Aim. IgA nephropathy (IgAN) is the most common form of glomerulonephritis. Recent genome-wide association study (GWAS) suggested that DEFA locus (which encodesα-defensins) may play a key role in IgAN.Methods. The levels ofα-defensins in 169 IgAN patients and 83 healthy controls were tested by ELISA.Results. We observed thatα-defensins human neutrophil peptides 1–3 (HNP1–3) in IgAN patients were elevated compared with healthy controls. The mean levels ofα-defensins of 83 healthy controls and 169 IgAN patients were 50 ng/mL and 78.42 ng/mL. When the results were adjusted to the mean levels ofα-defensins of IgAN patients, the percentage of individuals with high levels ofα-defensins increased in IgAN patients (22.5%) compared to healthy controls (9.6%) (p=0.013). The elevation ofα-defensins in IgAN patients was independent of renal function or neutrophil count, which were major sources ofα-defensins in circulation. More importantly, negative correlation was observed between galactose-deficient IgA1andα-defensins.Conclusion. Asα-defensin is a lectin-like peptide, we speculated that it might be involved in IgA galactose deficiency. The data implied that patients with IgAN had higher plasmaα-defensins levels and highα-defensins correlated with IgA galactose deficiency, further suggesting a pathogenic role ofα-defensins in IgAN.
Experimental evidence of pathogenic role of IgG autoantibodies in IgA nephropathy