As the most common glomerulonephritis worldwide,1 immunoglobulin A (IgA) nephropathy (IgAN) is a major contributor to the global kidney health burden. The pathogenesis of IgAN has been attributed to the “4-hit hypothesis”: increased production and circulation of galactose-deficient IgA1 (gd-IgA1), formation of autoantibodies against gd-IgA1, subsequent formation of circulating immune complexes containing gd-IgA1 and its autoantibodies, and deposition of those immune complexes in the glomerular mesangium, thereby leading to disease.