NPHS1 and membranous glomerulonephritis: Nephrin redistribution and dissociation from the podocyte actin cytoskeleton, thereby disrupting the integrity of the slit diaphragm, consequent to complement deposition, is a proposed mechanism of increased permeability of glomerular capillary barrier to protein [28], and a similar process was shown to occur in active human membranous nephropathy [29].