Immunoglobulin A vasculitis nephritis: Current understanding of pathogenesis and treatment

Table 1 Mechanism of immunoglobulin A vasculitis nephritis pathogenesis

No.	Mechanism of IgAVN pathogenesis
1	Infection triggers (Helicobacter pylori, Streptococcus pneumoniae and Haemophilus Influenzae[22-25]
2	Genetic factors[26-28]
3	Impaired glycosylation of IgA1 (Gd-IgA1)[29-41]
4	Complement activation[42-45]
5	TLR activation and B cell proliferation[46-48]
6	AECAs[49-51]
7	NAPIr[52,53]
8	Elevated plasma levels of IgE, eosinophil activation, higher levels of ECP and renal α-SMA[54-56]

IgAVN: Immunoglobulin A vasculitis nephritis; Gd-IgA1: Galactose-deficient-immunoglobulin A; TLR: Toll-like-receptor; AECAs: Anti-endothelial cell antibodies; NAPIr: Nephritis-associated plasmin receptor; α-SMA: α-smooth muscle; ECP: Eosinophil cationic protein.