|Year : 2020 | Volume
| Issue : 3 | Page : 189-196
An approach to allograft renal biopsy interpretation for the beginner- A narrative review
Department of Histopathology, Apollo Hospitals, Hyderabad, Telangana, India
|Date of Submission||09-Apr-2020|
|Date of Acceptance||05-Aug-2020|
|Date of Web Publication||30-Sep-2020|
Dr. Swarnalata Gowrishankar
Department of Histopathology, Apollo Hospitals, Jubilee Hills, Hyderabad - 500 096, Telangana
Source of Support: None, Conflict of Interest: None
Allograft renal biopsy remains the gold standard for diagnosing many conditions in the transplant recipient including rejections, infections, recurrent, and de-novo renal disease. The Banff schema of reporting is followed worldwide in arriving at the right diagnosis. The guidelines, the categories, and the Banff scores in this schema are constantly evolving and this has made the interpretation of the biopsy seem complex and difficult especially for the novice. In this review, a detailed description of the various patterns of injury specific to the graft, the Banff categories of diagnoses, the lesions, and the Banff scores are simplified and explained. Lastly, a systematic approach to these allograft biopsies, which can be followed in regular practice, and by which a tentative diagnosis can be made in most cases is laid out.
Keywords: Allograft renal biopsy, Banff, rejection
|How to cite this article:|
Gowrishankar S. An approach to allograft renal biopsy interpretation for the beginner- A narrative review. Indian J Transplant 2020;14:189-96
| Introduction|| |
Allograft renal biopsy interpretation remains the gold standard for diagnosing many conditions in the graft, including rejection, infections, recurrent, and de-novo disease among other conditions. However, the interpretation of the findings may be a little confusing and difficult for the beginner and this review attempts to simplify the approach to the light microscopic diagnosis of an allograft renal biopsy. Immunofluorescence (IF) and Electron Microscopy (EM) study are beyond the purview of this review
| How Is the Interpretation of an Allograft Biopsy Different from That of a Native Kidney Biopsy?|| |
There is no basic difference. However, as the lesions in an allograft include conditions mentioned above which are peculiar to the graft, injury patterns pertaining to these conditions need to be given importance. It should be kept in mind that all conditions affecting the native kidney can affect the graft as de novo conditions. Allograft biopsies are also peculiar in that there may be more than one condition affecting the graft, for example, rejections and concurrent recurrent disease.
The important broad categories of diagnoses in an allograft biopsy are:
- Rejections – acute/active and chronic, T-cell mediated, antibody mediated, or a combination
- Drug toxicity
- Recurrent disease
- De novo renal disease
| Methodology|| |
The Banff classification and Banff scores
Search of literature was done using words “Banff meeting”, “Allograft renal biopsy” and “rejection”. The first international conference on renal allograft pathology was held in the city of Banff, Canada in 1991, and subsequent meetings were held once in 2 years across the world. As a result of consensual discussions of all stakeholders at these meetings and correspondence between the meetings, the categories, the classification and criteria including Banff scores for diagnoses are constantly evolving. These meetings have also extended their activities to training programs and Banff working groups.,,,,,,,,,,,,,, The article is based on consensus from Banff meetings including the 2019 update.
| Results|| |
An algorithm for interpretation of renal allograft biopsies emerges from a study of the Banff meeting proceedings. This approach and algorithm are simplified and a systematic approach to the allograft renal biopsy is detailed in the Discussion which follows.
| Discussion|| |
Adequacy of the biopsy
Ten glomeruli and two arteries are considered adequate. It should be remembered that even in suboptimally sized biopsies, a diagnosis is often possible. The presence of medulla alone could help in the diagnosis of polyoma virus nephropathy (PVN) and C4d positivity. Every attempt should be made to give a diagnosis notwithstanding the size of the biopsy.
Processing of the allograft biopsy
This is similar to the native biopsy. Serial sections for hematoxylin and eosin (HE), periodic acid-Schiff (PAS), Jones and Trichrome stains need to be studied in all. A C4d stain either by immunohistochemistry or IF is mandatory. Routine IF is also mandated in all cases with proteinuria or with suspected recurrent disease. For these categories, an EM study also adds value.
