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ABSTRACT. To define the characteristics of malignancy we performed routine histology and an immunohistochemical study on seventeen aortic body tumors in dogs. We essayed tumors using a panel of immunohistochemical markers: neuron specific enolase (NSE), chromogranin A (CrA) and S-100. Among 17 cases, the neoplastic cells were positive for NSE (17 cases, 100%), S-100 (9 cases, 53%), and CrA (8 cases, 47%), respectively. The sustentacular cells density and chief cell staining intensity were both inversely related to tumor grade. The most relevant data was consistent with a negative staining of S-100 correlated with absence or decreased number of sustentacular cells in tumors grade III. This report indicates that the immunohistochemical panel has utility for the diagnosis of chemodectoma and the negative staining to CrA and S-100 markers in tumors grade III expresses an indication of malignant behaviour of the tumor. KEY WORDS: aortic body tumor, immunohistochemistry, tumor grade.

Tubulo-interstitial fibrosis in dogs may result from primary injury to the interstitium or develop secondary to other renal diseases. As in human renal pathology, tubular epithelial cells (TEC) are believed to actively participate in the mechanisms of renal fibrosis. In this study, we examined the changes in the tubular epithelial component in two specific canine diseases. Immunohistochemistry showed the expression of the epithelial marker cytokeratin, the smooth muscle marker alpha-SMA, the mesenchymal marker vimentin and PCNA in 20 dogs with membranous glomerulonephritis and membrano-proliferative glomerulonephritis. Results showed that the loss of the epithelial marker in TEC was directly correlated to the grade of tubulo-interstitial disease present and independent of the type of glomerulonephritis. Varying degrees of vimentin positivity were detected in tubular epithelium in areas of inflammation, and low numbers of scattered alpha-SMA-positive cells were also observed. Immunohistochemistry showed that epithelial tubular cells lose their cytokeratin staining characteristics and transdifferentiate into cells exhibiting key mesenchymal immunophenotypic feature of vimentin-positive staining in both diseases investigated. The integrity of the tubular basement membrane is likely to be fundamental in maintaining the epithelial phenotype of TEC. Animal models provide opportunities for investigating the pathogenesis of renal fibrosis in humans.

Abstract. In this report a 9-year-old female German Shepherd dog with a membranoproliferative glomerulonephritis (MPGN) type III associated with concomitant infection of Dirofilaria immitis and Leishmania infantum is presented. Light microscopic evaluation of kidney revealed a diffuse hypercellularity and thickening of glomerular basement membrane. Heavy and coarse granular complement C 3 deposition and a weaker positive reaction to immunoglobulin G were present along peripheral glomerular basement membrane and in the mesangium in the immunofluorescent study. Transmission electron microscopy revealed deposits in the mesangium, subendothelium, and subepithelium. These lesions are compatible with membranoproliferative glomerulonephritis type III in humans.Key words: Dirofilaria; dogs; Leishmania; membranoproliferative glomerulonephritis; transmission electron microscopy.Membranoproliferative glomerulonephritis (MPGN) is a histologic lesion characterized by intraglomerular hypercellularity (mesangial cells, endothelial cells, and inflammatory cells), matrix expansion, and thickening to the walls of the peripheral capillary loops. Immunocomplex deposits in the capillary walls and within mesangium are seen on electron microscopy. Membranoproliferative glomerulonephritis is usually associated with an immune complexmediated pathogenesis and may be idiopathic (primary) or secondary to viral, bacterial, and parasitic infections. According to the World Health Organization classification, MPGN is subdivided, based on ultrastructural alterations in the glomerular basement membrane (GBM), as type I (subendothelial deposits), type II (intramembranous dense deposits), and type III. 6,7 In MPGN type III, immune deposits are found in the subendothelial and mesangial region, similarly to type I; in addition, numerous subepithelial deposits are present. 1,6,7,13,14 This work describes the features of MPGN type III in a dog associated with simultaneous infection with Dirofilaria immitis and Leishmania infantum. To the authors' knowledge, this is the first description of MPGN type III in dogs.A 9-year-old female German Shepherd dog was referred with a 4-week history of poliuria/polydipsia, anorexia, vomiting, and diarrhea with melena. A hematologic evaluation 3 days earlier had revealed blood urea nitrogen increase and elevated serum creatinine and antibodies to Leishmania spp. (IFAT 10 ) and D. immitis antigens (SNAP a ). On clinical examination, the animal was in lateral recumbency with a severely dull and depressed mental state (uremic status). Its body condition score was poor, and it exhibited generalized muscle atrophy, tachypnea (60/min), and tachycardia (170/min). Mucous membranes were dry and a pale-yellowish color while all lymph nodes were subjectively normal to decreased in volume. After blood and urine collection and fine needle aspiration of lymph nodes, the dog was hospitalized. Fluid therapy (lactated Ringers) was infused, and antiemetic and gastro protective therapy (metoclopramide, ranitidine) was initiated. Hema...

Renal dysplasia is defined as a condition of disorganised development of renal parenchyma due to abnormal differentiation. The case of a 5-month-old intact male Norwegian Forest Cat with a history of polyuria and polydipsia is reported. Ultrasonographic examination showed a slight enlargement of kidneys. Biochemical parameters, haematological examinations and clinical signs were compatible with chronic renal failure (CRF). Histological examination was correlated with a primary tubular disorganisation and modification of glomerular compartment. The clinical history together with the histological lesions is consistent with bilateral juvenile renal dysplasia in this cat. To our knowledge, feline renal dysplasia has been reported in fetal infections with panleukopenia virus; no reports indicate the idiopathic origin in feline dysplastic lesions.