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Anti-angiotensin II type 1-receptor antibodies (AT1R-Ab) Induce a Specific Phenotype of Rejection Distinct from HLA antibody-Mediated Rejection

2018· article· en· W2884566262 on OpenAlexaff
Carmen Lefaucheur, Denis Viglietti, Olivier Aubert, Aurélie Philippe, Philip F. Halloran, Alexandre Loupy, Duska Dragun

Bibliographic record

VenueTransplantation · 2018
Typearticle
Languageen
FieldMedicine
TopicRenal Transplantation Outcomes and Treatments
Canadian institutionsThe Metabolomics Innovation Centre
Fundersnot available
KeywordsMedicineKidney transplantationTransplantationPathologyAngiotensin IIPeritubular capillariesArteritisVasculitisImmunologyAntibodyKidneyInternal medicineReceptor

Abstract

fetched live from OpenAlex

Anti-angiotensin II type 1-receptor antibodies (AT1R-Ab) have been associated with kidney allograft rejection; however, their ability to induce a specific rejection phenotype, independent of the presence of donor-specific anti-HLA antibodies (HLA-DSAs), has not been defined. In a prospective cohort of 881 kidney recipients transplanted between 2007 and 2010, we performed systematic screening for AT1R-Ab using quantitative ELISA and HLA-DSAs using single antigen bead assay, together with concomitant allograft biopsy, at the time of any clinical event in the first-year post-transplantation and at 1 year after transplantation. The allograft rejection phenotype was assessed by histopathology, immunochemistry for C4d complement fraction, and allograft gene expression measurement using microarray. We identified 233/881 (26%) patients with post-transplant AT1R-Ab (>10 U/mL). Compared to AT1R-Ab negative patients, AT1R-Ab positive patients showed increased levels of glomerulitis (p=0.01), peritubular capillaritis (p=0.01), endarteritis (p=0.01), similar level of interstitial inflammation (p=0.66) and tubulitis (p=0.23), and similar prevalence of C4d deposition in capillaries (p=0.24) and transplant glomerulopathy (p=0.99). After adjusting for the detection of HLA-DSAs, AT1R-Ab were independently associated with glomerulitis (aOR=1.7, p=0.006), peritubular capillaritis (aOR=1.8, p=0.002) and intimal arteritis (aOR=2.1, p=0.01). Among patients with microcirculation inflammation (g+ptc>1) (N=154), patients with AT1R-Ab and without HLA-DSA (N=23) showed increased prevalence of intimal arteritis (39%) and decreased prevalence of C4d deposition in capillaries (17%) compared to patients without AT1R-Ab and with HLA-DSA (N=80, 13% and 51%, respectively), to patients with AT1R-Ab and with HLA-DSA (N=31, 16% and 55%, respectively), and to patients without AT1R-Ab and without HLA-DSA (N=20, 5% and 10%, respectively) (p<0.001 and p=0.01, respectively). Compared to patients without AT1R-Ab and with HLA-DSA, patients with AT1R-Ab and without HLA-DSA exhibited increased expression of endothelial cell associated transcripts in allograft, including MEOX2, MEOX1 and FOSB (FC=3.9, 3.0 and 2.7, respectively, p<0.001 for all). Histomolecular rejection phenotype in patients with AT1R-Ab and without HLA-DSA was distinct from that of patients without AT1R-Ab and with HLA-DSA in unsupervised clustering. AT1R-Ab are associated with a specific histo-molecular phenotype of kidney allograft rejection, characterized by microvascular and arterial inflammation, expression of endothelial cell associated transcripts and low prevalence of complement deposition in capillaries, independent of the presence of HLA-DSAs.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.001
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.004

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.001
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.026
GPT teacher head0.297
Teacher spread0.271 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

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Citations1
Published2018
Admission routes1
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