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Introduction Immunoglobulin G4-related diseases encompass a growing list of organ involvement including membranous nephropathy, a disease entity generally associated with circulating antibodies to glomerular antigens and localised activation of complements. Although both immunoglobulin G4 and complements were present in the renal biopsy specimens, the mechanistic association link between them remains uncertain, particularly because immunoglobulin G4 is known to inhibit complement activation. The solution to this conundrum may lie in the recently discovered Fab arm exchange phenomenon. Hypothesis In this article, we hypothesise that immunoglobulin G4 molecules undergo structural perturbations via the dynamic Fab arm exchange phenomenon, which might then render it capable of complement activation and hence have a direct role in the pathogenesis of immunoglobulin G4-related membranous nephropathy. Evaluation of Hypothesis Investigation of the hypothesis is based on of recent discovery of newer biological properties of IgG4. Conclusion Membranous nephropathy may be just another endproduct of the newly discovered proinflammatory properties of IgG4.