Glomerular lesions induced in Pekin ducks by dietary administration of dimethylnitrosamine

Abstract

Histochemical and electron microscopic studies were completed on the kidneys of Pekin ducks receiving a dietary supplement of dimethylnitrosamine at a concentration of 0.005%. Ducks were given the diets when 36 hours of age; test and control ducks (fed only mash) were killed by decapitation at weekly intervals for 8 weeks for necropsy and collection of tissue for histopathology. Tissues for electron microscopic examination were obtained after 5 and 6 weeks, fixed in Palade's solution, and embedded in Epon. Necropsy findings included subcutaneous edema, ascites, hydropericardium, splenomegaly, hepatic necrosis, and swelling of the kidneys. Obvious alterations in the glomeruli were present after 3 weeks of feeding and consisted of a reduced cellularity of the glomerular tufts with diffuse thickening of the capillary loops; but, early, the basal stalk region was spared. In severely affected glomeruli, the normal architecture was replaced by a solid amorphous, hyaline, eosinophilic material. The deposits stained variably with Gomori's trichrome. The material in the glomeruli was negative for amyloid by Congo red staining, took the silver component of the Humason and Lushbaugh stain, was inconsistently stained by Weigert's method for fibrin, and was PAS positive. Since the PAS staining response was not removed by diastase or hyaluronidase digestion and was not metachromatic with toluidine blue, the material is apparently not a simple mucopolysaccharide. Ultrastructural alterations included thickening of the basement membrane of the glomerular capillaries by “deposits” of an electron dense material. The amorphous material was distributed through the various divisions of the basement membranes throughout the glomerulus. In severely affected glomeruli the ultrastructural features were obliterated by the deposited material. There were no recognizable signs of collagen, fibrin, or amyloid in the thickened basement membranes. The glomerular lesions resemble the glomerulosclerosis described in experimental diabetes and in experimental toxicoses characterized by severe hepatopathy.