4 4. Conclusion The mechanisms of proteinuria in primary glomerulopathies are complex and depend on all the components of the glomerular ﬁltration barrier. In primary membranous glomerulopathy, some molecules such as megalin and phos- pholipase A2 receptor have been considered as being the antigens responsible for subepithelial immune complexes, which change the glomerular permeability. In both FSGS and MCD podocytopathies, the molecular changes observed in proteins from the cytoskeleton, cell transmembrane, and slit diaphragm induce foot process eﬀacement and changes in negative charges, resulting in strong proteinuria. The understanding of the mechanisms involved in each clinical entity is extremely important for the best treatment choice and adequate patient followup. Authors’ Contributions J. R. Machado and L. P. Rocha have contributed equally to this work. 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