A systematic approach to the allograft biopsy
The four compartments, namely the glomeruli, tubules, interstitium, and vessels need to be studied systematically, and the important patterns of injury in each of these compartments are listed below.
| Glomeruli|| |
This can be segmental or global, the former being more common. This is manifest as swelling of the endothelial cells and a mononuclear or a neutrophilic infiltrate, the former being more common obliterating the capillary lumina [Figure 1]a and [Figure 1]b.
|Figure 1: (a) Segmental glomerulitis at 9'o clock position with neutrophils obliterating the capillary lumina. (b) Segmental glomerulitis with swelling of endothelium and lymphomononuclear cells at the 5'o clock position. (c) Transplant glomerulopathy with duplication and double contours of the glomerular basement membranes in several segments. (d) Transplant glomerulopathy with duplication of the glomerular basement membranes and glomerulitis|
Click here to view
These can be platelet or fibrin rich, within the capillary lumina. When fibrin rich, it is PAS positive and red on the trichrome. This can be accompanied by neutrophils and is then a clue to active antibody-mediated rejection (ABMR).
Basement membrane thickening and duplication. This again may be segmental or more widespread and best appreciated on the Jones silver stain. It must be emphasized that the duplication in even a single segment constitutes transplant glomerulopathy [Figure 1]c and [Figure 1]d.
| Tubules|| |
Dilatation, loss of brush border, flattening and denudation of the lining and presence of casts all constitute tubular injury. This can be of varying severity and may also be subtle with just apical blebbing of the brush border being an early sign.
Tubular lining cells
Fine isometric vacuoles are a sign of acute calcineurin inhibitor (CNI) toxicity, whereas larger coarse vacuoles could indicate osmotic nephrosis (has been reported with intravenous immunoglobulin infusions) or even hypokalemic nephropathy.
The cytopathic changes in PVN include nuclear enlargement, smudgy nuclei, intranuclear clearing, and cytomegalovirus (CMV) like nucleolar inclusions. Note that regenerative tubules in acute tubular injury can have enlarged nuclei. The index of suspicion for PVN needs to high and the threshold for ordering an SV40 immune stain low, so that a diagnosis of PVN can be confirmed [Figure 2]a,[Figure 2]b,[Figure 2]c.
|Figure 2: (a) Polyoma virus nephropathy – tubular lining cells having ground-glass type intranuclear inclusions. (b) Tubular lining cells having nucleolar like inclusion and an apoptotic cast is seen in the lower left in polyoma virus nephropathy. (c) SV 40 immunohistochemistry highlighting the positive nuclei in polyoma virus nephropathy. (d) Cytomegalovirus inclusion (at the pointer) – large with owl-eye nuclear inclusion and reddish smudged appearance of the cytoplasm|
Click here to view
The cytopathic changes in CMV, in contrast to PVN affect the tubular lining cells, the interstitial fibroblasts, the endothelium, and even the glomerular cells. The cells are typically large with prominent eosinophilic intranuclear inclusions and the cytoplasm also has smudged purple hue on the HE stain [Figure 2]d. A CMV IHC will help confirm the diagnosis.
Adenoviral infections also have similar enlarged smudged nuclei in the tubules. The infection is more common in the first 3 months posttransplant. On the biopsy, in addition to the cytopathic changes, which can be confirmed by an IHC stain, there is associated prominent hemorrhagic tubulo-interstitial nephritis simulating cortical necrosis, with surrounding inflammation including neutrophils and histiocytes forming ill-defined granulomas.
Granular casts could occur in tubular injury.
Refractile oxalate casts are a strong suspicion of recurrent hyperoxaluria. Attention to the details of the native kidney disease will help confirm the diagnosis. The recurrences are very early, and the biopsy may show just a few oxalate casts.
If the casts are refractile and brown, a 2,8 dyhydroxyadenine crystalluria due to an underlying deficiency of APRT enzyme would be the diagnosis.
Neutrophilic casts indicate an ascending infection, and urine culture studies are advised.
Casts with necrotic apoptotic cells with smudgy nuclei are a clue to PVN [Figure 2]b.
This finding in association with interstitial inflammation indicates a T-cell-mediated rejection (TCMR). Tubulitis is recognized by the presence of lymphocytes between the tubular lining cells or between the lining and the basement membrane. Hence, it is best recognized on the PAS stain. Note that tubulitis in very atrophic tubules, defined as tubules with a diameter of <25% of a normal tubule needs to be disregarded. Tubulitis is graded according to the maximum number of lymphocytes in a tubular cross section or in 10 consecutive lining cells when the tubule is cut longitudinally [Figure 3]a,[Figure 3]b,[Figure 3]c,[Figure 3]d. The maximum number is taken for grading. In practice, there should be more than one focus of tubulitis to be given a grade. Hence, just a single tubule with lymphocytes should prompt one to look at more tubules in serial sections before assigning a grade.
