The 2024 Banff meeting was from September 16-20 in Paris. We solicited the below input from the international transplant community to guide in-person discussions.
Note: The full meeting program and registration information can be found here: https://site.pheedloop.com/event/2024BanffPITOR/home)*
*some final changes to session and presentation titles might occur
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For the cumulative Banff activity index, consideration could be given to replacing the Banff i score with the total inflammation (ti) score, in order to capture all active interstitial inflammatory infiltrates in the biopsy, including both the non-scarred (i) and scarred areas (i-IFTA).
Chronic irreversible glomerular damage in renal allografts biopsies is not adequately represented by the present chronic Banff scores (cg, mm).
Non-specific irreversible chronic glomerular damage is common in late post-Tx allograft biopsies, but in the absence of Tx glomerulopathy will not be evident from the Banff scores alone.
Global glomerulosclerosis, focal segmental glomerulosclerosis, chronic ischemic glomerulopathy with periglomerular fibrosis and ischemic capillary tuft contraction, and probable atubular glomeruli with severe tuft contraction and detached podocytes in a cystically expanded Bowman’s space, are all easily quantified in renal allograft biopsies.
A quantitative chronic glomerular Banff score, which could be abbreviated as Banff gs (for glomerulosclerosis) would be easily scored based on the percentage of glomeruli showing these chronic lesions.
Banff gs1: <25% of glomeruli affected by global glomerulosclerosis, FSGS and chronic ischemic glomerulopathy.
Banff gs2: 25-50% of glomeruli affected by global glomerulosclerosis, FSGS and chronic ischemic glomerulopathy.
Banff gs3: >50% of glomeruli affected by global glomerulosclerosis, FSGS and chronic ischemic glomerulopathy.
Given the move towards adding activity and chronicity indices in renal allograft biopsies to the Banff-mandated pathology reporting, a chronic glomerular Banff score representative of the extent of irreversible chronic glomerular damage may add further granularity and prognostic relevance to a cumulative chronicity index.
Thanks for a great Banff 2024. Ian
We should recognize that recurrent disease may (often does) look different on biopsy in the transplant compared to the native kidney, and patients have different clinical presentations with recurrent disease compared to the native kidney. Should we use the same classification systems for the transplant as for the native kidney (if they exist), or do we need to develop new systems, or is that not even needed? How do those features interact with rejection phenotypes and other diseases that are relatively specific to transplants (eg, CNI toxicity)?
What should be standard practice for monitoring for recurrent or de novo glomerular disease? Should patients with a history of glomerulonephritis get surveillance biopsies, and if so at what times post transplant, and is this different depending on the native kidney disease (eg, if a disease tends to recur early versus late, if a disease could respond to treatment)?
One way to prevent confusing the features of recurrent GN with rejection (when the hx of ESKD is not available) is to do an upfront full panel IF for all transplant cases. Considering the cost and low yield of full IF especially for early transplant biopsies, is it recommended at all to do routine IF panel on all transplant cases? and if yes, how early post transplant? Thank you,
Will you review any evidence that recurrent GNs present with transplant specific pathology?