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defined a diagnostic algorithm for glomerular diseases classification in dog. Using hierarchical cluster analysis, two common patterns of glomerular injury were identified and these resulted very stable creating a simplified
and accurate guide for veterinary pathologists when evaluating renal biopsies. The analysis revealed 2
large categories of glomerular diseases based on the presence or absence of IC deposition: immune complex- mediated glomerulonephritis (ICGN) category including membranoproliferative GN, membranous GN and Mixed type glomerulonephritis. The second category including dogs with non-ICGN: glomerular amyloidosis, focal segmental glomerulosclerosis, Minimal Change Disease (MCD) and Juvenile Nephropathies (JN).
Focusing on the immune complex damage in ICGN,
this is characterized by a dynamic interaction between antigen and antibody and the injury is dependent by several factors such as mechanism of formation, the site of deposition, the composition of the deposits and the amount of the deposits. The ICs may be preformed from circulating antigens and antibodies and only ICs with
an antigen excess tend to deposit along the capillary walls and mesangium. Aetiology of ICGN has been associated with several and inflammatory diseases, but there are many reports in which the antigen source or underlying disease is not identified and in this case, the GN is referred to as idiopathic. Furthermore, ICs may form in situ in the glomerulus, and this occurs when circulating antibodies react with endogenous glomerular antigens or with “planted” non-glomerular antigens
(i.e. Dirofilariosis). The ICs can damage the glomerular structures by two mechanisms: attracting circulating inflammatory cells or activating resident glomerular
cells, which release vasoactive substances, cytokines, and activators of coagulation. Nonetheless, the most important glomerular injury mediator is the complement cascade, particularly C5b-9 membrane attack complex formation. Within the membranes of glomerular cells, this complex causes activation of both glomerular epithelial cells and mesangial cells to produce inflammatory mediators, such as oxidants and proteases. The glomerulus responds to this injury by cellular proliferation, thickening of the GBM subsequent to upregulation of epithelial cell receptors for transforming growth factor and epithelial detachment (causing proteinuria) and, if the insult persists, hyalinisation and sclerosis. The glomerular visceral epithelial cells (podocyte) gives a fundamental contribution in glomerular filtration permeselectivity and they respond to injury with reversible changes such
as hypertrophy, foot process effacement, cell body attenuation and microvillus formation.
An Urban Experience

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