|Figure 3: (a) Normal – no lymphocyte with a tubule. (b) Mild tubulitis: 2 lymphocytes within a tubule. (c) Moderate tubulitis: A cluster of up to 6 lymphocytes between the tubular cells. (d) Severe tubulitis with >10 lymphocytes within the tubular basement membrane|
Click here to view
These are recognized as small tubules with a thickened basement membrane with interstitial widening and fibrosis, best recognized on the PAS and the silver stains. The grading is according to the approximate percentage of cortex involved, estimated by eyeballing. Tubular atrophy and interstitial fibrosis go hand-in-hand [Figure 4]a,[Figure 4]b,[Figure 4]c,[Figure 4]d.
|Figure 4: Interstitial fibrosis and tubular atrophy: These two usually go hand-in-hand. (a) (periodic acid-Schiff) and (b) (trichrome) show moderate interstitial fibrosis and tubular atrophy, involving roughly a third of the cortex in this figure with the area being outlined (c) (periodic acid-Schiff) and (d) (trichrome) stains depict a case with diffuse involvement i3, t3 (>50%)|
Click here to view
| Interstitium|| |
Normally, the renal tubules are back-to-back and any separation of the tubules with a widening of the interstitium is abnormal. This widening may be due to edema or fibrosis.
In edema, the space is loose, fibrillary, or vacuolated and pale blue on the trichrome stain. In fibrosis, the space is more densely stained on HE and PAS and has a darker blue stain on trichrome, the latter stain being the most useful for assessing fibrosis. Fibrosis is also accompanied by tubular atrophy as mentioned above [Figure 4]a,[Figure 4]b,[Figure 4]c,[Figure 4]d.
The grading of inflammation is based on the percentage area of the cortex occupied by inflammatory cells, estimated by eyeballing. For the “i” score, it is the nonscarred cortex [Figure 5]a and [Figure 5]b, for the “ti” score, the total cortex and for the “i-IFTA score,” the cortex around atrophic tubules.
|Figure 5: (a) Mild interstitial inflammation (i1) About 15%–20% of the cortex occupied by inflammatory cells (b) Severe interstitial inflammation (i3) – A blue infiltrate of lymphoid cells scattered and in aggregates occupying >50% of the cortex|
Click here to view
Lymphocytes are the most common, scattered, or in aggregates and considered significant when they occupy more than 10% of the nonscarred cortex.
Eosinophils and plasma cells can accompany the lymphocytes and are considered significant when they form more than 10% of the infiltrating cells.
A plasma cell-rich infiltrate could indicate a PVN, and it may be a good policy to have a SV40 IHC in these cases.
A neutrophil-rich infiltrate, especially when accompanied by neutrophilic casts, is indicative of a pyogenic infection.
Sheets of histiocytes or even ill-defined granulomas are the manifestation of tuberculosis or fungal infections, which can be confirmed by demonstrating the organisms in special stains for acid-fast bacilli and fungal elements. Small inconspicuous granulomas have also been reported in drug toxicity. The presence of a granuloma warrants a search for infection notably tuberculosis and fungal infection.
| Blood Vessels|| |
The important changes in the vasculature which need to be noted in an allograft are:
The presence of lymphocytes and/or neutrophils within the lumina of peritubular capillaries which are thin-walled inconspicuous capillaries between the tubules, best seen in the PAS stain [Figure 6].
|Figure 6: Peritubular capillaritis: Many peritubular capillaries dilated and engorged with lymphocytes|
Click here to view
Changes are conspicuous in the arterioles and small vessels including the hilar vessels. Fibrin thrombi occluding their lumen, fibrinoid deposits and schistocytes or fragmented RBCs in the wall, intimal myxoid change, myointimal hyperplasia and onion-skinning constitute the spectrum of changes in thrombotic microangiopathy (TMA) [Figure 7]a,[Figure 7]b,[Figure 7]c. Fibrin is appreciated on all stains, whereas schistocytes and intimal myxoid change are easily recognized on the HE stain. The etiology of TMA in an allograft biopsy include active ABMR, acute CNI toxicity, de-novo (may be secondary to infections like CMV), and recurrent hemolytic uremic syndrome (due to an underlying defect of the alternate complement pathway).
