The pathogenesis of primary FSGS is unknown. Some investigators have suggested that FSGS and minimal-change disease are pa of a continuum and that minimal-change disease may transform into FSGS. Others believe them to be distinct clinicopathologic entities from the outset. In any case, injury to the podocytes is thought to represent the initiating event of primary FSGS. As with minimal change disease, permeability-increasing factors produced by lymphocytes have been proposed. The deposition of hyaline masses in the glomeruli represents the entrapment of plasma proteins and lipids in foci of injury where sclerosis develops.IgM and complement proteins commonly seen in the lesion are also believed to result from nonspecific entrapment in damaged glomeruli. The most common presentation is in the form of nephrotic syndrome with heavy proteinuria. Ref: Harsh Mohan textbook of pathology 6th edition page674