title: Association of soluble CD89 levels with disease progression but not susceptibility in IgA nephropathy.
abstract: The Fc-α receptor (FcαR/CD89) is involved in IgA complex formation and may affect the development of IgA nephropathy (IgAN). In this study, we tested the genetic variations of the CD89 gene in relation to disease susceptibility in IgAN and the expression of soluble CD89 (sCD89) in sera of patients with IgAN and in controls. There was a significant difference between the levels of sCD89-IgA complexes, measured by sandwich enzyme-linked immunosorbent assay (ELISA), in 177 patients with IgAN with and without disease progression at the time of first diagnosis. No such difference was found in 42 patients with other renal diseases. The patients with IgAN without disease progression had stable but high levels of sCD89 over 5-15 years of follow-up in contrast to stable but low levels of sCD89 in the disease progression group. Moreover, levels of sCD89 complexes were correlated with one of the five CD89 genetic variants in 212 patients with IgAN and 477 healthy Caucasians; the single-nucleotide polymorphism (SNP) rs11084377 was significantly associated with a lower expression of sCD89. However, no association between CD89 gene polymorphisms and susceptibility to IgAN was detected. Thus, we found an association between the levels of sCD89-IgA complexes in serum and the severity of IgAN, and a possible genetic component in regulating the production or expression of sCD89.
authors.affiliation: Rheumatology Unit, Department of Medicine, Karolinska Institutet, Karolinska University Hospital at Solna, Stockholm, Sweden.
authors.forename: Mai T
authors.initials: MT
authors.lastname: Vuong
authors.forename: Mirjana
authors.initials: M
authors.lastname: Hahn-Zoric
authors.forename: Sigrid
authors.initials: S
authors.lastname: Lundberg
authors.forename: Iva
authors.initials: I
authors.lastname: Gunnarsson
authors.forename: Cees
authors.initials: C
authors.lastname: van Kooten
authors.forename: Lars
authors.initials: L
authors.lastname: Wramner
authors.forename: Maria
authors.initials: M
authors.lastname: Seddighzadeh
authors.forename: Anders
authors.initials: A
authors.lastname: Fernström
authors.forename: Lars Å
authors.initials: LÅ
authors.lastname: Hanson
authors.forename: Lieu Thi
authors.initials: LT
authors.lastname: Do
authors.forename: Stefan H
authors.initials: SH
authors.lastname: Jacobson
authors.forename: Leonid
authors.initials: L
authors.lastname: Padyukov
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000936:Antigen-Antibody Complex / Q000378:metabolism; D015703:Antigens, CD / Q000097:blood* / Q000235:genetics*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D005922:Glomerulonephritis, IGA / Q000097:blood* / Q000235:genetics*; D006801:Humans; D007070:Immunoglobulin A / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000097:blood / Q000175:diagnosis / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide / Q000235:genetics; D011379:Prognosis; D011961:Receptors, Fc / Q000097:blood* / Q000235:genetics*; D012307:Risk Factors; D012720:Severity of Illness Index; D055815:Young Adult
chemical_list: D000936:Antigen-Antibody Complex; D015703:Antigens, CD; D015415:Biomarkers; C036832:Fc(alpha) receptor; D007070:Immunoglobulin A; D011961:Receptors, Fc