title: Association of interleukin-10 gene G-1082A polymorphism with the progression of primary glomerulonephritis.
abstract: BACKGROUND
  Interleukin-10 (IL-10) is a cytokine with immunosuppressive properties. We evaluated the influence of G-1082A polymorphism in the IL-10 gene promoter, which has been associated with modified IL-10 production, on the two most common forms of primary glomerulonephritis: IgA nephropathy (IgAN) and focal segmental glomerulosclerosis (FSGS).
  
  
  METHODS
  We studied Caucasian patients (N= 191) with biopsy-proven glomerulonephritis (IgAN: N= 123, FSGS: N= 68) followed-up for 6.5 +/- 5.5 years. Patients were classified according to the slope of reciprocal serum creatinine (>/= or <-0.1 dL(*)mg(-1) (*)year(-1)) into group A (slow progressors, IgAN: N= 75, FSGS: N= 47) and group B (fast progressors, IgAN: N= 48, FSGS: N= 21). One hundred healthy volunteers were analyzed as control patients. G-1082A polymorphism was determined by polymerase chain reaction (PCR) amplification.
  
  
  RESULTS
  The allele frequencies were similar in patients and control group (NS). Initial renal function, proteinuria, and blood pressure did not differ significantly between patients with different genotypes. G-1082A polymorphism was associated with the progression of both IgAN and FSGS: GA/AA genotypes were more frequent in group B (fast progressors) than in group A (slow progressors; P= 0.012 for IgAN, P < 0.05 for FSGS). Patients with the GA/AA genotypes showed a worse outcome in the Kaplan-Meier analysis of renal survival (P < 0.05 for both IgAN and FSGS). The IL-10 polymorphism remained an independent risk factor for progression in multivariate analysis (Cox regression model, P < 0.05 for IgAN and FSGS).
  
  
  CONCLUSIONS
  Our results suggest that IL-10 gene G-1082A polymorphism is an important marker of progression in patients with IgAN and FSGS.
authors.affiliation: Department of Nephrology and Rheumatology, Heinrich-Heine University, Düsseldorf, Germany.
authors.forename: Christos
authors.initials: C
authors.lastname: Bantis
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Heering
authors.forename: Sendogan
authors.initials: S
authors.lastname: Aker
authors.forename: Nicola
authors.initials: N
authors.lastname: Klein-Vehne
authors.forename: Bernd
authors.initials: B
authors.lastname: Grabensee
authors.forename: Katrin
authors.initials: K
authors.lastname: Ivens
mesh_terms: D000225:Adenine; D000328:Adult; D018450:Disease Progression; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D005922:Glomerulonephritis, IGA / Q000235:genetics / Q000503:physiopathology*; D005923:Glomerulosclerosis, Focal Segmental / Q000235:genetics / Q000503:physiopathology*; D006147:Guanine; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012189:Retrospective Studies
chemical_list: D016753:Interleukin-10; D006147:Guanine; D000225:Adenine