Banff classification so named because the first International Consensus Meeting on kidney allograft pathology was held in Banff, Canada (in 1991).1
The updated 2017 Banff classification is categorized into six broad categories.
Banff classification
Other changes not considered to be caused by acute or chronic rejection are listed under Banff category 6. These include
Acute tubular necrosis.
Polyoma (BK) virus nephropathy.
Calcineurin inhibitor nephrotoxicity.
Pyelonephritis.
Drug-induced interstitial nephritis.
Posttransplant lymphoproliferative disease.
Recurrent disease.
De novo glomerulopathy (other than transplant glomerulopathy [TG]).
Few lesions are not included in the Banff classification.
Category 1: normal biopsy or nonspecific changes
Nonspecific changes
Inflammation that does not meet any of the following diagnostic criteria
Mild glomerular injury that does not meet any of the following diagnostic criteria
TABLE 9-1 Banff Category 2
Antibody-mediated changes
Acute antibody-mediated rejection (ABMR)
Histologic and other features
Acute/active antibody-mediated injury
Microvascular inflammation (glomerulitis or peritubular capillaritis)
Arterial inflammation
Thrombotic microangiopathy without other cause
Acute tubular injury without other cause
Chronic antibody-mediated injury
Chronic active ABMR
Transplant glomerulopathy (TG); glomerular capillary double contours with new layers of subendothelial basement membrane material
Multilayered peritubular capillary basement membranes (seen by EM)
New onset arterial intimal fibrosis without other cause
Evidence of antibody-mediated vascular injury
Chronic ABMR
Peritubular capillary C4d staining in >10% by IF or >0% by immunohistochemistry
Expression of validated ABMR-associated gene transcripts in renal tissue
Moderate glomerulitis and/or peritubular capillaritis (see reference for details)
Histologic features of chronic antibody-mediated injuryb
Prior documented active or chronic active ABMR or prior documented DSA
Evidence of donor-specific antibodies (DSAs)
Positive test for DSA
Positive peritubular capillary C4d staining
Expression of validated ABMR-associated gene transcripts in renal tissue
C4d staining without evidence of rejection (see text)
Abbreviations: IF, immunofluorescence; EM, electron microscopy.
a Quantitative criteria for glomerular double contour score (also known as cg score) ranges from no glomerular basement membrane double contours by light microscopy or EM (cg0) to double contours affecting >50% of peripheral capillary loops in the most affected glomerulus (cg3). Detailed discussion is beyond the scope of this chapter.
b See left column for detailed criteria
Roufosse C, Simmonds N, Clahsen-van Gronigen M, et al. A 2018 reference guide to the Banff classification of renal allograft pathology. Transplantation. 2018;102(11):1795-1814.
Histologic features of antibody-mediated injury (Figure 9-1)
Acute/active antibody-mediated injury
Microvascular inflammation which is semiquantitated
Glomerulitis—glomerular endocapillary leukocytes and swollen endothelial cells
Peritubular capillaritis—leukocytes and swollen endothelial cells in cortical peritubular capillary lumens
Thrombotic microangiopathy without other cause
Acute tubular injury without other cause
Arterial inflammation
Chronic antibody-mediated injury
TG—glomerular capillary double contours with new layers of subendothelial basement membrane material
Figure 9-1 Features of Antibody-Mediated Rejection
A, Leukocytes, predominantly monocytes, and swollen endothelial cells within and occluding glomerular capillary lumens (arrows) (glomerulitis, active lesion) (Jones silver). B, Leukocytes and swollen endothelial cells in peritubular capillary lumens (peritubular capillaritis, active lesion) (arrows) (periodic acid-Schiff). C, Immunofluorescence for C4d showing linear staining of peritubular capillary walls (active lesion). D, Glomerular capillary wall double contours (transplant glomerulopathy, chronic lesion) (Jones silver). E, Electron microscopy of transplant glomerulopathy with new subendothelial layers of basement membrane material (arrow). F, Electron microscopy of a peritubular capillary showing multiple subendothelial layers of basement membrane material (arrow).
Identified by electron microscopy (EM) only (cg1a)
Identified by light microscopy (cg1b-cg3)
Multilayered peritubular capillary basement membranes
New onset arterial intimal fibrosis without other cause
Evidence of antibody-mediated vascular injury
Peritubular capillary C4d staining in ≥10% by immunofluorescence or >0% by immunohistochemistry
Moderate glomerulitis and/or peritubular capillaritis, with conditions
Expression of validated antibody-mediated rejection (ABMR)-associated gene transcripts in renal tissue
Evidence of donor-specific antibodies
Positive test for donor-specific antibody
Positive peritubular capillary C4d staining
Expression of validated ABMR-associated gene transcripts in renal tissue
Acute/active antibody ABMR
One or more histologic features of active antibody-mediated injury (see earlier discussion)
Evidence of antibody-mediated vascular injury
Evidence of donor-specific antibodies
Histologic features of chronic antibody-mediated injury (see earlier discussion)
Evidence of antibody-mediated vascular injury
Evidence of donor-specific antibodies
Chronic ABMR
Histologic features of chronic antibody-mediated injury (see earlier discussion)
Prior documented active or chronic active ABMR or prior documented donorspecific antibody
C4d staining without evidence of rejection7
Positive C4d stain
No histologic features of active or chronic active ABMR
No expression of validated ABMR-associated gene transcripts (if done)
No histologic features of T cell-mediated rejection (TCMR) or borderline lesions
In an ABO incompatible transplant, this may represent accommodation.
Figure 9-2 Chronic Active Antibody-Mediated Rejection
The glomerulus has many capillary wall double contours (transplant glomerulopathy) in addition to segmental occluding endocapillary inflammation (arrows, glomerulitis) (Jones silver).
Evaluated in renal cortex
Active/acute injury (Figure 9-3)
T lymphocytes in tubular walls between epithelial cells in non-atrophied tubules (tubulitis)
Number of lymphocytes per tubular cross section (up to 10 tubular epithelial cells) in the most affected tubule
Inflammation in the unscarred interstitium
Mononuclear inflammation in artery walls
This may be indicative of antibody-mediated injury.
Figure 9-3 Features of T cell-Mediated Rejection
A, Borderline lesion. Tubular inflammation (tubulitis) with one lymphocyte (arrow) in the tubular cross section and ≥25% interstitial inflammation (periodic acid-Schiff [PAS]). B, Banff grade 1A. Tubulitis with 5 to 10 lymphocytes in the tubular cross section (arrows) and ≥25% interstitial inflammation (Jones silver). C, Banff grade 1B. Tubulitis with >10 lymphocytes in the tubular cross section (arrows) and ≥25% interstitial inflammation (Jones silver). D, Banff grade 2A. Artery with endothelial cell swelling and intimal inflammation (arrow) with <25% luminal involvement (PAS). E, Banff grade 2B. Artery with circumferential intimal inflammation involving ≥25% of the artery lumen (hematoxylin and eosin). F, Banff grade 3. Artery with transmural inflammation (arrow) (PAS).
Chronic injury
Mononuclear inflammation in foci of tubular atrophy/interstitial fibrosis (interstitial fibrosis and tubular atrophy [IFTA])
Tubulitis in mildly or moderately atrophic tubules
Up to 25% interstitial inflammation with any degree of tubulitis
More than 25% interstitial inflammation and 1 to 4 lymphocytes/tubular cross section
Considered suspicious for acute TCMR
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