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Recurrence of Type 1 Diabetes After Simultaneous Pancreas–Kidney Transplantation in the Absence of GAD and IA‐2 Autoantibodies
Author(s) -
Assalino M.,
Genevay M.,
Morel P.,
DemuylderMischler S.,
Toso C.,
Berney T.
Publication year - 2012
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2011.03844.x
Subject(s) - medicine , pancreas transplantation , autoantibody , transplantation , kidney transplantation , pancreas , type 1 diabetes , diabetes mellitus , kidney , type 2 diabetes , immunology , endocrinology , antibody
We report herein the patterns of type 1 diabetes recurrence in a simultaneous pancreas–kidney transplant (SPK) recipient, in the absence of rejection. A 38‐year‐old female underwent SPK for end‐stage nephropathy secondary to type 1 diabetes. Fasting blood glucose, HbA1c, fructosamine, C‐peptide and autoantibodies (GAD‐65, IA‐2) were monitored throughout follow‐up. At 3.5 years post‐SPK, HbA1c and fructosamine increased sharply, indicating loss of perfect metabolic control, despite C‐peptide levels in the normal‐high range. Exogenous insulin was restarted 4 months later. C‐peptide levels abruptly fell and became undetectable at 5.5 years. Autoantibody levels, which were undetectable at the time of SPK, never converted to positivity. Pancreas retranspantation was performed at 6 years. The failed pancreas graft had a normal macroscopic appearance. On histology, there were no signs of cellular or humoral rejection in the kidney or pancreas. A selective peri‐islet lymphocytic infiltrate was observed, together with near‐total destruction of β cells. At 2.5 years post retransplantation, pancreatic graft function is perfect. This observation indicates unequivocally that pancreas graft can be lost to recurrence of type 1 diabetes in the absence of rejection. GAD‐65 and IA‐2 autoantibodies are not reliable markers of autoimmunity recurrence.