In mesangial IgA glomerulonephritis (Berger's disease), the immunoproteins appeared to gain access from the capillary lumen to the mesangium via endothelial fenestrae or via channels between the endothelial cells. The deposits are transported into the deeper mesangium by a process of inhibition or diffusion, with the matrix acting as the head. There are no true channels or grooves in the mesangial matrix for the transport of the immunoproteins. The contractility of the glomerular myoid fibrils may account for the movement of deposits to the hilus for possible removal. There was partial dissolution of the deposits in the mesangial matrix accompanied by loosening of the matrix. No evidence was found for any significant intracellular phagocytosis and digestion. The mesangial deposits directly or indirectly stimulated the cellular hypertrophy and hyperplasia and increased deposition of mesangial matrix. This was accompanied by formation of collagen fibrils within the thickened matrix and led to atrophy of the mesangial cells and sclerosis of the glomeruli.