Evidence map›Paper›PMID 27760523›Full record

ArticleBMC nephrology2016

Low level of MAp44, an inhibitor of the lectin complement pathway, and long-term graft and patient survival; a cohort study of 382 kidney recipients.

Julia Smedbråten, Geir Mjøen, Anders Hartmann, Anders Åsberg, Halvor Rollag, Tom Eirik Mollnes, Leiv Sandvik, Morten W Fagerland, Steffen Thiel, Solbjørg Sagedal

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 27% of its field
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

8 citing papers in PubMed, 14 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Julia SmedbråtenDepartment of Nephrology, Ullevål Oslo University Hospital, Postbox 4950, Nydalen, 0424, Oslo, Norway. yulsme@uus.no.ORCID 0000-0003-2189-9767
Geir MjøenDepartment of Transplant Medicine, Rikshospitalet Oslo University Hospital, Oslo, Norway.
Anders HartmannFaculty of Medicine, University of Oslo, Oslo, Norway.
Anders ÅsbergDepartment of Transplant Medicine, Rikshospitalet Oslo University Hospital, Oslo, Norway.
Halvor RollagFaculty of Medicine, University of Oslo, Oslo, Norway.
Tom Eirik MollnesFaculty of Medicine, University of Oslo, Oslo, Norway.
Leiv SandvikOslo Centre for Biostatistics and Epidemiology, Research Support Services, Oslo University Hospital, Oslo, Norway.
Morten W FagerlandOslo Centre for Biostatistics and Epidemiology, Research Support Services, Oslo University Hospital, Oslo, Norway.
Steffen ThielDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Solbjørg SagedalDepartment of Nephrology, Ullevål Oslo University Hospital, Postbox 4950, Nydalen, 0424, Oslo, Norway.
Oslo University Hospital · NOAarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHigher incidence of malignancy and infectious diseases in kidney transplant recipients is related to immunosuppressive treatment after transplantation and the recipient's native immune system. The complement system is an essential component of the innate immunity. The aim of the present study was to investigate the association of effector molecules of the lectin complement pathway with graft and patient survival after kidney transplantation.

methodsTwo mannan-binding lectin (MBL) associated proteases, MASP-2 and MASP-3 (activators of the lectin pathway) and two MBL-associated proteins, MAp44 and MAp19 (inhibitors of the lectin pathway) were measured at the time of transplantation in 382 patients (≥17 years old) transplanted in 2000-2001. The cohort was followed until December 31, 2014. Data on patient and graft survival were obtained from the Norwegian Renal Registry. Cox proportional hazard regression models were performed for survival analyses.

resultsLow MAp44 level (1st versus 2-4 quartile) was significantly associated with overall mortality; HR 1.52, 95 % CI 1.08-2.14, p = 0.017. In the sub analyses in groups below and above median age (51.7 years), low MAp44 as a predictor of overall mortality was statistically significant only in recipients of ≤51.7 years; HR 2.57, 95 % CI 1.42-4.66, p = 0.002. Furthermore, low MAp44 was associated with mortality due to infectious diseases; HR 2.22, 95 % CI 1.11-4.41, p = 0.023. There was no association between MASP-2, MASP-3 or MAp19 levels and patient mortality. No association between any measured biomarkers and death censored graft loss was found.

conclusionsLow MAp44 level at the time of transplantation was associated with increased overall mortality in kidney recipients of median age of 51.7 years or below and with mortality due to infectious diseases in the whole patient cohort after nearly 14-years of follow up after transplantation. No associations between other effector molecules; MASP-2, MASP-3 or MAp19 and recipient mortality were found, as well as no association of any biomarker with death censored graft loss.

Indexed as

AdolescentAdultAgedAged, 80 and overAge FactorsBiomarkersComplement Pathway, Mannose-Binding LectinFemaleGraft SurvivalHumansImmunity, InnateImmunosuppressive AgentsInfectionsKaplan-Meier EstimateKidney TransplantationLectinsBiomarkersImmunosuppressive AgentsLectinsMannose-Binding Protein-Associated Serine ProteasesMASP1 protein, humanMASP2 protein, humanComplementKidney transplantationRecipient survival

Identifiers

PMID27760523
PMCPMC5070230
OpenAlexW2532216643

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Registered trials

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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.