Type of publication:
Conference abstract
Author(s):
*Kaldindi S.R., *Moulik P., *Macleod A.
Citation:
Diabetic Medicine, March 2015, vol./is. 32/(117-118)
Abstract:
A 42-year-old Afro-Caribbean female presented with 1 week history of polyuria, polydypsia and vomiting. She had a background of transfusion associated iron overload and renal failure secondary to sickle cell disease. She underwent a live donor renal transplant 8 months prior to admission. Immunosuppressive therapy included tacrolimus, mycophenolate, prednisolone 5mg once a day. There was no family history of diabetes. She had a normal body mass index. Results revealed a pH of 7.08, bicarbonate of 6.6mmol/l, capillary blood glucose tests recorded as greater than 28.7mmol/l, ketones 7.0mmol/l, Hb 84 g/l. Her creatinine was 101mumol/l (baseline 90), eGFR 52 and tacrolimus levels were within therapeutic range. No obvious precipitant for diabetic ketoacidosis (DKA) was found. She responded well to intravenous fluids and insulin. Her glutamic acid decarboxylase (GAD) and islet antigen 2 (IA2) antibodies were negative. Possible causes for her diabetes include iron overload, steroid therapy, tacrolimus. In her case, she presented with a short timeline of symptoms along with severe DKA. This is typical of Type 1 diabetes, even though her antibodies were negative. NODAT usually behaves like Type 2 diabetes but, rarely, such patients can also present with an insulin deficient state similar to Type 1 diabetes. The Renal Association suggests lower levels of tacrolimus to decrease NODAT risk and screening for diabetes post-transplant. A steroid sparing immunosuppressive regimen may help in reducing the incidence of NODAT.
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