Etiology

• Sex: ♂ > ♀

• Age: more common in children

  • 90% of cases < 10 years

  • Peak incidence: 6 years

The exact pathogenesis is unknown and assumed to be multifactorial. Factors that likely play a role include:

• Preceding infection

  • Up to 90% of cases preceded by viral or bacterial infection 1–3 weeks prior

  • Most commonly an upper respiratory tract infection caused by group A Streptococcus

  • GI infections also possible

  • Many other organisms have also been associated with IgAV

• IgA nephropathy

• Genetic predisposition

• Hypothesized pathophysiological mechanism: exposure to allergen/antigen (e.g., infection, drugs) → stimulation of IgA production → deposition of IgA immune complexes in vascular walls (e.g., in the skin, GI tract, joints, kidneys) → activation of complement → vascular inflammation and damage