title: Single nucleotidic polymorphism 844 A->G of FCAR is not associated with IgA nephropathy in Caucasians.
abstract: BACKGROUND
  IgA nephropathy is characterized by a high heterogeneity of clinical expression with 10-30% of patients progressing to end-stage renal failure. The gene of the FcαRI or CD89 presents a single-nucleotide polymorphism responsible for a proinflammatory phenotype of neutrophils in vitro and ex vivo. The aim of our study was to assess whether this CD89 polymorphism 844 A->G is (i) a marker of disease susceptibility and/or (ii) associated with a more severe prognosis.
  
  
  METHODS
  All patients diagnosed with IgA nephropathy and for whom DNA frozen sample was available were included in this European monocentric retrospective analysis and compared to a cohort of healthy volunteers. Allelic discrimination was performed by real-time quantitative polymerase chain reaction (Applied Biosystems™). We first compared the distribution of A and G alleles between patients and volunteers and then studied the relationships between alleles and renal survival, histological score, proteinuria and renal function at diagnosis.
  
  
  RESULTS
  Seven hundred and twenty-six patients were analyzed for the study of susceptibility and 425 in the association study. The presence of the G allele was not associated with the occurrence of IgA nephropathy (χ(2) test 0.57, ns). Likewise, renal survival and the criteria for disease activity at time of diagnosis were not affected by the presence of the G allele.
  
  
  CONCLUSIONS
  No significant association between 844 A->G CD89 polymorphism and the expression of the IgA nephropathy in Caucasians exists. This result does, however, not preclude the implication of other CD89 polymorphisms neither the possibility for a role of CD89 in the pathogenesis of IgA nephropathy.
authors.affiliation: EA3064, GIMAP, Université Jean Monnet, Saint Etienne, France. nicolas.maillard@univ-st-etienne.fr
authors.forename: Nicolas
authors.initials: N
authors.lastname: Maillard
authors.forename: Lise
authors.initials: L
authors.lastname: Thibaudin
authors.forename: Farida
authors.initials: F
authors.lastname: Abadja
authors.forename: Ingrid
authors.initials: I
authors.lastname: Masson
authors.forename: Olivier
authors.initials: O
authors.lastname: Garraud
authors.forename: François
authors.initials: F
authors.lastname: Berthoux
authors.forename: Eric
authors.initials: E
authors.lastname: Alamartine
authors.forename: Christophe
authors.initials: C
authors.lastname: Mariat
mesh_terms: D000328:Adult; D000483:Alleles; D000704:Analysis of Variance; D015703:Antigens, CD / Q000235:genetics*; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology*; D005838:Genotype; D005922:Glomerulonephritis, IGA / Q000235:genetics* / Q000401:mortality* / Q000473:pathology; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D020641:Polymorphism, Single Nucleotide; D011379:Prognosis; D016016:Proportional Hazards Models; D011961:Receptors, Fc / Q000235:genetics*; D012189:Retrospective Studies; D018570:Risk Assessment; D012720:Severity of Illness Index; D016019:Survival Analysis; D044465:White People / Q000235:genetics*
chemical_list: D015703:Antigens, CD; C036832:Fc(alpha) receptor; D011961:Receptors, Fc