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Kidney Allograft Inflammation and Fibrosis, Causes and Consequences
Author(s) -
Gago M.,
Cornell L. D.,
Kremers W. K.,
Stegall M. D.,
Cosio F. G.
Publication year - 2012
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2011.03911.x
Subject(s) - medicine , fibrosis , inflammation , subclinical infection , kidney , kidney transplantation , biopsy , chronic allograft nephropathy , gastroenterology , pathology , urology
This study assessed the development of allograft interstitial fibrosis and inflammation (GIF+“i”), a histologic pattern associated with reduced graft survival. Included are 795 adults, recipients of kidney allografts from 2000 to 2006. GIF+“i” was diagnosed in surveillance and clinical biopsies that had no transplant glomerulopathy. With time, posttransplant increasing number of grafts showed GIF+“i” and these patients had reduced death‐censored graft survival (HR = 4.33 (2.49–7.53), p < 0.0001). Development of GIF+“i” was related to prior acute cellular rejection (ACR), BK nephropathy (PVAN), increasing number of HLA mismatches, retransplantation and DGF. However, 46.4% of GIF+“i” cases had no history of ACR or PVAN. Anti‐HLA antibodies at transplant did not relate to GIF+“i” and these patients had no increased frequency of new antibody formation posttransplant. Post‐ACR biopsies showed that GIF+“i” developed more commonly after clinically and/or histologically more severe ACR. Graft inflammation persisted in 38.7 and 29.6% of grafts 2 and 12 months post‐ACR. Twelve months post‐ACR, 27.1% of biopsies developed moderate‐severe GIF and 51.8% showed GIF and inflammation. Persistent inflammation and progressive GIF is often subclinical but may lead to graft failure. GIF+“i” can be initiated by multiple etiologies but it is often postinfectious or due to persistent cellular immune‐mediated injury.