title: Serological and genetic factors in early recurrence of IgA nephropathy after renal transplantation.
abstract: BACKGROUND
  The relative role of IgA anomalies and genetic factors in IgA nephropathy (IgAN) recurrence after transplantation has never been investigated in a single cohort.
  
  
  METHODS
  Sixty-one transplanted patients who had IgAN as an original disease (30 with biopsy-proved early recurrence, median 2.9 yr post-transplant), and 120 controls, were investigated for aberrantly glycosylated IgA1, IgA binding to mesangial matrix, macromolecular IgA (IgA/fibronectin and uteroglobulin/IgA/fibronectin complexes), and polymorphisms of cytokines [tumor necrosis factor alpha (TNFalpha), interleukin 10 (IL-10), IL-6, interferon gamma and transforming growth factor beta 1] and renin-angiotensin system (angiotensinogen converting enzyme, angiotensin II receptor 1, and angiotensinogen) genes.
  
  
  RESULTS
  At multivariate logistic regression analysis, recurrence showed a border-line association with aberrantly glycosylated IgA1 [odds ratio (OR) 8.172, p = 0.077], and was significantly less frequent in carriers of -308 AG/AA TNF-alpha"high producer" genotype (OR 0.125, p = 0.036) and -1082, -819, -592 ACC/ATA IL-10 "low producer" (OR 0.038, p = 0.009) genotypes.
  
  
  CONCLUSIONS
  High levels of aberrantly glycosylated IgA1 do not appear to play a strong crucial role in recurrence of IgAN. Polymorphisms of TNFalpha and IL-10 known to condition Th1 prevalence were associated with protection from early recurrence of IgAN.
authors.affiliation: Nephrology, Dialysis and Transplantation Unit, Regina Margherita (Turin), Italy. rosanna.coppo@unito.it
authors.forename: Rosanna
authors.initials: R
authors.lastname: Coppo
authors.forename: Alessandro
authors.initials: A
authors.lastname: Amore
authors.forename: Monica
authors.initials: M
authors.lastname: Chiesa
authors.forename: Federica
authors.initials: F
authors.lastname: Lombardo
authors.forename: Paola
authors.initials: P
authors.lastname: Cirina
authors.forename: Simeone
authors.initials: S
authors.lastname: Andrulli
authors.forename: Patrizia
authors.initials: P
authors.lastname: Passerini
authors.forename: Giovanni
authors.initials: G
authors.lastname: Conti
authors.forename: Licia
authors.initials: L
authors.lastname: Peruzzi
authors.forename: Roberta
authors.initials: R
authors.lastname: Giraudi
authors.forename: Maria
authors.initials: M
authors.lastname: Messina
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Segoloni
authors.forename: Claudio
authors.initials: C
authors.lastname: Ponticelli
mesh_terms: D000328:Adult; D000888:Antibodies, Anti-Idiotypic / Q000276:immunology*; D015415:Biomarkers; D001706:Biopsy; D016207:Cytokines / Q000235:genetics*; D004247:DNA / Q000235:genetics*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005500:Follow-Up Studies; D005922:Glomerulonephritis, IGA / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D006801:Humans; D007070:Immunoglobulin A / Q000276:immunology*; D007668:Kidney / Q000473:pathology; D016030:Kidney Transplantation; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D012008:Recurrence; D012189:Retrospective Studies; D013997:Time Factors
chemical_list: D000888:Antibodies, Anti-Idiotypic; D015415:Biomarkers; D016207:Cytokines; D007070:Immunoglobulin A; D004247:DNA