Histology of the pancreas transplant

Abstract The early detection and effective treatment of acute rejection has been a major challenge in pancreas transplantation. Numerous non-invasive markers of pancreas rejection and function have been studied such as serum or urine levels of amylase, lipase, or anodal trypsinogen or functional measures such as glucose disappearance rates. [1–3]. Although widely used, none of these biochemical markers or functional measures have proven to be specific for acute rejection. Similarly imaging studies such as magnetic resonance imaging (MRI) scanning or ultrasound have not shown adequate sensitivity or specificity on which to base treatment of rejection [4–6]. The diagnosis of acute pancreas rejection has until recently relied on evidence of renal allograft rejection in patients receiving simultaneous kidney and pancreas transplantation. In these patients, renal allograft dysfunction is used as a surrogate marker for pancreas rejection as most rejection episodes occur simultaneously in both the kidney and pancreas, and the renal allograft is easily biopsied.