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

Authors:
Anthony Chang
Anthony Chang
University of Chicago
United States
Michelle L Cowan
Michelle L Cowan
University of Colorado
Boulder | United States
Michelle A Josephson
Michelle A Josephson
University of Chicago
Chicago | United States
Roger Sciammas
Roger Sciammas
University of Chicago
United States
Zeying Du
Zeying Du
UCLA Immunogenetics Center
Los Angeles | United States
Susana R Marino
Susana R Marino
University of Chicago Medicine

Transpl Int 2012 Oct 17;25(10):1050-8. Epub 2012 Jul 17.

Departments of Pathology, University of Chicago Medical Center, Chicago, IL 60637, USA.

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.

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http://dx.doi.org/10.1111/j.1432-2277.2012.01531.xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439557PMC

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October 2012
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