 2 months post kidney transplant with hyperglycemia for 1 week. Labs showed DKA with anion gap (AG) 28 mEq/L, CO2 6 mEq/L, pH 7.18, blood glucose (BG) >1500 mg/dL, beta hydroxybutyrate (BHB) 5.91 mmol/L. Immunosuppressants included prednisone, MMF, and TAC with a serum level of 13.1 ng/mL. Pretransplant A1C was 5.8% and increased to 10.3% at admission. Glutamic acid decarboxylate (GAD), islet cell, zinc transporter 8 Ab were negative, and C-peptide was 0.2ng/mL. He was treated with IV insulin and TAC dose adjusted. DKA resolved and he was discharged on insulin and a DPP4 inhibitor. 2: 57yo female with T2D, hypertension, congestive heart failure, presented 1-year post heart transplant with vomiting and abdominal pain for 1 day. Labs showed DKA with AG 22 mEq/L, CO2 19 mEq/L, pH 7.38, BG 267 mg/dL, BHB 3.16 mmol/L. Immunosuppressants included prednisone and TAC with level >30 ng/ml. A1C was 5.2%. She was treated with IV insulin. TAC was held and resumed after the level returned to range. DKA resolved and she was discharged on basal/bolus insulin and DPP4 inhibitor. 3: 68yo male with T2D, hypertension, ischemic cardiomyopathy presented 8 months post heart transplant with 1 month of hyperglycemia and weight loss. Labs showed DKA with AG 16 mEq/L, CO2 13 mEq/L, pH 7.38, BG 735 mg/dL, BHB 5.1 mmol/L Immunosuppressants included prednisone, MMF, and TAC with level of 7.0 ng/mL. Pretransplant A1C 7.1% and noted to be 12.2% at admission. Negative GAD, zinc transporter 8 Ab, and C-peptide 2.1ng/mL. He was treated with IV insulin. DKA resolved and he was discharged on basal/bolus insulin. We describe DKA in post-transplant patients within 12 months of transplant while on TAC without any other cause identified. All 3 had rapid improvement with insulin and adjustment of TAC doses. The negative effects of TAC on beta cells function causing an insulin deficient state could be an important precipitant of DKA in these patients. Close glucose monitoring is essential for early recognition and prevention. The risk factors for TAC associated DKA needs further study.