In this study, we aimed to investigate the molecular basis for patient subtyping to form the basis for clinical differentiation of SLE patients with high versus low levels of C3dg as well as high versus low SLEDAI scores. Our study applied primarily applied a high-throughput LC-MS/MS method capable of analyzing 500 samples per day (SPD) , global assessment of autoantibody profiles as well as inflammatory markers. The ob-jective of this study is to investigate the biological processes associated with these two measures, and to determine whether these markers reflect overlapping or distinct bi-ological processes.