| 1. Normal |
Absent 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
|
| 2. Indeterminate |
|
|
| 3. Acute TCMR |
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
-
o
Focal acinar inflammation (two or fewer foci per lobule) with absent or minimal acinar cell injury.
Grade II (moderate acute TCMR [requires differentiation from ABMR]):
-
o
Multifocal (but not confluent or diffuse) acinar inflammation (three or more foci per lobule) with spotty (individual) acinar cell injury and dropoutand/or
-
o
Mild intimal arteritis (with minimal [<25%] luminal compromise)
Grade III (severe acute TCMR [requires differentiation from ABMR]):
-
o
Diffuse (widespread, extensive) acinar inflammation with focal or diffuse multicellular/confluent acinar cell necrosisand/or
-
o
Moderate or severe intimal arteritis (>25% luminal compromise)and/or
-
o
Transmural inflammation—necrotizing arteritis
|
| 4. Acute/active ABMR |
One of three diagnostic components: requires exclusion of ABMR Two of three diagnostic components: consider acute ABMR Three of three diagnostic components: definite acute ABMR Diagnostic components:
Histologic evidence of acute tissue injury:
Grade I (mild acute ABMR): Well‐preserved architecture, mild interacinar monocytic‐macrophagic or mixed (monocytic‐macrophagic/neutrophilic) infiltrates with rare acinar cell damage (swelling, necrosis) Grade II (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 Grade III (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)
C4d positivity in interacinar capillaries (≥1% of acinar lobular surface for immunohistochemistry) Serologic evidence of DSA (HLA or other antigens)
|
| 5. Chronic active ABMR |
Combined features of category 3 and/or 4 with active chronic arteriopathyb and/or category 6 Specify whether TCMR, ABMR, or mixed
|
| 6. Chronic arteriopathyc
|
Fibrointimal arterial thickening with narrowing of the lumen
Distinguish on the most affected artery:
-
o
Grade 0, negative: no narrowing of the luminal area
-
o
Grade 1, mild: ≤25% narrowing of luminal area
-
o
Grade 2, moderate: 26–50% narrowing of luminal area
-
o
Grade 3, severe: ≥50% narrowing of luminal area
|
| 7. Chronic graft fibrosis |
Grade I (mild graft fibrosis): Expansion of fibrous septa; the fibrosis occupies <30% of the core surface but the acinar lobules have eroded, irregular contours. The central lobular areas are normal Grade II (moderate graft fibrosis): The fibrosis occupies 30–60% of the core surface. The exocrine atrophy affects the majority of the lobules in their periphery (irregular contours) and in their central areas (thin fibrous strands criss‐cross between individual acini) Grade III (severe graft fibrosis): The fibrotic areas predominate and occupy >60% of the core surface with only isolated areas of residual acinar tissue and/or islets present
|
| 8. Islet pathology |
Recurrence of autoimmune diabetes mellitus (insulitis and/or selective β cell loss) Islet amyloid (amylin) deposition Islet cell calcineurin inhibitor toxicity
|
| 9. Other histologic diagnosis |
|
|
