Elevated Plasma α-Defensins (HNP1–3)‎ Levels Correlated with IgA1 Glycosylation and Susceptibility to IgA Nephropathy

Abstract EN

Aim.

IgA nephropathy (IgAN) is the most common form of glomerulonephritis.

Recent genome-wide association study (GWAS) suggested that DEFA locus (which encodes α-defensins) may play a key role in IgAN.

Methods.

The levels of α-defensins in 169 IgAN patients and 83 healthy controls were tested by ELISA.

Results.

We observed that α-defensins human neutrophil peptides 1–3 (HNP1–3) in IgAN patients were elevated compared with healthy controls.

The mean levels of α-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 of α-defensins of IgAN patients, the percentage of individuals with high levels of α-defensins increased in IgAN patients (22.5%) compared to healthy controls (9.6%) ( p = 0.013 ).

The elevation of α-defensins in IgAN patients was independent of renal function or neutrophil count, which were major sources of α-defensins in circulation.

More importantly, negative correlation was observed between galactose-deficient IgA1and α-defensins.

Conclusion.

As α-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 plasma α-defensins levels and high α-defensins correlated with IgA galactose deficiency, further suggesting a pathogenic role of α-defensins in IgAN.