Experimental Mycotoxic Nephropathy in Pigs Provoked by a Diet Containing Ochratoxin A and Penicillic Acid

Mycotoxic nephropathy was induced in 18 young pigs by diets contaminated with strains of Aspergillus ochraceus containing ochratoxin A (OTA) and penicillic acid (PA) at levels corresponding to those naturally encountered in animal feeds in Bulgaria. Haematological and biochemical parameters, as well as the morphological and ultrastructural changes in various internal organs, and especially in the kidneys, were examined at different stages of development of the disease. A mottled surface of the kidneys was only seen in pigs exposed to a mouldy diet containing 180 ppb OTA for 3 months, but microscopic lesions, as well as changes in various haematological and biochemical parameters, were observed in all groups exposed to the same mouldy diet containing only 90 or 180 ppb OTA. Histological examination showed two types of change: degenerative changes affecting the epithelial cells of the proximal tubules, which predominated at the initial stage, and proliferative changes in the interstitium, which predominated at the later stage of the disease. Telangiectasis and lymph stasis were also seen, as well as degenerative changes in the capillary endothelium. The characteristic renal lesions were similar to those observed in spontaneous cases of mycotoxic porcine nephropathy in Bulgaria, but they were a little different from the classic Danish porcine nephropathy. The enhanced toxicity of OTA in our study may be due to a synergistic effect between OTA and PA or to some other unknown metabolites produced by the same ochratoxinogenic strains of A. ochraceus.     

IgM-mesangial nephropathy in callithricids

Spontaneous IgM-mediated mesangioproliferative nephropathy was detected in 91% of tamarins and marmosets over 6 months old. The disease remains silent for long periods but is progressive. It is responsible for, or is at least related to, the cause of death in 20% of animals. Morphological characteristics are those of mesangial hyperplasia accompanied by subacute to chronic interstitial inflammation. The immunopathological demonstration of early accumulation of IgM within the mesangial cells and matrix, followed by interstitial deposition of C3, suggests that the lesion is mediated by immunological mechanisms.     

Familial nephropathy in cocker spaniels

In 21 normal dogs of different breeds and ages the number of nephrons was calculated from paraffin sections in comparison with a maceration method. With these methods the number of glomeruli x 1000 per kidney appeared to be 502 +/- 213 and 515 +/- 230 respectively. The histological method appeared to be acceptable for the determination of the number of glomeruli in incomplete kidneys. The examined Cocker Spaniels consisted of 5 animals without renal problems for control and 21 animals with nephropathy: 12 of 1-2 years, 6 of 4-6 years and 3 of 9-10 years old dogs. As indication for the present number of nephrons the glomeruli were counted in bands of whole cortex with a width of 1 mm. The number of glomeruli per band of cortex in the nephropathic Cocker Spaniels (15.0 +/- 3.0) was not drastic lower than those of the normal Cockers (20.8 +/- 2.5) and of 7 normal adult dogs of different breeds (17.2 +/- 2.2). On pathological examination the nephropathic kidneys showed a membranoproliferative-sclerosing glomerulonephritis with extra-capillary reaction leading to glomerular obsolescence. The animals showed evident proteinuria and final renal insufficiency. It was concluded that the pathogenesis of the familial nephropathy in this breed will not be caused by cortical hypoplasia, but by a primary glomerulopathy.     

Membranous nephropathy in the dog

Membranous nephropathy, a disease syndrome characterized by severe proteinuria and often accompanied by the nephrotic syndrome, was identified in 29% of a population of 46 proteinuric dogs. Renal lesions were characterized by the presence of subepithelial immunoglobulin deposits distributed diffusely along the glomerular capillary wall. Advanced stages were associated with progressive thickening of capillary basement membranes and incorporation of the immune deposits. These changes were followed by either glomerulosclerosis or recovery. Characteristic morphologic stages were correlated with clinical pathologic findings which showed that the level of proteinuria, hypoalbuminemia, and consequent nephrotic syndrome was most severe in the initial stages of membranous nephropathy while the level of azotemia increased in the more advanced stages of the syndrome.     

Acute nephropathy in young lambs

Acute renal failure was diagnosed by clinical, necropsy and histological criteria in 39 flocks (20 low ground, 13 hill and six marginal upland) in areas served by six veterinary investigation centres. Forty-eight lambs of 12 different breeds or crosses were investigated. The mean age of affected lambs was 38 days (range seven to 84 days); 21 lambs (44 per cent) were aged seven to 28 days, while only eight (17 per cent) were older than two months. Mortality in clinically affected lambs was almost 100 per cent, with no response to various treatments. Histological examination showed that 40 lambs (83 per cent) had nephrosis, while the rest had toxic tubular necrosis, interstitial nephritis or tubular damage associated with oxalate crystal deposits. Only about half of the lambs had any evidence of enteric infections or enteropathy. Acutely ill lambs had azotaemia, haemoconcentration and proteinuria; some lambs had glycosuria or haematuria. Samples of plasma from 22 lambs with nephrosis were compared with similar samples from 82 incontact but asymptomatic lambs. The clinically affected group had significantly elevated plasma urea, creatinine, total protein, globulin, phosphorus and chloride concentrations and significantly reduced plasma calcium concentrations compared with healthy lambs. Affected lambs had a significant reduction also in the calcium:phosphorus ratio. No significant differences between groups was found in plasma concentrations of albumin, glucose, lactate, glycerol, creatine kinase, alkaline phosphatase, sodium, potassium or magnesium.     

