Chauvet S, Berthaud R, Devriese M, et al. - In this retrospective analysis of 34 children suffering from acute postinfectious GN and having low C3 level at onset, researchers inquired about mechanisms of complement activation. They screened a panel of anticomplement protein autoantibodies, performed associated functional characterization, and contrasted outcomes with those of 60 children with C3 glomerulopathy and persistent hypocomplementemia who were identified from the National French Registry. They noted that the alternative pathway of the complement system was activated in all children with acute postinfectious GN. At onset, a significantly higher proportion of children with the disorder had autoantibodies targeting factor B (a component of the alternative pathway C3 convertase), relative to children with hypocomplementemic C3 glomerulopathy. Experts found anti-factor B autoantibodies as contributors in alternative complement pathway activation. Screening for anti-factor B antibodies at the commencement of nephritic syndrome with low C3 level might assist in guiding indications for kidney biopsy to avoid misdiagnosed chronic glomerulopathy, such as C3 glomerulopathy, and might aid therapy selection.