scholarly journals Antibody-mediated rejection as a contributor to previously unexplained early liver allograft loss

2014 ◽  
Vol 20 (2) ◽  
pp. 218-227 ◽  
Author(s):  
Jacqueline G. O'Leary ◽  
Hugo Kaneku ◽  
Anthony J. Demetris ◽  
John D. Marr ◽  
S. Michelle Shiller ◽  
...  
Nephron ◽  
2020 ◽  
pp. 1-5
Author(s):  
Takahiro Tsuji ◽  
Sari Iwasaki ◽  
Keishi Makita ◽  
Teppei Imamoto ◽  
Naomichi Ishidate ◽  
...  

<b><i>Aim:</i></b> Chronic active antibody-mediated rejection (CAABMR) is an important cause of late-stage renal allograft loss. Early inflammatory events such as acute rejection and infection after transplantation are considered to be the risk factors of de novo donor-specific antibody (dnDSA) production. In this study, we investigated the relationship between pre­disposing T-cell-mediated rejection and dnDSA-positive CAABMR. <b><i>Methods:</i></b> We recruited 365 patients who underwent ABO-compatible renal transplantation at our hospital. Among them, 16 patients diagnosed as having dnDSA-positive CAABMR were designated as a CAABMR group, and 38 randomly selected patients were designated as a control group. All biopsies from 1 month after transplantation were included in the study. The presence or absence of borderline changes (BLCs), acute T-cell-mediated rejection (ATMR), microvascular inflammation (MVI), and C4d positive on peritubular capillaries (C4d-P) was examined. <b><i>Results:</i></b> In the CAABMR group, BLC/ATMR was found in 12 cases (75%), and the mean duration until appearance of BLC/ATMR was 282.7 ± 328.7 days. C4d-P was found in 11 cases (68.8%), and the mean duration until its appearance was 1,432 ± 1,307 days. MVI was found in all cases, and the mean duration until its appearance was 1,333 ± 1,126 days. The mean duration until diagnosis of CAABMR was 2,268 ± 1,191 days. In the control group, BLC/ATMR was found in 13 cases (34.2%), and the mean duration until the appearance of BLC/ATMR was 173.1 ± 170.4 days. C4d-P was found in 2 cases (5.3%), and the durations until its appearance were 748 and 1,881 days. No cases of MVI were found in the control group. The frequency of BLC/ATMR was significantly higher in the CAABMR group (<i>p</i> &#x3c; 0.01). <b><i>Conclusion:</i></b> Preceding BLC/ATMR is associated with the development of CAABMR with dnDSA.


2016 ◽  
Vol 16 (10) ◽  
pp. 2816-2835 ◽  
Author(s):  
A. J. Demetris ◽  
C. Bellamy ◽  
S. G. Hübscher ◽  
J. O'Leary ◽  
P. S. Randhawa ◽  
...  

2012 ◽  
Vol 26 (1) ◽  
pp. 62-69 ◽  
Author(s):  
Sharif Ali ◽  
Adrian Ormsby ◽  
Veena Shah ◽  
Maria C. Segovia ◽  
Kristin L. Kantz ◽  
...  

2015 ◽  
Vol 15 (2) ◽  
pp. 489-498 ◽  
Author(s):  
B. J. Orandi ◽  
E. H. K. Chow ◽  
A. Hsu ◽  
N. Gupta ◽  
K. J. Van Arendonk ◽  
...  

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0249934
Author(s):  
Dominique Bertrand ◽  
Rangolie Kaveri ◽  
Charlotte Laurent ◽  
Philippe Gatault ◽  
Maïté Jauréguy ◽  
...  

De novo donor-specific antibodies (dnDSA) are associated with antibody-mediated rejection (ABMR) and allograft loss. We tested Immucor* (IM) Luminex Single-antigen beads (LSAB) assay and C3d-fixing antibodies in the setting of dnDSA and subclinical (s) ABMR. This retrospective multicentric study included 123 patients biopsied because of the presence of subclinical de novo DSA detected by One Lamda* Labscreen (MFI > 1000). In 112 patients, sera of the day of the biopsy were available and tested in a central lab with IM Lifecodes LSAB and C3d fixing antibodies assays. In 16 patients (14.3%), no DSA was detected using Immucor test. In 96 patients, at least one DSA was determined with IM. Systematic biopsies showed active sABMR in 30 patients (31.2%), chronic active sABMR in 17 patients (17.7%) and no lesions of sABMR in 49 KT recipients (51%). Intensitity criteria (BCM, BCR and AD-BCR) of DSA were not statistically different between these 3 histological groups. The proportion of patients with C3d-fixing DSA was not statistically different between the 3 groups and did not offer any prognostic value regarding graft survival. Performing biopsy for dnDSA could not be guided by the intensity criteria of IM LSAB assay. C3d-fixing DSA do not offer added value.


Author(s):  
David N. Rush ◽  
Peter W. Nickerson

Rejection of the transplanted kidney is an important cause of graft loss despite modern cross-matching techniques and immunosuppressive agents. The incidence of acute rejection episodes in the first post-transplant year is down to less than 15% in low-risk recipients, but as many as one-third of allograft losses over 10 years result from alloimmunity. Rejection may occur at any time following transplantation, from minutes—hyperacute, to days—acute, or in the longer term—chronic. Rejection can be predominantly through either T-cell-mediated or antibody-mediated mechanisms. It may present clinically as either abrupt or insidious dysfunction of the graft, or it may be subclinical and thus silent, detected only by protocol biopsy or other technology. The prevention and treatment of T-cell-mediated rejection is usually successful with current immunosuppressive agents. Antibody-mediated rejection, on the other hand, is not easily treated and is the principal cause of late renal allograft loss. This chapter presents the concepts and details of this central issue in clinical transplantation.


2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
C. Lefaucheur ◽  
D. Viglietti ◽  
M. Mangiola ◽  
A. Loupy ◽  
A. Zeevi

The purpose of the present review is to describe how we improve the model for risk stratification of transplant outcomes in kidney transplantation by incorporating the novel insights of donor-specific anti-HLA antibody (DSA) characteristics. The detection of anti-HLA DSA is widely used for the assessment of pre- and posttransplant risks of rejection and allograft loss; however, not all anti-HLA DSA carry the same risk for transplant outcomes. These antibodies have been shown to cause a wide spectrum of effects on allografts, ranging from the absence of injury to indolent or full-blown acute antibody-mediated rejection. Consequently, the presence of circulating anti-HLA DSA does not provide a sufficient level of accuracy for the risk stratification of allograft outcomes. Enhancing the predictive performance of anti-HLA DSA is currently one of the most pressing unmet needs for facilitating individualized treatment choices that may improve outcomes. Recent advancements in the assessment of anti-HLA DSA properties, including their strength, complement-binding capacity, and IgG subclass composition, significantly improved the risk stratification model to predict allograft injury and failure. Although risk stratification based on anti-HLA DSA properties appears promising, further specific studies that address immunological risk stratification in large and unselected populations are required to define the benefits and cost-effectiveness of such comprehensive assessment prior to clinical implementation.


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