Human pregnancy and generation of anti‐angiotensin receptor and anti‐perlecan antibodies. (12th March 2014)

• Record Type: Journal Article
• Authors: Hönger, Gideon; Cardinal, Heloise; Dieudé, Mélanie; Buser, Andreas; Hösli, Irene; Dragun, Duska; Hébert, Marie‐Josée; Schaub, Stefan
• Is Part Of: Transplant international. Volume 27:Number 5(2014:May)
• Page Start: 467
• Page End: 474
• Publication Date: 2014-03-12
• Subjects: Transplantation of organs, tissues, etc -- Periodicals; 617.95405
• DOI: 10.1111/tri.12282
• Languages: English
• ISSNs: 0934-0874

Abstract

<abstract abstract-type="main" id="tri12282-abs-0001"> <title>Summary</title> <p>Non‐HLA antibodies against the angiotensin II type 1 receptor (AT<sub>1</sub>R) and the C‐terminal fragment of perlecan (i.e., LG3) are associated with the development of renal allograft rejection. It is currently unknown how humans develop anti‐AT<sub>1</sub>R or anti‐LG3 antibodies. The aim of this study was to investigate whether pregnancy—as a model of sensitization to polymorphic proteins—induces anti‐AT<sub>1</sub>R and/or anti‐LG3 antibodies. We included 104 samples from women obtained after physiologic full‐term pregnancy and 80 samples from healthy nonsensitized controls (40 women and 40 men). Both anti‐AT<sub>1</sub>R and anti‐LG3 antibody levels were lower in pregnancy samples than in controls (both <italic>P </italic>< 0.05). By multivariate analysis, male gender was an independent predictor for high anti‐AT<sub>1</sub>R antibody levels (OR 3.66, <italic>P</italic> = 0.04) and pregnancy was predictive for low anti‐LG3 antibody levels (OR 6.53, <italic>P</italic> = 0.0001). There was no correlation of anti‐AT<sub>1</sub>R with anti‐LG3 antibody levels, either in the pregnancy or in the control samples (<italic>r</italic><sup>2</sup> ≤ 0.03, <italic>P</italic> ≥ 0.26). In conclusion, physiologic full‐term pregnancy does not induce anti‐AT<sub>1</sub>R or anti‐LG3 antibodies and may even lower their levels. Therefore, anti‐AT<sub>1</sub>R and anti‐LG3 antibodies are likely not caused by allosensitization. The lack of correlation of anti‐AT<sub>1</sub>R with anti‐LG3 antibodies suggests different mechanisms of generation, which remain to be elucidated.</p> </abstract>