Future studies should aim to characterize (i) the binding properties of physiological and/or neutrophil‐derived properdin (instead of unfractionated) to acute phase reactants (e.g. mCRP and other pentraxins) and neutrophil proteases (e.g. myeloperoxidase), and (ii) the functional consequences of these interactions on alternative pathway activity, especially in the context of known disease mutations or polymorphisms associated with dysregulated alternative pathway activity, such as in aHUS or C3 glomerulopathies.37 Here, CFP is linked to complement 3 glomerulopathy.