Noncongophilic fibrillary glomerulonephritis in a cat

This report describes an uncommon case of nonamyloidotic fibrillary glomerulonephritis. A 5-year-old female European cat was presented with nephrotic syndrome. Serum biochemistry and urinalysis revealed a mild increase in cholesterol, low total protein, severe hypoalbuminemia, and high proteinuria with a high protein-to-creatinine ratio. An histologic examination revealed an interstitial nephritis and a diffuse glomerulonephritis, with multifocal thickening of the Bowman's capsule. Transmission electron microscopy showed widespread fibrillary deposits in the glomerular basement membrane and in the mesangium. These fibrils ranged between 18 and 26 nm in diameter and were Congo red negative, which allowed their differentiation from amyloid. Immunohistochemistry demonstrated expression for immunoglobulin M (IgM) and immunoglobulin G (IgG) within the mesangium. Renal deposits of Congo red-negative amyloid-like fibrils have been described in humans, horses, monkeys, and dogs. This is the first report of noncongophilic fibrillary glomerulopathy in a cat.     

Chronic renal failure in young Old English Sheepdogs

Chronic renal failure was diagnosed in three young Old English Sheepdogs. Clinical signs were characterised by ill-thrift, polydipsia, polyuria, nervous signs and behavioural changes. Laboratory findings showed azotaemia, non-regenerative anaemia, hyperphosphataemia and isosthenuria. The kidneys were characterised histologically by interstitial fibrosis, and thickening and calcification of the tubular and glomerular basement membrane. A familial incidence could not be confirmed in these cases. (New Zealand Veterinary Journal 38, 118–121, l990)     

Primary bilateral corneal nerve sheath neoplasm in a dog

A 15‐year‐old, neutered male, Shih Tzu cross developed progressive corneal stromal thickening and vascularization of the right eye, and 5 months later, of the left eye. Both eyes became blind due to extensive corneal opacification and were enucleated. Light microscopic examination revealed a diffuse corneal infiltrate of neoplastic mesenchymal cells, and immunohistochemistry revealed diffuse cytoplasmic vimentin immunoreactivity and variable cytoplasmic and nuclear immunoreactivity for S100 in the neoplastic cells. Transmission electron microscopy revealed desmosomes between contiguous cells, thread‐like cytoplasmic processes coated with basement membrane, extracellular bundles of collagen, and axonal degeneration consistent with features of a nerve sheath neoplasm. This is the first report of primary, bilateral corneal nerve sheath sarcoma in a canine.     

Mesangioproliferative Glomerulonephritis in Mink with Encephalitozoonosis

Renal specimens from 6 mink with encephalitozoonosis were studied by light and electron microscopy and immunohistochemistry. The glomeruli of affected kidneys had a mesangioproliferative glomerulonephritis which was characterized by an increase in mesangial cells and matrix in most glomeruli. Some glomeruli were partially or completely sclerosed. There were protein or granular casts in the cortical and medullary tubules. Interstitial nephritis, vasculitis and tubular cysts were found. Electron microscopy demonstrated extensive matrix and increased cellularity in the mesangial areas. Glomeruli showed segmentally thickened or wrinkled capillary basement membranes. Electron dense deposits were found in the glomerular basement membranes and mesangium. Peroxidase-anti-peroxidase immunohistochemistry demonstrated that IgG and IgM positive material was present as granular deposits in the glomerular basement membrane and occasionally in the mesangium.     

Chronic renal failure in young Old English Sheepdogs

Chronic renal failure was diagnosed in three young Old English Sheepdogs. Clinical signs were characterised by ill-thrift, polydipsia, polyuria, nervous signs and behavioural changes. Laboratory findings showed azotaemia, non-regenerative anaemia, hyperphosphataemia and isosthenuria. The kidneys were characterised histologically by interstitial fibrosis, and thickening and calcification of the tubular and glomerular basement membrane. A familial incidence could not be confirmed in these cases.     

