Recent results indicate that intrinsic glomerular cells (podocytes, mesangial and endothelial cells) are active participants in the inflammatory process in the glomerulus. Particular attention is drawn to podocyte injury in glomerulonephritis. Podocytes are end-differentiated cells which have lost their proliferation abilities and can only compensate by hypertrophy. The inability to proliferate is the cost which a podocyte must pay for the development of highly specialized structures and ability to adhere to the glomerular basement membrane. Collapsing focal-segmental glomerulosclerosis is a condition in which podocytes proliferate, but this process is associated with loss of their maturity markers as well as with abnormalities in the expressions of cell cycle proteins. Dysfunction of slit diaphragms is an important element in the pathogenesis of glomerulopathies with marked proteinuria. Recent studies also underline the importance of neprilysin in the pathogenesis of glomerulonephritis. This is the first podocytic antigen which has been shown to induce human membranous glomerulonephritis.