Familial nephropathy in Cocker Spaniels

A clinical diagnosis of chronic renal failure associated with nephron atrophy and fibrosis was made in 4 blue roan Cocker Spaniels. The lesion was considered to be the result of a primary glomerulopathy. All dogs were closely related. The findings were similar to those previously described for renal cortical hypoplasia. On the basis of the morphological findings and genetic characteristics, the use of the more appropriate term, familial nephropathy is encouraged.     

Mycotoxic tremorgens of Claviceps paspali and Penicillium cyclopium: a comparative study of effects on sheep and cattle in relation to natural staggers syndromes

Claviceps paspali sclerotia were dosed orally at various levels to sheep and cattle and the neurotoxic effects are described. Evidence is presented which indicates that the tremors are produced by a neutral tremorgen fraction. The ergot alkaloids, principally D-lysergic acid alpha-hydroxyethylamide and its isolysergic acid isomer, are not involved. The mixture of C paspali tremorgens has not been separated and characterised but its components are chemically related to other known tremorgens, such as penitrem A, produced by saprophytic moulds, notably Penicillium cyclopium. P cyclopium mycelium and C paspali sclerotia were dosed to produce comparable effects in sheep and in cattle. Similarly, effects of penitrem A and tremorgen concentrate of C paspali were compared after intravenous dosage to sheep. Observed enurotoxic effects of both moulds were identical in most respects. A low level of tremorgenic activity was detected at the honeydew stage of C paspali. These findings are discussed in relation to staggers syndromes occurring in grazing livestock.     

Juvenile nephropathy in 37 boxer dogs

OBJECTIVES: The purpose of this study was to review and characterise the clinical presentation of young boxer dogs with chronic kidney disease referred to the authors' institutions. METHODS: Records were collected retrospectively from 37 boxer dogs, less than five years of age, which had presented with azotaemia, inappropriately low urine concentrating ability, and ultrasound or radiographic evidence of abnormal kidneys. RESULTS: Clinicopathological findings included azotaemia, hyperphosphataemia, anaemia, isosthenuria and proteinuria. Ultrasonographic findings included hyperechoic renal cortices, loss of corticomedullary junction definition, dilated pelves and irregularly shaped small kidneys. Renal histopathological findings included pericapsular and interstitial fibrosis, inflammatory cell infiltration, dilated tubules, sclerotic glomeruli and dystrophic calcification. Survival time of the dogs varied from zero to over five years after diagnosis. CLINICAL SIGNIFICANCE: This paper documents features of the presentation and progression of juvenile nephropathy in boxer dogs. While juvenile nephropathy has been reported in individual cases of boxer dogs previously, this is the first reported case series.     

Feline kaliopenic polymyopathy/nephropathy syndrome

The prevalence of hypokalemia in cats has probably been underestimated until recently. Like many other "contemporary" diseases, this syndrome is probably not new; however, it is now more easily recognized because of the identification of associated dietary and disease risk factors, clinical signs, and laboratory abnormalities, which have been linked to the expected pathophysiology of potassium depletion in the cat.     

Juvenile nephropathy in a Weimaraner dog

A case of juvenlle nephropathy In a two-year-old Welmaraner bitch Is reported. Although juvenlle nephropathy has been described in several breeds of dogs, this is the first report In a Welmaraner. Clinical aspects, blood analysis, renal pathology and extrarenal changes are described. The renal changes consisted of tubular as well as glomerular lesions, similar to those described in the miniature schnauzer. The main extrarenal lesion was degeneration and necrosis of subendocardial myocytes in the left atrial wail associated with an inflammatory reaction and focal necrotising arteritis.     

Juvenile nephropathy in a Samoyed bitch

A case of juvenile nephropathy is reported in a 16-week-old Samoyed bitch. Clinical, laboratory and gross postmortem findings followed by histological analysis of kidney, liver and cerebrum and transmission electron microscopy of renal tissue are described. The histological and ultrastructural findings are similar to those found in a line of related Samoyeds in Canada, termed Samoyed hereditary glomerulopathy. The case is, however, distinct from those documented in Canada as the condition is present in a young female and the mode of inheritance elucidated in Canada is one of X-linked dominance, with the disease only developing in its juvenile form in males.     

Familial nephropathy in the Cocker Spaniel

Eight cases of familial nephropathy in Cocker Spaniels aged between 10 and 24 months were referred to the Renal Unit of the Small Animals Centre from 1977–1982 (cases 1–8). The disease took a rapid course and progressed to a fatal outcome within 2 months of what may have been an insidious onset. Five of these cases were from litters in which at least one other dog had died with uraemia. Autopsy material was received from twelve other young Cocker Spaniels. In four of these cases urinalysis was performed and in a further four; biochemical evidence of renal failure was obtained. The most striking pathological changes in the kidneys were found in the glomeruli.     

Familial progressive nephropathy in young Bull Terriers

The clinical, clinicopathological and pathological findings are described in three Bull Terrier bitches with advanced renal disease. The bitches were less than four years old and showed variable presenting signs but anorexia, lethargy and polydipsia were the most frequent. All three dogs were azotaemic and isosthenuric. Urinary protein was measured in two of the three cases. Both were proteinuric. At necropsy all dogs had shrunken kidneys. Histological examination revealed nephron loss, atrophy of glomerular tufts, interstitial fibrosis, and mineralisation of basement membranes.

The progressive renal disease in these dogs was similar to the condition reported in Bull Terriers in Australia, and is probably familial and inherited.