Glomerulonephropathy in aged captive Key Largo woodrats (Neotoma floridana smalli)

A retrospective review of mortality records of Key Largo woodrats (Neotoma floridana smalli) in a captive breeding program revealed chronic renal disease in 5 of 6 woodrats older than 4 years of age. Two of the 5 woodrats with chronic renal disease also had clinical evidence of diabetes mellitus. Kidneys from all 5 woodrats were examined via light microscopy, histochemical staining, immunohistochemical staining, and transmission electron microscopy. The dietary histories of the affected animals were examined as well. The most striking histopathologic abnormality in the affected kidneys was the presence of large protein casts within cortical and medullary tubules in combination with lesions of membranous glomerulopathy and glomerulosclerosis. Transmission electron microscopy revealed thickening and undulation of the tubular and glomerular mesangial basement membranes with the variable presence of electron-dense deposits within the capillary endothelial basement membrane. Patchy glomerular immunoreactivity for IgG was noted in 2 cases, but IgA and IgM immunoreactivity were not present. The pathologic changes in the kidneys of the Key Largo woodrats mirrored many of the features of chronic progressive nephropathy commonly diagnosed in laboratory rats. Woodrats in the captive population were fed an ad libitum high-protein diet similar to diets that have been shown in laboratory rats to exacerbate the development and progression of chronic progressive nephropathy. It is concluded that Key Largo woodrats develop glomerulonephropathy with features similar to chronic progressive nephropathy described in laboratory rats. Age, concomitant disease, and dietary factors may contribute to the development and severity of this potentially age-limiting disease in Key Largo woodrats.     

Antitubular basement membrane autoantibody in a dog with chronic tubulointerstitial nephritis

Linear deposition of immunoglobulin G was seen by direct immunofluorescence along the tubular basement membranes in the kidney of a dog with chronic tubulointerstitial nephritis. Autoantibody eluted from the affected kidney bound to the tubular basement membrane of normal canine kidney, but not to several other normal canine basement membranes. The pathogenic significance of the autoantibody in this dog was not determined.     

Chronic tubulointerstitial nephropathy in six okapis (Okapia johnstoni).

Renal tubular atrophy with conical and medullary interstitial fibrosis with severe thickening of the basement membranes of atrophic tubules was found in six okapis (Okapia johnstoni). Focal glomerular atrophy, probably secondary to ischemic collapse of the glomerular capillary tuft, was also observed. Although the etiologies and pathogeneses of these nephropathies are unclear, primary damage of the tubular epithelium appears to be the most likely cause, and toxicity from ingested plant material, possibly willow (Salix sp.), is a possibility.     

Origin of enzootic intranasal tumor in the goat (Capra hircus): a glycohistochemical approach

Enzootic intranasal tumor (EIT) appears glandular in type and has recently been classified as an adenocarcinoma of low malignancy. The aim of this study was to characterize the secretion of surface glycoconjugates (GCs) in EIT and in normal respiratory and olfactory mucosae of the goat by means of conventional and lectin histochemistry, in order to shed light on the histogenesis of EIT. Morphologic and ultrastructural investigations showed two growth types of EIT: i.e., tubular and papillary patterns. Conventional histochemistry revealed the presence of neutral and carboxylated GCs in the olfactory glands and in the tubular part of EIT, as well neutral and sulphated GCs in the respiratory glands and in the papillary part of EIT, suggesting that the papillary pattern tumor arises from the respiratory glands, whereas the tubular portion of EIT arises from the olfactory glands. Lectin histochemistry gave further information on the expressed GCs.     

