The Pathophysiology and Impact of Inflammation in Nonscarred Renal Interstitium: The Banff i Lesion.

Transplantation
Brian J NankivellJeremy R Chapman

Abstract

Interstitial inflammation (i-INT) is the driver of T-cell-mediated rejection. Its causes, pathophysiology, kinetics, and outcomes are poorly documented. The role of i-INT was evaluated in 2055 biopsies from 775 renal transplant recipients. i-INT was present in 374 (18.2% prevalence) from acute and subclinical rejection (67.4%); interstitial fibrosis and tubular atrophy (14.4%); BK virus nephropathy (BKVAN) 9.9%; and acute tubular necrosis (ATN with i-INT) in 5.9% of cases. i-INT was predicted by prior T-cell-mediated rejection and BKVAN, human leukocyte antigen mismatch, cyclosporine therapy, and indication biopsy for dysfunction. It correlated with tubulitis, arteritis, and antibody markers within concurrent histology (P < 0.001). After treatment, renal functional recovery was best with histological ATN, milder i-INT, and early posttransplant biopsy times. The initial histological improvement of inflammation depended on baseline i-INT severity. Complete resolution to Banff i0 was predicted by early biopsy time, antilymphocyte therapy, recipient age, and medication compliance (all P < 0.001). Clearance i-INT was followed by delayed resolution of tubulitis (P < 0.001). i-INT was associated with histological ATN, renal dysfunctio...Continue Reading

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Citations

Aug 1, 2020·Transplantation·Edward John Filippone, John L Farber
Sep 18, 2021·Journal of the American Society of Nephrology : JASN·Luisa Ricaurte ArchilaAndrew D Rule

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Methods Mentioned

BETA
biopsies
biopsy
PCA

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