Acute cytomegalovirus glomerulonephritis: an experimental model.

HA/ICR mice injected intraperitoneally with an LD(10) of murine cytomegalovirus develop a transiet acute glomerulonephritis characterized by cytomegalic intranuclear inclusions limited to mesangial cells. Viruria and proteinuria occur on the 3rd day and usually subside by the 10th day, accompanied by resolution of the glomerular lesion. By electron microscopy, virus synthesized within mesangial cell nuclei accumulates in intercelluar channels that course through the mesangial matrix. Virus and cellular debris are also found in channels surrounded by matrix in the juxtaglomerular area and between the epithelial cells of the macula densa. By immunofluorescence, viral antigen first concentrated in glomerular mesangial cells on the 5th day is cleared centripetally, appearing as fine granules in the juxtaglomerular area by the 7th day after infection. By the 10th day, changes are restricted to the juxtaglomerular region, and thereafter hyalinization at the glomerular vascular pole or cellular disarray of the juxtaglomerular zone with lymphocytic infiltration extending into the renal interstitium from few glomeruli occurs in approximately 40 per cent of the mice associated with persistence of viral antigen in these foci. These findings indicate that at least one route of transport resulting in viruria involves the glomerular mesangium, juxtaglomerular zone, and the distal convoluted tubule. Persistence of viral antigen or other noxious substances along this route may result in a unique juxtaglomerular lesion and interstital nephritis.