Renal pathology of polycystic kidney disease and concurrent hereditary nephritis in Bull Terriers

OBJECTIVE: To describe the renal lesions in Bull Terrier polycystic kidney disease (BTPKD), to confirm that the renal cysts in BTPKD arise from the nephron or collecting tubule, and to identify lesions consistent with concurrent BTPKD and Bull Terrier hereditary nephritis (BTHN). DESIGN: Renal tissue from five Bull Terriers with BTPKD and eight control dogs was examined by light and transmission electron microscopy. Clinical data were collected from all dogs, and family history of BTPKD and BTHN for all Bull Terriers. RESULTS: In BTPKD the renal cysts were lined by epithelial cells of nephron or collecting duct origin that were usually squamous or cuboidal, with few organelles. They had normal junctional complexes, and basal laminae of varying thicknesses. Glomeruli with small, atrophic tufts and dilated Bowman's capsules, tubular loss and dilation, and interstitial inflammation and fibrosis were common. Whereas the lesions seen in BTHN by light microscope were nonspecific, the presence of characteristic ultrastructural glomerular basement membrane (GMB) lesions and a family history of this disease indicated concurrent BTHN was likely in three of five cases of BTPKD. CONCLUSION: This paper provides evidence that renal cysts in BTPKD are of nephron or collecting duct origin. In addition, GBM lesions are described that strongly suggest that BTPKD and BTHN may occur simultaneously.     

Localization of extracellular matrix receptors in ICGN mice, a strain of mice with hereditary nephrotic syndrome.

Fibrotic degeneration was examined in the kidneys of ICR-derived glomerulonephritis (ICGN) mice, a novel inbred mouse line with a hereditary nephrotic syndrome of unknown etiology considered to be a good model of human idiopathic nephrotic syndrome. In the present study, we histochemically revealed changes in accumulation of extracellular matrix (ECM) components and in localization of integrins, cellular receptors for ECM, in the kidneys of ICGN mice with the progression of renal failure. Excessive accumulation of basement membrane (laminin and collagen IV) and interstitial (type III collagen) ECM components were demonstrated in the glomeruli and tubulointerstitum of ICGN mice. Marked deposition of type I collagen and tenascin was seen only in the glomeruli of ICGN mice but not in those of ICR mice as normal controls. Increased expression of integrin alpha1-, alpha2-, alpha5- and beta1-subunits in glomeruli with fibrotic degeneration and abnormal distribution of alpha6-subunit were noted in the kidneys of ICGN mice. Excessive laminin, a ligand of alpha6beta1-integrin, was demonstrated on the tubular basement membrane, but alpha6-subunit diffusely disappeared on the basal side of the tubular epithelial cells. We presumed that abnormal integrin expression in renal tubules causes epithelial cell detachment, and consequently tubular nephropathy, and results in disorder of ECM metabolism causing excessive accumulation of ECM components in the kidneys of ICGN mice.     

Spontaneous early-onset glomerulonephritis in a 8-week-old male Crj:CD1 (ICR) mouse

Glomerular lesions including membranoproliferative glomerulonephritis occur spontaneously in aged mice, but they are rare in young animals. In our laboratory, spontaneous glomerulonephritis was observed in an 8-week-old male Crj:CD1 (ICR) mouse. Macroscopically, the bilateral kidneys were discolored, but no edema or ascites was observed. Glomerular lesions were characterized by a thickening of capillary walls, a double-contoured basement membrane and mesangial expansion due to increased amounts of matrix. Ultrastructurally, mesangial interposition in the capillary wall and subendothelial deposition of basement membrane-like material were observed. No evidence of immune complex deposition or amyloid was found. On the basis of the observed clinical pathology and histopathology, a secondary form of glomerular lesion was excluded. The glomerular lesion was compatible with glomerulonephritis in a young Crj:CD1 (ICR) mouse.     

