IgA nephropathy (IgAN) is an autoimmune disease that involves galactose-deficient IgA1 (Gal-deficient IgA1) recognized by autoantibodies to form circulating immune complexes (IgA1-IC). Some of these complexes deposit in the glomeruli and induce kidney injury. Gal-deficient IgA1 alone is not sufficient to induce kidney damage. Additional proteins are required to form nephritogenic complexes. In this study, we isolated different molecular forms of serum IgA1, including IgA1-IC, monomeric (mIgA1), and polymeric (pIgA1) by SEC from patients with IgAN and healthy control donors. These three chromatographic fractions of molecular forms of IgA1 were analyzed by LC-MS. An analysis of the proteomes of the IgA1 molecular forms yielded several serum proteins enriched in the IgA1-IC. These proteins were also enriched in patients with IgAN when compared to healthy controls. The ability to characterize the proteome of IgA1-IC provides critical information relevant to IgAN pathogenesis and the nephritogenic characteristics of the ICs.