Abstract

renal sections, glomeruli contained large 5 to 40 pm clear structures which stained black in osmicated tissues (Figs. 1, 2) (2 hours in 2% OsO, in 0.1 M phosphate buffer, pH 7.4). Similar structures, interpreted as lipid emboli, were present rarely in renal arteriolar lumens. In PAS and Masson's tri- chrome-stained renal sections, there were diffuse and nodular glomerulosclerosis and thickened glomerular capillary base- ment membranes. Proximal tubular basement membranes also contained multifocal subepithelial nodular aggregates of PAS-positive material covered by normal tubular epithelium (Fig. 3). Transmission electron microscopy of Spurr resin8 embed- ded sections post-fixed in OsO, confirmed the presence of osmophilic emboli within glomerular capillary lumens (Fig. 4). Capillary basement membranes were thickened and vac- uolated. Some vacuoles within these membranes contained an osmophilic substance similar in staining to the capillary emboli. Capillary basement membranes were frequently folded, and podocyte foot processes appeared thickened and multifocally fused. Mesangial cells were often present in pe- ripheral capillary loops between the thickened basement membrane and additional subendothelial branching deposits of basement membrane-like material. The light and ultrastructural lesions seen with canine di- abetic nephropathy have been previously de~cribed'.~ and may account for the diffuse and nodular glomerulosclerosis, thickened glomerular capillary basement membranes, and mesangial cell and matrix proliferations. Lipid emboli have been previously reported in glomerular capillaries and he- patic sinusoids of diabetic dogs. Renal lipid emboli may also be a component of post-traumatic systemic lipid emboliza- tion in dogs and h~mans.~.~ In humans, emboli are found in small arterioles and capillaries of the lung, kidneys, heart, and brain.' Glomerular lipid may also occur in mesangial cell vacuoles in spontaneous glomerular lipoidosis of dogs.9 The lipid deposits in the present case are unusual due to their localization only in renal arterioles and glomerular cap- illary lumens. No emboli were detected in osmicated sections of brain, heart, liver, or lung as previously noted in dogs with diabetes mellitus or post-traumatic embolization. Electron microscopy confirmed the lipid was within capillary lumens thus excluding spontaneous glomerular lipoidosis. The in- termittent lipidemia present in this case may have produced lipid droplets in glomerular capillary lumens but probably would not have resulted in selective renal distribution of such lumenal emboli. Other possible sources include the fatty de- posits on renal arteriolar walls with release secondary to sur- gical trauma. Post-surgical release of cholesterol crystals from atheromatous vessel walls with renal embolization occurs in humans, and diabetic humans are at higher risk for such

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