Evidence map›Paper›PMID 41309447›Full record

ArticleScandinavian journal of immunology2025

The Impact of Complement Factor H-Related Protein Gene Deletions on Kidney Transplantation.

Salla Markkinen, A Inkeri Lokki, Ilkka Helanterä, Jarmo Ritari, Jukka Partanen, Seppo Meri, Kati Hyvärinen

Erratum issuedAbstract read
In one paragraph

Article in Scandinavian journal of immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Novel Aspects of Immunogenetics and Post-Transplant Events in Kidney Transplantation.Transplant international : official journal of the European Society for Organ Transplantation · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Salla MarkkinenResearch and Development, Finnish Red Cross Blood Service, Helsinki, Finland.ORCID https://orcid.org/0000-0002-4892-1269
A Inkeri LokkiTranslational Immunology Research Program and Department of Bacteriology and Immunology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0003-4397-8415
Ilkka HelanteräTransplantation and Liver Surgery, Helsinki University Hospital, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0002-2954-2538
Jarmo RitariResearch and Development, Finnish Red Cross Blood Service, Helsinki, Finland.ORCID https://orcid.org/0000-0002-3458-9314
Jukka PartanenResearch and Development, Finnish Red Cross Blood Service, Helsinki, Finland.ORCID https://orcid.org/0000-0001-6681-4734
Seppo MeriTranslational Immunology Research Program and Department of Bacteriology and Immunology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.ORCID https://orcid.org/0000-0001-9142-501X
Kati HyvärinenResearch and Development, Finnish Red Cross Blood Service, Helsinki, Finland.ORCID https://orcid.org/0000-0003-4605-2837

Funding

Helsinki University Hospital Diagnostic Center funds Y780023006MunuaissäätiöSigrid Jusélius FoundationState Research FundingSuomen Transplantaatiokirurginen Yhdistys ryThe State Subsidy to Hospitals TYH2019311The State Subsidy to Hospitals TYH2022315
6 · The paper itself

Abstract

We recently reported that a homozygous deletion in the complement factor H-related (CFHR) locus predisposed kidney transplant patients to rejection. As donors carried intact genes, the susceptibility may have resulted from an alloimmune reaction to FHR proteins. However, we found no evidence for an anti-FH response. It is therefore possible that CFHR deletions as such affect the rejection risk. Here, we used MLPA and WGS to fine-map and sequence the CFHR region in rs7542235-GG patients, a SNP tagging for ΔCFHR3-1 deletion. Our results confirmed that all patients with this SNP harboured deletions of various sizes encompassing CFHR1. Furthermore, patients with homozygous ΔCFHR3-1 were homozygous for rs6677604-A, a SNP tagging for deletions of CFHR3-1 locus, confirming that allele A tags for deletion of both CFHR3 and CFHR1. Proteomics analyses in a larger population demonstrated that rs7542235-G and rs6677604-A associate with expression levels of several proteins involved in regulating alloimmune response. We observed that while increasing the rejection risk, the ΔCFHR3-1 did not associate with baseline disease or specific clinical characteristics. To conclude, the various deletion types found in patients shared the deletion of the CFHR1 gene confirming its association with variant rs7542235. Also, both deletion-tagging alleles are associated with altered expression of FHR proteins.

Indexed as

Blood ProteinsComplement C3b Inactivator ProteinsGene DeletionGraft RejectionKidney TransplantationAdultFemaleGenetic Predisposition to DiseaseHomozygoteHumansMaleMiddle AgedPolymorphism, Single NucleotideBlood ProteinsCFHR1 protein, humanCFHR3 protein, humanComplement C3b Inactivator Proteinsallograft rejectionCFHRcomplement factor H‐relatedgene deletionkidney transplantation

Identifiers

PMID41309447
PMCPMC12660060

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Registered trials

None linked

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.