|Figure 7: Thrombotic microangiopathy. (a) Fibrin thrombi are seen obliterating the capillary lumina of the glomerulus as well as the lumina of two small arterioles on the left. (b) Fibrinoid deposits and schistocytes in the wall and intimal myxoid change imparting a blue tinge on hematoxylin and eosin stain. (c) This is concentric myointimal hyperplasia or onion skinning|
Click here to view
In contrast to fibrin, hyalinosis is homogeneous smooth eosinophilic, PAS positive, silver negative and bluish red on trichrome stain. This may be intimal or peripheral, circumferential or noncircumferential. Peripheral nodular hyalinosis secondary to smooth muscle degeneration is the lesion described in cyclosporine toxicity, and this is coded as aah in the Banff scores [Figure 8]a and [Figure 8]b.
|Figure 8: Arteriolar hyalinosis. (a) There is marked circumferential homogeneous periodic acid-Schiff positivity with a faint nodular pattern. (b) The arteriole marked shows faint early peripheral nodular hyalinosis|
Click here to view
This is the presence of lymphocytes under the endothelium of arteries with lifting and usually a swelling of the overlying endothelium [Figure 9]a. Even a single lymphocyte under the endothelium is significant. As endarteritis progresses, there is an obliteration of the lumen and in severe cases, transmural inflammation and necrosis are evident. Endarteritis may be seen in arterioles, and this is indicated by an asterisk under hyalinosis lesion.
|Figure 9: (a) Endarteritis. The endothelium is lifted off with few lymphocytes under it, beginning to occlude the lumen. (b) Transplant arteriopathy: There is prominent intimal fibrosis with inflammatory cells, partially occluding the lumen. The above two lesions can be seen in T-cell-mediated rejection and antibody-mediated rejection|
Click here to view
There is normally no space between the intima and media of renal arteries. When this is so, it is intimal fibrosis and can be accompanied by the duplication of the internal elastic lamina when due to hypertension. Intimal fibrosis without elastosis and with lymphocytes and/or histiocytes away from the intima is transplant arteriopathy and more likely to reflect chronic rejection, T-cell, or antibody mediated [Figure 9]b.
| Banff Scores|| |
The Banff lesions, definitions, and scores are elaborated in [Table 1].
| Banff Categories|| |
The Banff categories and the criteria for the diagnosis (based on 2017 Banff update).
Category I: When the biopsy is normal or the changes are nonspecific and do not fit into any of the categories below.
Category II: ABMR: This can be active, chronic active, or chronic. For each of the above, there are three sets of criteria and at least one criterion from each set needs to be fulfilled to give a definitive diagnosis.
Active ABMR: Note the terminology in ABMR is active whilst that in TCMR is acute for the reason that ABMR is not always acute in presentation.
- Criteria 1: Evidence of injury mediated by antibody, which can be in the form of:
- Microvascular inflammation, namely glomerulitis and/or peritubular capillaritis
- Endarteritis (Note: endarteritis can also be seen in TCMR)
- TMA, in the absence of other cause
- Tubular injury, in the absence of other cause
- Criteria 2: Evidence that the injury was indeed mediated by antibody
- C4d positivity by IF or IHC (Note: As IF is more sensitive, a score of >0 is considered positive on IHC and a score >1 for IF)
- Moderate microvascular inflammation (g + ptc score ≥2 with none being 0). Note: This criterion can be used when C4d is negative, but there should be no evidence of recurrent or de-novo disease, borderline or acute TCMR, or infection
- Increased expression of genes which are upregulated in ABMR. This should be a validated assay. Note: These assays are RNA-based assays on renal biopsies and for practical purposes, there is no laboratory in India which offers a validated assay at the present
- Criteria 3: Demonstration of the antibody
- Donor-specific antibody (DSA). This can be anti-HLA or non-HLA antibodies directed against the graft
- C4d positivity. As C4d positivity is a very strong indicator of the presence of antibody at the site of reaction, the requirement for checking for DSA has been dispensed with, when C4d is positive
- Increased expression of validated gene transcripts (if this test is available and increased expression of a set of validated genes demonstrated, then ABMR can be diagnosed even if C4d and DSA are negative)
Chronic active ABMR: Here, the injury is presumed to be due to persistent antibodies and the pattern of injury chronic and different from that in active ABMR. Criteria 2 and 3 remain the same as above.
Criteria 1: Evidence of chronic injury mediated by antibodies, which can be in the form of
- Transplant glomerulopathy, by LM or IF, by light microscopy (LM) or EM. Cases of chronic TMA due to other causes are excluded.
- Peritubular capillary basement membrane multilayering, demonstrated on EM (7 or more layers in one capillary and 5 or more layers in two more).
