scholarly journals The Banff 2019 Kidney Meeting Report (I): Updates on and clarification of criteria for T cell– and antibody‐mediated rejection

2020 ◽  
Vol 20 (9) ◽  
pp. 2318-2331 ◽  
Author(s):  
Alexandre Loupy ◽  
Mark Haas ◽  
Candice Roufosse ◽  
Maarten Naesens ◽  
Benjamin Adam ◽  
...  
2019 ◽  
Vol 70 (1) ◽  
pp. e830
Author(s):  
Anne Höfer ◽  
Danny Jonigk ◽  
Björn Hartleben ◽  
Robert Geffers ◽  
Murielle Verboom ◽  
...  

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.


2020 ◽  
Vol 34 (1) ◽  
pp. S15-S15
Author(s):  
Hyunwook Kwon ◽  
Sung Shin ◽  
Duck Jong Han ◽  
Young Hoon Kim ◽  
Joo Hee Jung ◽  
...  

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Anna Buxeda ◽  
Laura Llinàs ◽  
Javier Gimeno ◽  
Carlos Arias Cabrales ◽  
Carla Burballa Tarrega ◽  
...  

Abstract Background and Aims Antibody-mediated rejection (ABMR) associated with donor-specific HLA antibodies (DSA) is the leading cause of late allograft failure after kidney transplantation. Microvascular inflammation (MVI) without detectable circulating DSA or C4d + cannot be classified as ABMR according to Banff-2017. The involvement of intragraft lymphocyte subsets in the development of humoral damage in kidney transplantation (KT) is relevant. We aimed to analyze lymphocyte subset distribution in kidney transplant biopsies (KTBx) with ABMR compared with MVI and with normal KTBx. Method KTBx with ABMR, MVI (g+ptc≥2, without DSA) or normal findings were included. DSA were identified with Luminex single antigen assays. Intragraft lymphocyte subsets’ characterization was performed by immunohistochemistry: T-lymphocytes (CD3, CD4, CD8, Foxp3), B-lymphocytes / plasmatic cells (CD20, CD138), NK cells (CD56), macrophages / monocytes (CD68), cytotoxic cells (TIA1) and activated cells (PD1) were evaluated. Results We analyzed 34 KTBx: 21 ABMR, 5 MVI and 8 KTBx with normal findings. KT with ABMR and MVI had more proteinuria at the time of the biopsy compared with the normal group (575 mg/24h and 964 mg/24h vs 147 mg/24h, p=0.002 and p=0.005 respectively). DSA were more frequently detected in patients with ABMR (95.2% vs 0% and 37.5%, p&lt;0.001 and p=0.003 respectively). KTBx with ABMR and MVI had increased cytotoxic T-cell infiltration apparently corresponding to NK cells in peritubular capillaries (ptc) compared to normal group. Moreover, both groups showed a greater number of macrophages and monocytes in glomeruli. KT with MVI but not with ABMR had a significantly increased activated cell infiltration (PD1+) in ptc compared to the normal group, and showed an increased cytotoxic T-cell infiltration in glomeruli compared to ABMR and normal groups. Conclusion ABMR and MVI have an increased infiltration of NK cells with cytotoxic activity in ptc that differs from the normal group. However, KT with MVI show greater infiltration of activated cells in ptc and cytotoxic T-cell in glomeruli compared to ABMR suggesting the possibility of different activation pathways.


2010 ◽  
Vol 64 (1) ◽  
pp. 47-53 ◽  
Author(s):  
C. Bellan ◽  
T. Amato ◽  
M. Carmellini ◽  
M. Onorati ◽  
A. D'Amuri ◽  
...  

2015 ◽  
Vol 88 (3) ◽  
pp. 560-568 ◽  
Author(s):  
Kin Y. Shiu ◽  
Laura McLaughlin ◽  
Irene Rebollo-Mesa ◽  
Jingyue Zhao ◽  
Vikki Semik ◽  
...  

1970 ◽  
Vol 2 (3) ◽  
pp. 172-179
Author(s):  
G Aryal ◽  
DS Shah

Background:  Renal allograft biopsy remains the gold standard for the diagnosis of graft dysfunction. Protocol renal allograft biopsies have provided insights into pathogenesis of early and late allograft injury and guided clinical management. The aim of this study was to find out the causes of early and late graft dysfunction in renal allograft biopsies taken at different time points after transplantation. Materials and Methods: Between August 2008 and February 2011, a total of 98 renal allograft biopsies from 62 kidney transplants recipients were received in the department of Pathology, KIST Medical College and Teaching Hospital. Renal allograft biopsies were interpreted according to the Schemes of Banff ’09 update. Results: The maximum numbers of recipients were in the age group of 31-40 years. Age ranges from 16 to 61 years. Out of 62 recipients, there were 47(75.8%) males and 15 (24.2%) females. The time of biopsy ranges from 0 hour to 6 years after transplantation. There were 9 (9.18%) cases of acute T cell-mediated rejection, 8 (8.16%) cases of acute antibody-mediated rejection, 6 (6.12%) cases of acute ischemic injury, 6 (6.12%) cases of borderline lesions and 4 (4.08%) cases of chronic calcineurin inhibitor toxicity. Conclusion: In the early post-transplant period (0-6 months), acute antibody-mediated rejection, acute ischemic injury and T cell-mediated rejection are the major causes for graft dysfunction. In the late post transplant period (> 6 months after transplant), transplant glomerulopathy, chronic calcineurin inhibitor toxicity, viral infections and graft senescence including donor derived disease result in poor late graft survival.DOI: http://dx.doi.org/10.3126/jpn.v2i3.6016 JPN 2012; 2(3): 172-179


2021 ◽  
Vol 12 ◽  
Author(s):  
Zhe Yang ◽  
Fei Han ◽  
Tao Liao ◽  
Haofeng Zheng ◽  
Zihuan Luo ◽  
...  

Immunological rejection is an important factor resulting in allograft dysfunction, and more valid therapeutic methods need to be explored to improve allograft outcomes. Many researches have indicated that artemisinin and its derivative exhibits immunosuppressive functions, apart from serving as a traditional anti-malarial drug. In this assay, we further explored the therapeutic effects of artemisinin for transplant rejection in a rat cardiac transplantation model. We found that it markedly attenuated allograft rejection and histological injury and significantly prolonged the survival of allograft. Upon further exploring the mechanism, we demonstrated that artemisinin not only attenuated T cell-mediated rejection (TCMR) by reducing effector T cell infiltration and inflammatory cytokine secretion and increasing regulatory T cell infiltration and immunoregulatory cytokine levels, but also attenuated antibody-mediated rejection (ABMR) through inhibition of B cells activation and antibody production. Furthermore, artemisinin also reduced macrophage infiltration in allografts, which was determined to be important for TCMR and ABMR. Moreover, we demonstrated that artemisinin significantly inhibited the function of pure T cells, B cells, and macrophages in vitro. All in all, this study provide evidence that artemisinin significantly attenuates TCMR and ABMR by targeting multiple effectors. Therefore, this agent might have potential for use in clinical settings to protect against transplant rejection.


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