IGHA1 and Glomerular sclerosis: The subsequent hits are (2) the production of anti-Gd-IgA1 antibodies, including IgM, IgG, or IgA [13]; (3) the formation of immune complexes containing Gd-IgA1, anti-glycan antibodies, and various other biological proteins, such as sCD89 shedding from mononuclear/neutrophils [14]; and (4) the deposition of immune complexes in the renal mesangium, leading to complement system activation, mesangial matrix expansion, and inflammation, and ultimately resulting in glomerular sclerosis and interstitial fibrosis.