- Arterial intimal fibrosis of new onset
Criteria 2: Same as above
Criteria 3: Same as above
Note: In practice, a C4d negative ABMR (active or chronic active) diagnosis is made when the histologic changes are present but C4d is negative and DSA is positive at the time of biopsy.
Chronic ABMR (no active in the name). This diagnosis can be made when there is evidence of chronic injury (criteria 1 of chronic active ABMR above), negative C4d, with a prior documented diagnosis of active/chronic active ABMR or a prior DSA positivity.
Category III: Suspicious (borderline) for acute TCMR.
This is diagnosed when there is interstitial inflammation and tubulitis line 18: (t≥1 and i≥1) but the minimum criteria of acute TCMR (namely at least i2 and t2) are not met.
Note: If the Banff 2005 guidelines are followed (and that should be mentioned in the report) t > 0 and i ≤ 1is permitted. A minimum score of i1 is required for borderline category according to the 2019 update.
This diagnosis is often met with skepticism by the nephrologist as it does not help in the management. Oftentimes, however, a discussion with the nephrologist, the clinical correlation and the presence of activated “angry looking” lymphoid cells could help one favor rejection. Borderline changes may also be seen when the biopsy is done soon after or during a course of antirejection therapy.
Category IV: TCMR. This can be acute or chronic active. Chronic TCMR unlike chronic ABMR is not diagnosed.
Acute TCMR: This is graded into Type I (A and B) and Type II. The presence of endarteritis will upgrade the rejection to type II irrespective of the grade of interstitial inflammation and tubulitis
- IA: Interstitial inflammation (i2 or i3) and moderate tubulitis (t2)
- IB: Interstitial inflammation (i2 or i3) and severe tubulitis (t3)
- IIA: Any grade of interstitial inflammation and tubulitis with mild endarteritis (v1)
- IIB: Any grade of interstitial inflammation and tubulitis with moderate endarteritis (v2)
- III: Any grade of interstitial inflammation and tubulitis with severe transmural arteritis (v3).
Isolated 'v' lesions: This refers to the presence of endarteritis without tubulo-interstitial inflammation. This can be considered as ABMR when C4d positive and TCMR when the diagnostic criteria for ABMR are not met.
Chronic active T-cell-mediated rejection
- Grade IA: Total inflammation at least moderate (ti ≥ 2), moderate inflammation in atrophic areas (iIFTA ≥ 2) and moderate tubulitis (t2)
- Grade IB: Total inflammation at least moderate (ti ≥ 2), moderate inflammation in atrophic areas (iIFTA ≥ 2), and severe tubulitis (t3).
- Grade II: Presence of transplant arteriopathy.
Category V: interstitial fibrosis, tubular atrophy (IFTA) This is divided into mild (ci1 and/or ct1), moderate (ci2 and/or ct2), and severe (ci3 and/or ct3).
Note: An underlying cause for the IFTA needs to be always searched for by correlating with the other histologic, IF and EM findings, clinical details, and other investigations including imaging before a case is diagnosed as IFTA of no special type.
Category VI: All other changes which are considered not rejection are in this category. The important conditions include acute tubular injury, infections including PVN, drug toxicity including that due to CNI, recurrent and de-novo renal disease.
The diagnosis of PVN requires the demonstration of tubular cytopathic changes by LM which should be confirmed by IHC staining using the SV40 antigen. PVN has three grades depending on the percentage of tubules with positive nuclei and the degree of IFTA.
Acute CNI toxicity manifests as TMA, tubular necrosis, and isometric vacuolization of the tubular lining cells. Late toxicity is suspected with medial and adventitial hyalinosis of the arterioles, intermittent areas of interstitial fibrosis (striped fibrosis), and glomerular and vessel changes of chronic TMA.
Points to consider
The diagnosis should not just mention category but what the category is. For example, the diagnostic line should read “acute T-cell-mediated rejection IA” rather than “Category 4, IA”
Different categories can co-exist. For example, rejection can co-exist with infection, infection can co-exist with recurrent disease and so on.
When the criteria of chronic active and acute TCMR are fulfilled, the grade of chronic and active rejection needs to be separately mentioned. Similarly, in a diagnosis of chronic active ABMR, the severity of chronic and active lesions are mentioned in the diagnostic line to aid in treatment.
Where the criteria for active ABMR are fulfilled, and there is associated interstitial inflammation and tubulitis but not fulfilling the criteria for TCMR, it is best that the diagnostic line reads only ABMR. Having an associated borderline TCMR is unlikely to change the management. If, however, the criteria for an acute TCMR are fulfilled, a diagnosis of a combined active ABMR and an acute TCMR is made.
