Glomerulopathies are currently considered one of the most important causes of chronic renal failure in both humans and dogs. These can be induced by a primary kidney disease, by genetic mutations or by secondary glomerulopathies caused by systemic diseases such as lupus, infections, tumors or in response to medications. Glomerulopathies cause significant morbidity and mortality and are a potentially preventable factor of end-stage renal disease in all species, so early diagnosis is considered vital. The typical clinical manifestation of glomerulopathies is proteinuria, which implies the failure of the glomerular filtration process. In the present work, a complex histopathological study on renal specimens of canines was carried out and a subsequent structural and gene level measurement of podocin, nephrine, alpha actinin-4 proteins and transforming growth factor beta-1 in human kidney biopsies and canine tissues, in order to compare the different mechanisms of podocyte injury. The results allowed to define three groups of renal conditions with glomerular damage in the canines: renal dysplasia, focal and segmental glomerulosclerosis and glomerulonephritis. High degree of similarity was determined between the glomerular structure of the two species. Additionally, it was possible to define that there are changes in the expression and location of the filtration diaphragm and cytoskeleton proteins as a response of the podocyte to different injuries. It was determined that the pathogenesis of glomerulopathies in canines and humans shows similar mechanisms of injury and that can be considered an adequate model of spontaneous glomerular diseases.