INTERLEUKIN-1 RECEPTOR ANTAGONIST ALLELE - IS IT A GENETIC LINK BETWEEN HENOCH-SCHONLEIN NEPHRITIS AND IGA NEPHROPATHY

Henoch-Schonlein purpura nephritis (HSPN) is a multi-organ systemic va sculitis, which shares many clinical, histological and immunological f eatures with IgA nephropathy (IgAN). To address whether these two dise ases have a common genetic background, the polymorphism of the variabl e number tandem repeal (VNTR) of IL-1 receptor antagonist (IL-1ra) gen e has been analyzed using PCR in patients diagnosed with HSPN (N = 43) and IgAN (N = 97), together with normal controls (N = 98) and patient s with acute post-infectious glomerulonephritis (APGN), under the conc ept that IL-1 might play an important role in mediating pathogenesis o f vasculitis and glomerulonephritis. It was found that the allele freq uency and carriage rate of the interleukin-1 receptor antagonist allel e (IL1RN2) of the IL-1ra gene increased significantly in HSPN patient s as compared to IgAN (P < 0.01), APGN (P < 0.05) and normal subjects (P < 0.01). Interestingly, varied carriage rates of IL1RN2 were found among various groups of IgAN patients presenting with different clini cal manifestations. The carriage rate of IL1RN2 was significantly hig her in patients with recurrent gross hematuria than other groups of Ig AN patients (P < 0.01). Furthermore, although the carriage rate of IL1 RN2 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 IL 1RN2 between HSPN and those IgAN patients with recurrent gross hematu ria (42.8%1 P > 0.05). It suggested that the IL1RN2 allele might be a genetic marker shared by HSPN and a special group of IgAN patients wi th recurrent gross hematuria. Our preliminary observation provided a g enetic evidence to support the hypothesis that HSPN and certain subgro up of IgAN are closely related diseases. Such an association of the ge ne polymorphism of IL-1ra between HSPN and IgAN with recurrent gross h ematuria might serve as a key to explore their pathogenesis and eventu ally a specific intervention.