The categories suspicious for acute/active ABMR, suspicious for chronic ABMR and suspicious for chronic active ABMR mentioned in the Banff 2015 update have now been deleted.
[Table 2] outlines the algorithmic approach to the allograft biopsy.
| Conclusions|| |
A systematic approach with particular emphasis on lesions in the Banff scores and a correlation with the clinical features the other laboratory investigations will lead one to a reasonably accurate diagnosis in most allograft biopsies.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Roufosse C, Simmonds N, Clahsen-van Groningen M, Haas M, Henriksen KJ, Horsfield C, et al
. A 2018 reference guide to the Banff classification of renal allograft pathology. Transplantation 2018;102:1795-814.
Solez K, Axelsen RA, Benediktsson H, Burdick JF, Cohen AH, Colvin RB, et al
. International standardization of criteria for the histologic diagnosis of renal allograft rejection: The Banff working classification of kidney transplant pathology. Kidney Int 1993;44:411-22.
Solez K, Benediktsson H, Cavallo T, Croker B, Demetris AJ, Drachenberg C, et al
. Report of the Third Banff Conference on Allograft Pathology (July 20-24, 1995) on classification and lesion scoring in renal allograft pathology. Transplant Proc 1996;28:441-4.
Racusen LC, Solez K, Colvin RB, Bonsib SM, Castro MC, Cavallo T, et al
. The Banff 97 working classification of renal allograft pathology. Kidney Int 1999;55:713-23.
Racusen LC, Halloran PF, Solez K. Banff 2003 meeting report: New diagnostic insights and standards. Am J Transplant 2004;4:1562-6.
Solez K, Colvin RB, Racusen LC, Sis B, Halloran PF, Birk PE, et al
. Banff '05 Meeting Report: Differential diagnosis of chronic allograft injury and elimination of chronic allograft nephropathy ('CAN'). Am J Transplant 2007;7:518-26.
Solez K, Colvin RB, Racusen LC, Haas M, Sis B, Mengel M, et al
. Banff 07 classification of renal allograft pathology: Updates and future directions. Am J Transplant 2008;8:753-60.
Sis B, Mengel M, Haas M, Colvin RB, Halloran PF, Racusen LC, et al
.. Banff '09 meeting report: Antibody mediated graft deterioration and implementation of Banff working groups. Am J Transplant 2010;10:464-71.
Mengel M, Sis B, Haas M, Colvin RB, Halloran PF, Racusen LC, et al
. Banff 2011 Meeting report: New concepts in antibody-mediated rejection. Am J Transplant 2012;12:563-70.
Haas M, Sis B, Racusen LC, Solez K, Glotz D, Colvin RB, et al
. Banff 2013 meeting report: Inclusion of c4d-negative antibody-mediated rejection and antibody-associated arterial lesions. Am J Transplant 2014;14:272-83.
Solez K, Racusen LC. The Banff classification revisited. Kidney Int 2013;83:201-6.
Loupy A, Haas M, Solez K, Racusen L, Glotz D, Seron D, et al
. The Banff 2015 kidney meeting report: Current challenges in rejection classification and prospects for adopting molecular pathology. Am J Transplant 2017;17:28-41.
Haas M, Loupy A, Lefaucheur C, Roufosse C, Glotz D, Seron D, et al
. The Banff 2017 Kidney Meeting Report: Revised diagnostic criteria for chronic active T cell-mediated rejection, antibody-mediated rejection, and prospects for integrative endpoints for next-generation clinical trials. Am J Transplant 2018;18:293-307.
Liapis H, Gaut JP, Klein C, Bagnasco S, Kraus E, Farris AB 3 rd
, et al
.Banff histopathological consensus criteria for preimplantation kidney biopsies. Am J Transplant 2017;17:140-50.
Solez K. Kim Solez, Edmonton, Alberta, Canada Banff: A unique start setting standards for consensus conferences. Transplantation 2017;101:2264-6.
Loupy A, Haas M, Roufosse C, Naesens M, Adam B, Afrouzian M et al
. The Banff 2019 Kidney Meeting Report (I): Updates on and clarification of criteria for T cell- and antibody-mediated rejection [published online ahead of print,2020 28]. Am J Transplant. 2020;10.1111/ajt. 15898. doi: 10.1111/ajt. 15898
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
[Table 1], [Table 2]