title: Interleukin-1 receptor antagonist allele: is it a genetic link between Henoch-Schönlein nephritis and IgA nephropathy?
abstract: Henoch-Schönlein purpura nephritis (HSPN) is a multi-organ systemic vasculitis, which shares many clinical, histological and immunological features with IgA nephropathy (IgAN). To address whether these two diseases have a common genetic background, the polymorphism of the variable number tandem repeat (VNTR) of IL-1 receptor antagonist (IL-1ra) gene has been analyzed using PCR in patients diagnosed with HSPN (N = 43) and IgAN (N = 97), together with normal controls (N = 98) and patients with acute post-infectious glomerulonephritis (APGN), under the concept that IL-1 might play an important role in mediating pathogenesis of vasculitis and glomerulonephritis. It was found that the allele frequency and carriage rate of the interleukin-1 receptor antagonist allele (IL1RN*2) of the IL-1ra gene increased significantly in HSPN patients as compared to IgAN (P < 0.01), APGN (P < 0.05) and normal subjects (P < 0.01). Interestingly, varied carriage rates of IL1RN*2 were found among various groups of IgAN patients presenting with different clinical manifestations. The carriage rate of IL1RN*2 was significantly higher in patients with recurrent gross hematuria than other groups of IgAN patients (P < 0.01). Furthermore, although the carriage rate of IL1RN*2 was higher in HSPN (46.5%) than average IgAN patients (26.8%; P < 0.01), there was no significant difference in the carriage rate of IL1RN*2 between HSPN and those IgAN patients with recurrent gross hematuria (42.8%l P > 0.05). It suggested that the IL1RN*2 allele might be a genetic marker shared by HSPN and a special group of IgAN patients with recurrent gross hematuria. Our preliminary observation provided a genetic evidence to support the hypothesis that HSPN and certain subgroup of IgAN are closely related diseases. Such an association of the gene polymorphism of IL-1ra between HSPN and IgAN with recurrent gross hematuria might serve as a key to explore their pathogenesis and eventually a specific intervention.
authors.affiliation: Research Institute of Nephrology, Jinling Hospital, Nanjing University School of Medicine, People's Republic of China.
authors.forename: Z H
authors.initials: ZH
authors.lastname: Liu
authors.forename: Z H
authors.initials: ZH
authors.lastname: Cheng
authors.forename: Y S
authors.initials: YS
authors.lastname: Yu
authors.forename: Z
authors.initials: Z
authors.lastname: Tang
authors.forename: L S
authors.initials: LS
authors.lastname: Li
mesh_terms: D000293:Adolescent; D000328:Adult; D000483:Alleles; D002648:Child; D005260:Female; D005787:Gene Frequency; D008040:Genetic Linkage; D005921:Glomerulonephritis / Q000209:etiology / Q000235:genetics; D005922:Glomerulonephritis, IGA / Q000235:genetics*; D006579:Heterozygote; D006801:Humans; D011695:IgA Vasculitis / Q000235:genetics*; D007239:Infections / Q000150:complications; D008297:Male; D008875:Middle Aged; D009393:Nephritis / Q000235:genetics*; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors*
chemical_list: D017472:Receptors, Interleukin-1