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dc.contributor.authorMjøen, Geir
dc.contributor.authorHartmann, Anders
dc.contributor.authorÅsberg, Anders
dc.contributor.authorRollag, Halvor
dc.contributor.authorMollnes, Tom Eirik
dc.contributor.authorSandvik, Leiv
dc.contributor.authorFagerland, Morten
dc.contributor.authorThiel, Steffen
dc.contributor.authorSagedal, Solbjørg
dc.contributor.authorSmedbråten, Julia
dc.date.accessioned2017-03-16T09:40:43Z
dc.date.available2017-03-16T09:40:43Z
dc.date.created2016-10-23T10:16:33Z
dc.date.issued2016
dc.identifier.issn1471-2369
dc.identifier.urihttp://hdl.handle.net/11250/2434302
dc.description.abstractBackground Higher 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. Methods Two 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. Results Low 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. Conclusions Low 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. Keywords Kidney transplantation – Complement – Recipient survivalnb_NO
dc.language.isoengnb_NO
dc.publisherBioMed Centralnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleLow level of MAp44, an inhibitor of the lectin complement pathway, and long-term graft and patient survival; a cohort study of 382 kidney recipientsnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.volume17nb_NO
dc.source.journalBMC Nephrologynb_NO
dc.source.issue1nb_NO
dc.identifier.doi10.1186/s12882-016-0373-9
dc.identifier.cristin1393719
dc.relation.projectNorges forskningsråd: 223255nb_NO
dc.description.localcode© 2016 The Author(s).Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, andreproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link tothe Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.nb_NO
cristin.unitcode194,65,15,30
cristin.unitcode194,65,15,0
cristin.unitnameCentre of Molecular Inflammation Research (SFF-CEMIR)
cristin.unitnameInstitutt for kreftforskning og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal