Plasma cell densities and glomerular filtration rates predict renal allograft outcomes following acute rejection Journal Article

Authors: Chang, A; Moore, J. M.; Cowan, M. L.; Josephson, M. A.; Chon, W. J.; Sciammas, R.; Du, Z.; Marino, S. R.; Meehan, S. M.; Millis, M.; David, M. Z.; Williams, J. W.; Chong, A. S.
Article Title: Plasma cell densities and glomerular filtration rates predict renal allograft outcomes following acute rejection
Abstract: The contribution of T cells and graft-reactive antibodies to acute allograft rejection is widely accepted, but the role of graft-infiltrating B and plasma cells is controversial. We examined 56 consecutive human renal transplant biopsies classified by Banff schema into T-cell-mediated (N = 21), antibody-mediated (N = 18), and mixed (N = 17) acute rejection, using standard immunohistochemistry for CD3, CD20, CD138, and CD45. In a predominantly African-American population (75%), neither Banff classification nor C4d deposition predicted the return to dialysis. Immunohistochemical analysis revealed CD3(+) T cells as the dominant cell type, followed by CD20(+) B cells and CD138(+) plasma cells in all acute rejection types. Using univariate Cox Proportional Hazard analysis, plasma cell density significantly predicted graft failure while B-cell density trended toward significance. Surprisingly T-cell density did not predict graft failure. The estimated glomerular filtration rate (eGFR) at diagnosis of acute rejection also predicted graft failure, while baseline eGFR >/=6 months prior to biopsy did not. Using multivariate analysis, a model including eGFR at biopsy and plasma cell density was most predictive of graft loss. These observations suggest that plasma cells may be a critical mediator and/or an independently sensitive marker of steroid-resistant acute rejection.
Journal Title: Transplant international : official journal of the European Society for Organ Transplantation
Volume: 25
Issue: 10
ISSN: 1432-2277; 0934-0874
Publisher: European Society for Organ Transplantation  
Journal Place: England
Date Published: 2012
Start Page: 1050
End Page: 1058
Language: eng
Notes: LR: 20150224; CI: (c) 2012 The Authors. Transplant International (c) 2012; GR: R01 AI083452/AI/NIAID NIH HHS/United States; GR: R01AI083452/AI/NIAID NIH HHS/United States; GR: R03AI069284/AI/NIAID NIH HHS/United States; GR: R56 AI043631/AI/NIAID NIH HHS/United States; GR: UL1 RR024999/RR/NCRR NIH HHS/United States; JID: 8908516; 0 (Antigens, CD20); 0 (Antigens, CD3); 0 (Peptide Fragments); 0 (Syndecan-1); 80295-50-7 (Complement C4b); 80295-52-9 (complement C4d); NIHMS389104; OID: NLM: NIHMS389104; OID: NLM: PMC3439557; 2012/07/17 [aheadofprint]; ppublish