Patients with other familial podocytopathies, such as ACTN4, CD2AP, or LMX1B, showed variable histological phenotypes in the biopsies including membranous proliferative glomerulonephritis (MPGN), dense deposits, and tubular atrophy, suggesting a wide spectrum of glomerular alterations apart from FSGS [24,25]. This evidence concerns the gene ACTN4 and primary membranoproliferative glomerulonephritis.