Reduced anchoring fibril formation and collagen VII immunoreactivity in feline dystrophic epidermolysis bullosa

Dystrophic epidermolysis bullosa was diagnosed in a cat with juvenile-onset epithelial sloughing of the oral mucosa, footpads, and haired skin. Dermoepidermal separation occurred in the absence of inflammation or cytolysis of basal epidermal cells. Collagen IV-specific immunostaining corroborated the fact that clefting took place below the epidermal basement membrane. Ultrastructural examination revealed that the proband's anchoring fibrils exhibited a filamentous morphology and were decreased in number compared with those in a normal cat. Finally, the attenuated immunoreactivity for collagen VII in our patient led us to suspect that its encoding gene, COL7A1, could be mutated in this case of feline dystrophic epidermolysis bullosa.     

Spinal arachnoid cyst in four dogs: diagnosis, surgical treatment and follow-up results

Spinal arachnoid cysts were diagnosed in four dogs; two schipperkes and two rottweilers. Myelography showed the cysts to be localised either at the second to third caudal vertebrae or between the eighth and tenth thoracic vertebrae. The cysts were drop-shaped with a dorsal midline localisation, intradural in the arachnoid space, and with a cranial opening. Surgical treatment was performed by one of two techniques; durotomy with drainage or durectomy with resection. As the pathological examination in one case revealed a lining of hyperplastic pia-arachnoid meningothelial cells in the cyst, it was assumed that the cyst originates from a developmental disturbance during formation of the arachnoid membrane. Follow-up studies were carried out from 10 months to four years postoperatively and revealed that there were no further problems in three out of four of the dogs during this period.     

Ultrastructural glomerular changes in experimental infection with the classical swine fever virus

Ultrastructural studies of glomerular changes were performed on 16 pigs experimentally infected with a highly virulent strain of the classical swine fever virus. Our observations revealed the thickening of glomerular basement membranes, swelling of endothelial cells and cytoplasmic vacuolization within podocytes containing abundant viral particles. An early viral infection of podocytes was suggested as the cause of selective swelling of the foot processes of these cells with the consequent obliteration of the glomerular urinary spaces. To our knowledge this is the first report of ultrastructural evidence of classical swine fever virions infecting glomerular podocytes.     

Immune complex-mediated glomerulopathy in Marek's disease

Chickens infected with Marek's disease (MD) virus developed immune complex (IC)-mediated glomerulopathy. Fluorescent antibody staining technique using antichicken globulin and antichicken complement was used to demonstrate IC in the kidney glomeruli. During the initial stages of MDV infection, IC deposits were seen on the glomerular basement membrane, but subsequently the entire glomerulus was involved. Mesangial cells also had IC deposits. Chicken complement was demonstrated in the glomeruli which had IC deposits. The number of glomeruli with IC deposition was higher in tumor-bearing birds than in non-tumor-bearing birds. Histologically, kidney lesion were characterized by thickening of basement membrane and proliferation of mesangial cells. It is suggested that IC-mediated glomerulopathy might be one of the major causes of death in MD.     

Glomerular lesions in renal biopsies of Saimiri boliviensis (primate) examined by light and electron microscopy and immunohistochemistry

In order to determine the existence of glomerular lesions in Saimiri boliviensis, renal biopsies were performed in 20 clinically healthy animals of similar age and both sexes. Biopsies were obtained by laparotomy with a Tru-Cut biopsy needle. Mesangioproliferative glomerulonephritis characterized by an increased number of mesangial cells and increased mesangial matrix was present in 35% of the animals. Proliferative glomerulonephritis characterized by increased numbers of epithelial and endothelial cells with narrowed capillary lumen, and membranous glomerulonephritis characterized by diffuse thickening, wrinkling, and occasional lamellation of basement membranes, were present in 15% of the samples. Ultrastructural features included increased mesangial matrix, fusion of the visceral epithelial foot processes, thickened glomerular basement membranes, and incipient lamellation. Immunohistochemical examination revealed granular deposits of immunoglobulin M in the cytoplasm of mesangial cells and in the mesangial matrix in 50% of the samples.     

