The efficacy of 4-methylpyrazole (4-MP) and ethanol as treatment for ethylene glycol (EG) intoxication in cats was compared. Twenty-two cats were assigned at random to 6 experimental groups. Cats of 1 experimental group were given only 4-MP; those of another experimental group were given only EG. Cats of 3 experimental groups were intoxicated with EG and given 4-MP at 0 hour or 2 or 3 hours after EG ingestion, and those of 1 experimental group were given EG and treated with ethanol 3 hours after EG ingestion. Physical, biochemical, hematologic, blood gas, serum and urine EG concentrations, and urinalysis findings were evaluated at 0, 1, 3, 6, 9, 12, 24, 48, and 72 hours, 1 week, and 2 weeks after EG ingestion, or 4-MP treatment in cats of the 4-MP only group. The half-life of EG and percentage of ingested EG excreted unchanged were determined for each group. 4-Methylpyrazole treatment at 0 hour was most effective at preventing metabolism of EG. 4-Methylpyrazole was not effective in preventing development of renal failure when given 2 or 3 hours after EG ingestion. Ethanol given 3 hours after EG ingestion was successful in preventing development of renal dysfunction in 2 of the 6 cats treated 3 hours after EG ingestion. Of the remaining 4 cats treated with ethanol, 2 developed transient renal dysfunction and 2 developed acute oliguric renal failure and were euthanatized. 4-Methylpyrazol given 2 or 3 hours after EG ingestion was less effective in preventing EG metabolism than was ethanol given 3 hours after EG ingestion. Therefore 4-MP, at the dose found to be effective in dogs, cannot be recommended as an alternative to ethanol for treatment of EG intoxication in cats.

Amino acid profiles and serum albumin and serum total protein concentrations were evaluated in dogs with renal disease. Nine dogs ranging in age from 1 to 15 years were identified as having mild to moderate chronic renal failure (CRF; exogenous creatinine clearance, 0.5 to 2.13 ml/kg of body weight/min). These dogs and a group of 10 clinically normal control dogs were fed a diet containing 31% protein for 8 weeks, at which time serum and urine amino acid assays and clearance studies were performed. All dogs then were fed a diet containing 16% protein for 8 weeks and then reevaluated. Chronic renal failure was associated with mild abnormalities in serum concentrations of amino acids. When fed the higher protein diet, dogs with CRF had lower serum concentrations of glutamine, leucine, proline, and serine and higher serum concentrations of cystathionine and 3-methylhistidine than clinically normal control dogs. When fed the low protein diet, dogs with CRF had lower serum serine concentrations and higher serum concentrations of cystathionine, phenylalanine, and 3-methylhistidine. Urine excretion of amino acids in all dogs on both diets was low, and dogs with CRF had lower renal clearances of 3-methylhistidine than control dogs. There were no significant differences in concentrations of serum albumin and total solids between either group, regardless of diet. We concluded that dogs with mild to moderately severe CRF have mild abnormalities of serum free amino acid concentrations, but renal conservation of essential amino acids is not impaired.

Four diets were formulated to contain: 16% protein and 0.4% phosphorus-diet 1; 16% protein and 1.4% phosphorus-diet 2; 32% protein and 0.4% phosphorus-diet 3; and 32% protein and 1.4% phosphorus-diet 4. Forty-eight dogs were fed diet 1 for 3 months after surgical reduction of renal mass, then were allotted to 4 groups of 12 dogs each, with equal mean values for glomerular filtration rate (GFR). Dog of groups 1-4 were fed diets 1-4, respectively, for 24 months. Data collected from the dogs during and at termination of the study were analyzed statistically for effects of dietary protein, phosphorus (P), time, and interactions between these factors. During the 24 months of study, 24 dogs developed uremia and were euthanatized for necropsy. Necropsy also was performed on the remaining 24 dogs after they were euthanatized at the end of the study. Dog survival was significantly enhanced by 0.4% P diets (vs 1.4% P diets), but survival was not significantly influenced by amount of dietary protein. The 0.4% P diets (vs 1.4% P diets) significantly increased the period that GFR remained stable before it decreased, but dietary protein did not have significant effect. Significant blood biochemical changes attributed to P, protein, and time were identified during the study. Terminally, plasma parathyroid hormone concentration was significantly increased from prediet values in all groups of dogs. Urine protein excretion was not significantly affected by dietary amount of either protein or P, when measured by either timed urine collection or urine protein-to-creatinine ratio. A tendency was seen for increased protein excretion with passage of time. Histologic and mineral analyses of kidneys removed at necropsy revealed some significant difference attributable to diet, but differences were more marked when diet was ignored, and the 24 surviving dogs were compared with the 24 that developed uremia. Overall, amount of dietary P was more important than amount of dietary protein for preventing adverse responses. However, because renal damage specifically attributable to either dietary component was not obvious, it is possible that the effects of P were manifested by extrarenal mechanisms.

