Lytic disarrangement of mesangial matrix was noted in acute proliferative glomerulonephritis induced in the rabbit by injection of duck nephrotoxic antibody. The severity of the change was variable depending upon dose of the antibody injected. With severe mesangiolysis, mesangial areas were highly obscured by marked hypertrophy and proliferation of mesangial cells along with massive infiltration of monocytes into the loosened mesangium and subendothelial space. There was random mobilization of the mesangial cells as shown by peripheral interposition and intraluminal projection with capillary subdivision. Glomerular capillaries were thus narrowed and distorted. The ultrastructural hallmark of the proliferated mesangial cells was prominence of the Golgi complex and endoplasmic reticulum which suggested accelerated protein synthesis, most likely for repair of the damaged matrix. In the affected glomeruli, exclusive of those undergoing rapid obliteration due to basement membrane rupture, resolution of the acute inflammatory process occurred within 2 wk. At this stage 2 types of glomerular changes became manifest; prominent mesangial stalk thickening and cellularity with occasional peripheral interposition of mesangial cells, and segmental capillary subdivisions due to mesangial bridges built between the original mesangium and peripheral loop. Chronic glomerular disease may develop based upon these persistent alterations of the glomerular structure. When a smaller dose of the duck antibody was employed, the process was much less prominent and complete recovery from acute glomerulonephritis took place.