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In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients
Published on: August 12, 2017
The Diversity of Transplant Glomerulitis and its Relationship to Alloantibody
Brian J Nankivell1, Seethalakshmi Viswanathan2, Xinyi Ding3
1Department of Renal Medicine, Westmead Hospital, Sydney, New South Wales, Australia.
Introduction:
Although transplant glomerulitis often signifies antibody-mediated rejection (AMR), the pathophysiology of complement degradation split-product 4d (C4d) staining of peritubular capillaries (C4dptc) and donor-specific antibodies (DSAs) negative cases is unclear.
Methods:
We compared Banff 1997 defined glomerulitis (n = 271, from 4300 biopsies) using serological and pathological dichotomization, against rejection without glomerulitis (g0REJ, n = 612) and normal controls (NIL, n = 1442).
Results:
Epidemiological risk factors were female recipients, living donation, early T-cell-mediated rejection (TCMR) or AMR, and previous corticosteroid rejection treatment. Glomerulitis associated with sensitization in 38.0%, ischemic endothelial injury in 20.7%, iatrogenic minimization in 30.3%, and nonadherence in 21.4%. Banff g score correlated with DSA+, C4dptc+, endothelial C4d staining of glomerular capillaries positive (C4dglom+), Banff cg, i, t, ti scores, serum creatinine, and proteinuria. DSA+ glomerulitis was typified by inflammation, chronic scarring, C4d+, later presentation, treatment resistance, and functional deterioration (P < 0.001 vs. DSA-). DSA- glomerulitis from CD3+ TCMR (pure 43.3% and mixed 28.7% with AMR) presented earlier with excellent graft outcomes. C4dptc- glomerulitis was etiologically classified TCMR in 36.8%, pure AMR in 28.1%, and mixed AMR in 31.3%. Isolated glomerulitis in 20.3% was diagnosed by surveillance sampling in 70.9%, displayed CD3+ in 51.9% and a distinct but minimal spatial transcriptomic phenotype, with superior allograft outcomes compared with glomerulitis with inflammation. Kidneys with glomerulitis and g0REJ failed more frequently than normal control samples (P < 0.001). Graft survival was independently determined by DSA+, C4dptc+, transplant glomerulopathy, and chronic interstitial fibrosis using multivariable Cox regression, but not by glomerulitis score.
Conclusion:
Glomerulitis is a heterogenous biological lesion that frequently signifies AMR, however TCMR or innate cellular inflammation caused many DSA- and/or C4dptc- episodes.
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