Evidence map›Paper›PMID 39154645›Full record

ArticleAmerican journal of nephrology2024

C4d, rather than C3d and C5b-9, Is Associated with Graft Loss in Recurrent IgA Deposition after Kidney Transplantation.

Firas F Alkaff, Audrey Uffing, Gesa Tiller, Rosa G M Lammerts, Marius C van den Heuvel, Ingeborg M Bajema, Mohamed R Daha, Jacob van den Born, Stefan P Berger

Abstract read
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Article in American journal of nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Firas F AlkaffDivision of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Audrey UffingDivision of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Gesa TillerDivision of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Rosa G M LammertsTransplantation Immunology, Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Marius C van den HeuvelDepartment of Pathology and Medical Biology, Pathology Section, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Ingeborg M BajemaDepartment of Pathology and Medical Biology, Pathology Section, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Mohamed R DahaDivision of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Jacob van den BornDivision of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Stefan P BergerDivision of Nephrology, Department of Internal Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionRecurrent IgA deposition is common after kidney transplantation. However, it is difficult to define whether IgA deposition is innocuous or contributes to organ damage. Next, although complement is known to be involved in the pathogenesis of IgA nephropathy (IgAN), its involvement has not been studied systematically in kidney transplant recipients (KTRs).

methodsKTRs with biopsy-proven native IgAN who underwent kidney biopsy after transplantation between 1995 and 2020 were included. Recurrent IgA deposition was defined as IgA deposit in the glomerulus. Staining of complement factors C4d, C3d, and C5b-9 was quantitatively evaluated using ImageScope.

resultsSixty-seven KTRs (85% male, 46 ± 13 years old, 12 [6-24] months after transplantation, 58% with indication biopsy) were included in the analyses. Of them, 25 (37%) had recurrent IgA deposition. There were no clinical differences between KTR with and without recurrent IgA deposition. C3d and C5b-9 were always present in biopsies with IgA deposition, while C4d was present in 48% of the biopsies. During a median follow-up of 9.6 [4.8-14] years, 18 (27%) KTRs developed death-censored graft failure. Recurrent IgA deposition was not associated with graft failure. Of the evaluated complement factors, only C4d staining was associated with graft failure in KTR with recurrent IgA deposition (hazard ratio = 2.55, 95% confidence interval = 1.07-6.03, p = 0.034).

conclusionsRecurrent IgA deposition was not associated with graft failure in itself. C4d, when present, is strongly associated with graft loss in KTR with recurrent IgA deposition, suggesting a pathogenic role for the lectin pathway in recurrent IgAN.

Indexed as

Complement C3dComplement C4bGlomerulonephritis, IGAGraft RejectionImmunoglobulin AKidney TransplantationPeptide FragmentsRecurrenceAdultBiopsyComplement Membrane Attack ComplexFemaleGraft SurvivalHumansMaleMiddle AgedComplement C3dComplement C4bcomplement C4dComplement Membrane Attack ComplexImmunoglobulin APeptide FragmentsComplementGraft survivalIga nephropathyKidney transplantationRenal biopsy

Identifiers

PMID39154645
PMCPMC11651231

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.