Progressive renal disease in Soft-coated Wheaten Terriers: possible familial nephropathy

Clinical and pathological features are described in seven young Soft-coated Wheaten Terriers with chronic renal disease. The oldest dog was 21/2 years; in the other six, ages at death ranged from one to 15 months. Two of the puppies were littermates: one died at 4 weeks, the other at 12 months. Two of the dogs were examined at intervals up to 14 months, during which time there was progressive deterioration in renal function. All seven dogs had abnormal kidneys with cortical narrowing. The histological features were not consistent and included: tubular dilatation and basement membrane thickening; an unusually large proportion of immature glomeruli; persistence of interstitial connective tissue resembling foetal mesenchyme. Inflammatory change was minimal except in two dogs with super-imposed pyelonephritis. The clinical and laboratory data suggest that these dogs had dysplasia of the kidneys that progressed to chronic renal disease during early life. In three dogs there was a familial relationship.     

Membranous Glomerulonephropathy in a Hatano Low-avoidance Rat

Membranous glomerulonephropathy can be experimentally induced in rats, but spontaneous cases have been rarely reported. In this report, we present a typical case of spontaneous membranous glomerulonephropathy in a rat. A male Hatano low-avoidance (LAA) strain rat had a tumor mass on the right auricle, and was sacrificed at 41 weeks of age. Urinary screening by reagent strips revealed intense proteinuria. Histological tests revealed frequent presence of irregularly sized eosinophilic hyaline materials on the capillary wall and in the mesangium of renal glomeruli. Immunofluorescence revealed granular deposits of IgG, IgM, and C3 in the glomeruli. Subepithelial dense deposits were observed by electron microscopy accompanied by podocyte foot process effacement and occasional irregular thickening of the glomerular basement membrane. The rat also developed chronic lymphocytic pancreatitis, and the tumor mass on the right auricle was diagnosed as a fibrosarcoma. Screening tests for antibodies against major infectious agents and antinuclear antibody were negative. Western blot and indirect immunofluorescence analyses suggested the presence of an autoantibody against the pancreatic component. The glomerulopathy was considered an early stage of membranous glomerulonephropathy.     

End-stage kidney disease probably due to reflux nephropathy with segmental hypoplasia (Ask-Upmark kidney) in young Boxer dogs in Norway. A retrospective study

This paper is a retrospective morphologic study of 7 young Boxer dogs, showing end-stage kidney lesions compatible with chronic pyelonephritis with severe segmental cortical atrophy and fibrosis, associated with chronic tubulointerstitial inflammation of varying degree. Azotemia was observed in 6 of the 7 cases. The gross kidney lesions were as follows: bilateral small kidneys with numerous segmental cortical scars causing depression of the renal cortical surface. Histologic examination revealed salient atrophy of nephrons, including paucity of glomeruli, glomerulocystic lesions, colloid-filled tubular microcysts, and a conspicuously increased occurrence of arteries with narrowed lumina caused by intimal thickening. These segmental abnormalities were accompanied by pronounced interstitial fibrosis. All but 1 dog showed salient tubulointerstitial lympho-plasmacytic infiltration, which in 3 cases also included diffuse infiltration of polymorphonuclear neutrophilic leukocyte (PMN)-cells and occurrence of tubular PMN-casts. Morphologic signs of abnormal metanephric differentiation (renal dysplasia) were observed in all cases in the form of atypical tubules or asynchronous nephronic development (immature glomeruli) or both. However, other morphologic primary dysplastic features were absent. Based on the morphologic features, it is concluded that the end-stage kidney disease in these young Boxer dogs was the result of chronic atrophic nonobstructive pyelonephritis, most probably caused by vesico-ureteral reflux, compatible with reflux nephropathy causing segmental hypoplasia (Ask-Upmark kidney) in man. It is proposed that atypical tubular epithelium in the form of adenomatoid proliferation of collecting duct epithelial cells should be considered an acquired compensatory lesion, rather than the result of disorganized metanephric development.