Abstract. Glomerulonephritis constitutes an important category of renal diseases in animals and has been recognized with increasing frequency in the last decade. We report here the comparative morphologic aspects of glomerulonephritis as a naturally occurring disease of animals. We briefly review the immunopathogenesis of glomerulonephritis. The morphology of renal lesions occurring in glomerulonephritis in dogs, cats, cattle, sheep, horses and swine has been reviewed with emphasis on the range and specificity of various glomerular lesions and on the comparison of lesions between various species. A distinction was made between glornerulonephritis as a primary disease entity and glomerulonephritis associated with other disease processes. Primary idiopathic glomerulonephritis occurred in all species but was most commonly recognized as a clinically important disease in dogs and cats. Glomerulonephritis also occurred in association with other diseases such as equine infectious anemia, chronic hog cholera, canine pyometra, dirofilariasis, feline leukemia virus infection and canine systemic lupus erythematosus.Glomerulonephritis is responsible for substantial morbidity and mortality in many species of animals. Although the cause is basically unknown, it is a disease generally thought to result from the interaction of immunologic and inflammatory reactants at a fixed tissue site (the glomeruli) with subsequent loss of structural and functional integrity of the injured tissues. It is not the purpose of this paper to detail the pathogenesis of glomerulonephritis. For a better understanding of the disease as it occurs in animals, however, it will be useful to review briefly what is known about the pathways potentially leading to glomerular injury [25, 61, 71, 73, 77, 82, 831. Two major immunologic mechanisms of glomerular injury have been identified. In one, antibodies react with antigens in the glomerular basement membrane. In the other, antibodies react with nonglomerular antigens in the circulation to form immune complexes that are deposited in the glomerulus. With conventional light microscopy, it is difficult to infer the pathogenetic mechanisms responsible for glomerulonephritis from the histologic lesion. Differentiating these two mechanisms usually requires fluorescence and electron microscopy. Glomerular lesions induced by soluble immune complexes have characteristic discrete, interrupted, focal deposits of host IgG and complement when examined by fluorescence microscopy. In contrast, the fluorescence staining pattern of glomeruli injured by anti-glomerular basement membrane antibody is uniform, smooth and linear. To further implicate anti-glo-
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