title: Experimental proliferative glomerulonephritis in the cat.
abstract: A model of chronic serum sickness was used to induce immune-complex glomerulonephritis in seven experimental cats, by daily intravenous inoculation of an increasing dose (5 to 35 mg) of human serum albumin (HSA). At week four, two of the seven animals developed anterior uveitis. At week 23, two different animals developed the subcutaneous oedema characteristic of the nephrotic syndrome (NS), whilst the other five cats appeared clinically normal. The kidneys were examined at necropsy by light microscopy and by transmission electron microscopy. The glomeruli of four animals (three with both proteinuria and uraemia, and one with proteinuria only) showed morphological changes under light microscopy. The abnormalities suggested that a diffuse mesangial proliferative glomerulonephritis (GN) had been induced in three cats and diffuse membranoproliferative GN induced in another. Ultrastructural studies revealed electron-dense deposits (immune-complexes) in six of the seven cats. Two cats without glomerular abnormalities by light microscopy had mesangial deposits and three cats with mesangial proliferative GN had deposits at mesangial, subendothelial and/or subepithelial sites. The single cat with membranoproliferative GN had deposits at mesangial, subendothelial, subepithelial and intramembranous sites. Immunohistological examination (peroxidase-antiperoxidase technique) showed that HSA and immunoglobulin (IgG and IgM) were deposited in the glomeruli of these cats. Deposits were the most dense in cats with more severe renal lesions. Deposits of IgM were most abundant. An extensive cellular infiltrate, comprising macrophages, neutrophils and plasma cells, was observed only in the four animals which showed abnormalities in glomerular ultrastructure. The disease induced in these cats thus appears to differ from the membranous nephropathy previously described in the cat and bears a close resemblance to immune complex (IC) disease in man. In view of the relatively few specific animal models of IC-mediated proliferative GN, this model has potential for application to the study of human IC disease.
authors.affiliation: Department of Veterinary Medicine, University of Bristol, Langford, U.K.
authors.forename: S A
authors.initials: SA
authors.lastname: Bishop
authors.forename: C R
authors.initials: CR
authors.lastname: Stokes
authors.forename: V M
authors.initials: VM
authors.lastname: Lucke
mesh_terms: D000818:Animals; D000936:Antigen-Antibody Complex / Q000032:analysis; D002415:Cats; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D015432:Glomerulonephritis, Membranoproliferative / Q000139:chemically induced* / Q000473:pathology; D007124:Immunoenzyme Techniques; D007136:Immunoglobulins / Q000032:analysis; D007150:Immunohistochemistry; D007275:Injections, Intravenous; D007678:Kidney Glomerulus / Q000737:chemistry / Q000473:pathology / Q000648:ultrastructure; D008854:Microscopy, Electron; D012709:Serum Albumin / Q000009:adverse effects*
chemical_list: D000936:Antigen-Antibody Complex; D007136:Immunoglobulins; D012709:Serum Albumin