A wide variety of glomerular lesions express circumferential mesangial interposition (CMI). The pathomorphogenesis of CMI involves low-grade mesangiolysis and subsequent passive dislocation of mesangial cells towards the lateral wall of glomerular capillaries through a high hydraulic pressure of blood flow penetrating the lytic mesangium. This is in contrast to the previous theories which advocate an active movement of mesangial cells. Moreover, circumferential mesangial interposition can disappear spontaneously or after treatment, suggesting that mesangial cells may return to the original site with their inherent contractility after the insults are removed, in order to restore handicapped filtering surfaces. But the precise mechanisms of its regression will be a subject for future investigation.