The feasibility of renal arterial infusion of nonbiodegradable microspheres as a model of chronic renal disease in dogs was evaluated. Resin-coated, styrene-divinyl benzene copolymer microspheres were infused into the kidneys of healthy adult Beagles by direct injections of both renal arteries in a single surgical procedure. Injections of 25-micrometer diameter microspheres had minimal effect on either the clinical status or serum values of the dogs. Histologic examination revealed the majority of the microspheres lodged within the capillary beds of the glomeruli, and little change to the kidneys. However, injections of 50-micrometer diameter microspheres caused significant increases in serum concentrations of urea nitrogen and creatinine. Histologically, the larger microspheres obstructed afferent arterioles and small arteries, which caused diffuse glomerular necrosis and nephron damage. With doses ranging from 1 to 3 million microspheres/dog, a correlation between the quantity of microspheres injected and severity of renal damage was observed. The optimal dose for producing a model of moderate renal disease was determined to be 1.8 million microspheres/dog (0.9 million microspheres/kidney). During long-term studies, microsphere-injected dogs fed a moderately restricted protein ration remained relatively azotemic, compared with control dogs on the identical ration. During the 5-month postsurgical period, the serum urea nitrogen concentration averaged 18.41 +/- 1.59 mg/dl (mean +/- SE) for the microsphere-injected dogs vs 9.31 +/-0.38 for the control dogs (P < 0.001). Similarly, the mean serum creatinine value was significantly higher (P = 0.020) for the microsphere-injected dogs, compared with the controls (1.23 +/- 0.12 mg/dl vs 0.94 +/- 0.03). In addition, the difference in mean endogenous creatinine clearance rates was statistically significant (microsphere-injected 1.02 0.05 ml/min/kg, vs control 1.53 +/- 0.06, P < 0.001).

In order to investigate the renal pathology of spontaneously occurring renal lesions, basic macroscopic inspection was conducted to 3,850 pigs randomly collected from local slaughter houses, and a total of 355 pigs (9.2 %) were detected with various gross pathological conditions. Renal morphologic patterns for gross lesions were classified histopathologically as 123 (34.5 %) congestion, 81 (22.8 %) acute interstitial nephritis, 52 (14.7 %) chronic interstitial nephritis, 49 (13.8 %) hemorrhage, 39 (11.0 %) renal cyst, 29 (8.2 %) chronic glomerulonephritis, 18 (5.1 %) acute glomeruonephritis, 14 (3.9 %) infarction, 11 (3.1 %) thrombosis, 5 (1.4 %) atrophy, 5 (1.4 %) pyelonephritis and 1 (0.3 %) lymphosarcoma.

In this study, we aimed to evaluate the oxidative damage caused by lipid peroxidation due to renal coccidiosis by histopathological and immunohistochemical methods. Material-The material of this study was made up of tissue samples taken from 139 geese whose average age was 10 weeks, who were brought to our department dead between 2013-2020. Tissue samples taken were fixed in 10% buffered formaldehyde solution. 5 µm-thick sections were taken from the paraffin blocks prepared after routine tissue follow-up procedures. Hematoxylin & Eosin staining was applied to the sections in order to detect histopathological changes. Sections were examined and photographed under a light microscope.Various clinical signs such as fever, respiratory distress, weakness, anorexia, tremors, inability to get up from the ground, balance disorders, rotational movement, diarrhea, wheezing were detected in geese. In systemic necropsies of geese, large and small white nodular structures were detected in the kidney. In histopathological examinations, coccidiosis agents (E. truncata) were found in the tubular epithelium of the kidney. Necrosis and mononuclear cell infiltration were observed in the tubules due to the presence of E. truncata. In addition, edema and hyperemia in the lungs, multifocal necrosis in the liver, cell infiltration in the portal spaces and enteritis were other important histopathological findings. In one case, aspergillosis was detected together with renal coccidiosis. We observed that MDA expression was more severe in oocyst stages, which is the mature form of the parasite, compared to other parasitic life stages.Based on the results obtained from this study, it was revealed that renal coccidiosis in geese caused lipid peroxidation / oxidative damage through the increase in MDA expression.

Urinary liver-type fatty acid-binding protein (uL-FABP) is a clinically useful biomarker for monitoring chronic kidney disease (CKD) in humans. However, long-term monitoring of uL-FABP in CKD cats has not been reported. The objective of this preliminary study was to investigate whether the urinary excretion of L-FABP could predict the deterioration of renal function in 2 CKD model cats. Urinary liver-type fatty acid-binding protein (uL-FABP) increased before standard renal biomarkers, including serum creatinine, blood urea nitrogen, and symmetric dimethylarginine, in 1 cat with deteriorating renal function, but remained low and relatively stable in another cat with stable renal function. Our results suggest that uL-FABP is a potential clinical biomarker for predicting the progression of CKD in cats, as it is in humans.