Literature DB >> 30578675

Molecular signatures and clinical outcomes of transplant glomerulopathy stratified by microvascular inflammation and donor-specific antibody.

Michelle Lubetzky1, Nicole Hayde2, Pilib Ó Broin3, Maria Ajaimy2, Yi Bao2, Omar Mohammed2, Daniel Schwartz4, James Pullman4, Enver Akalin2.   

Abstract

BACKGROUND: We investigated clinical outcomes and molecular signatures of transplant glomerulopathy (TG) stratified by microvascular inflammation (MVI) and donor-specific antibody (DSA) status.
METHODS: We performed a retrospective review of 749 kidney transplant patients who received a for-cause kidney biopsy from 2009 to 2014. We classified TG as MVI positive (MVI+) or MVI negative (MVI-), and with or without DSA. We obtained gene expression profiles for 44 biopsies by Affymetrix HuGene 1.0 ST expression arrays.
RESULTS: A total of 100 patients had TG; 49 were MVI+, and 51 were MVI-. After a median post-biopsy follow-up of 2.08 years (range 0.43-4.59), Kaplan-Meier survival analysis demonstrated worse allograft survival in MVI+ TG patients compared with MVI- TG patients (P = 0.01), and time to graft failure was significantly shorter in MVI+ patients (1.08 ± 1.01 years vs 2.3 ± 1.8 years; P = 0.002). DSA status did not affect graft survival within MVI+ or MVI- groups. Analysis of pathogenesis-based transcripts (PBT) showed that MVI+ TG biopsies had increased expression of gamma interferon and rejection (GRIT) and DSA-associated transcripts (DSAST), as observed in antibody-mediated rejection. MVI- TG biopsies had increased expression of cytotoxic and regulatory T cell- and B cell-associated transcripts but not GRIT or DSAST. DSA status had no effect on expression of any PBTs studied in MVI- TG biopsies.
CONCLUSIONS: Graft survival in TG is significantly worse in the presence of MVI. Gene expression profiles of MVI+ TG resemble antibody-mediated rejection while gene expression profiles of MVI- TG resemble cell-mediated rejection regardless of DSA status.
© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Entities:  

Keywords:  kidney transplant; microarray; transplant glomerulopathy

Mesh:

Substances:

Year:  2019        PMID: 30578675     DOI: 10.1111/ctr.13469

Source DB:  PubMed          Journal:  Clin Transplant        ISSN: 0902-0063            Impact factor:   2.863


  4 in total

1.  Proposed Definitions of Antibody-Mediated Rejection for Use as a Clinical Trial Endpoint in Kidney Transplantation.

Authors:  Candice Roufosse; Jan Ulrich Becker; Marion Rabant; Daniel Seron; Maria Irene Bellini; Georg A Böhmig; Klemens Budde; Fritz Diekmann; Denis Glotz; Luuk Hilbrands; Alexandre Loupy; Rainer Oberbauer; Liset Pengel; Stefan Schneeberger; Maarten Naesens
Journal:  Transpl Int       Date:  2022-05-20       Impact factor: 3.842

Review 2.  Molecular Assessment of Kidney Allografts: Are We Closer to a Daily Routine?

Authors:  A Trailin; P Hruba; O Viklicky
Journal:  Physiol Res       Date:  2020-03-23       Impact factor: 1.881

3.  B-cell Deficiency Attenuates Transplant Glomerulopathy in a Rat Model of Chronic Active Antibody-mediated Rejection.

Authors:  Shannon R Reese; Nancy A Wilson; Yabing Huang; Lucille Ptak; Kenna R Degner; Ding Xiang; Robert R Redfield; Weixiong Zhong; Sarah E Panzer
Journal:  Transplantation       Date:  2021-07-01       Impact factor: 5.385

4.  Integrative Analyses of Circulating Small RNAs and Kidney Graft Transcriptome in Transplant Glomerulopathy.

Authors:  Canan Kuscu; Manjari Kiran; Akram Mohammed; Cem Kuscu; Sarthak Satpathy; Aaron Wolen; Elissa Bardhi; Amandeep Bajwa; James D Eason; Daniel Maluf; Valeria Mas; Enver Akalin
Journal:  Int J Mol Sci       Date:  2021-06-09       Impact factor: 5.923

  4 in total

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