Pancreas Transplantation Guidelines

Updated: Apr 13, 2022
  • Author: Joseph Sushil Rao, MD; Chief Editor: Ron Shapiro, MD  more...
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Guidelines Summary

Banff pancreas allograft rejection grading schema

In 2017, an update to the Banff pancreas allograft rejection grading schema was published. [20]  The current criteria are outlined below.

Normal criteria are as follows:

  • No inflammation  or inactive septal, mononuclear inflammation not involving ducts, veins, arteries, or acini
  • No graft sclerosis
  • The fibrous component is limited to normal septa, and its amount is proportional to the size of the enclosed structures (ducts and vessels).
  • The acinar parenchyma shows no signs of atrophy or injury

When septal inflammation appears active, but the overall features do not fulfill the criteria for mild acute rejection, rejection is deemed indeterminate.

Acute T-cell–mediated rejection (TCMR) has three grades. Criteria are as follows:

Grade I - Mild acute TCMR: Active septal inflammation (activated blastic lymphocytes and/or eosinophils) involving septal structures: venulitis (subendothelial accumulation of inflammatory cells and endothelial damage in septal veins), ductitis (epithelial inflammation and damage of ducts) and/or focal acinar inflammation (two or fewer foci per lobule) with absent or minimal acinar cell injury.

Grade II - Moderate acute TCMR: Multifocal (but not confluent or diffuse) acinar inflammation (three or more foci per lobule) with spotty (individual) acinar cell injury and dropout and/or mild intimal arteritis 

Grade III - Severe acute TCMR: Diffuse (widespread, extensive) acinar inflammation with focal or diffuse multicellular/confluent acinar cell necrosis and/or moderate or severe intimal arteritis and/or transmural inflammation-necrotizing arteritis

The diagnostic criteria for acute/active antibody‐mediated rejection (ABMR) are as follows:

  • Histologic evidence of acute tissue injury
  • C4d positivity in interacinar capillaries (≥1% of acinar lobular surface for immunohistochemistry)
  • Serologic evidence of donor-specific antibodies (HLA or other antigens)

Histologic evidence is categorized into three grades as follows:

  • Mild acute ABMR: Well‐preserved architecture, mild interacinar monocytic‐macrophagic or mixed (monocytic‐macrophagic/neutrophilic) infiltrates with rare acinar cell damage (swelling, necrosis)
  • Moderate acute ABMR: Overall preservation of the architecture with interacinar monocytic‐macrophagic or mixed (monocytic‐macrophagic/neutrophilic) infiltrates, capillary dilatation, interacinar capillaritis, intimal arteritis, a congestion, multicellular acinar cell dropout, and extravasation of red blood cells
  • Severe acute ABMR: Architectural disarray, scattered inflammatory infiltrates in a background of interstitial hemorrhage, multifocal and confluent parenchymal necrosis, arterial and venous wall necrosis, transmural/necrotizing arteritis, a and thrombosis (in the absence of any other apparent cause)

ABMR is diagnosed when all three diagnostic criteria are met.  If only 2 criteria are present, the diagnosis may be considered. ABMR is excluded if only one criterion is met.