Abstract
It was found that Masugi nephritis induced in cholesterol-fed rabbits was characterized by accumulation of foam cells in glomeruli. In order to investigate the origin of these foam cells, electron microscopic observations of glomerular lesions were performed. Prior to the experiment, 9 rabbits were fed a diet containing 0.5% cholesterol for 4 weeks. The serum cholesterol level ranged from 450 to 690 mg/dl at the beginning of the experiment. The animals were maintained on the same diet during the subsequent experiment. Masugii nephritis was induced in 7 animals by single intravenous injection of 2 ml of nephrotoxic duck serum and the remaining two were used as controls. Kidney specimens were obtained by either surgical biopsies or autopsies at different stages from 6 to 28 days after injection of nephrotoxic serum. The results obtained were as follows: 1. The number and extent of glomerular foam cells roughly paralleled the natural course of Masugi nephritis. At the peak of the disease, they were seen not only in the glomeruli but also in extracapillary portions forming crescents. They disappeared when glomerular lesions were subsided. 2. Foam cells were apparently derived from migrant blood monocytes and mesangial cells with a wide variety of intermediate forms. Monocytic foam cells were seen in the capillary lumens as well as in the subendothelial space and mesangium. They often migrated in Bowman's space at the peak of the disease. Furthermore, they transformed into multinucleate giant cells including Touton type's. 3. There was no evidence that endothelial cells underwent a transformation into foam cells. 4. Lipid deposits filling the cytoplasm of foam cells seemed to be in two forms, free cytoplasmic droplets and membrane-bounded structures containing debris. The latter developed later preferentially in the central portion of the cytoplasm and were considered to be originated from lysosomes. 5. It seemed unlikely that glomerular lesions in Masugi nephritis were aggravated by foam cell accumulation. Foam cells were most probably a reflection of systemic hyperlipemia in the kidneys with active glomerular damage.
