oxalates and Cat-Diseases

The detection, treatment, and prevention of the causes underlying urolithiasis depend on knowledge of the composition and structure of the entire stone. Therefore, proper and complete analysis of uroliths is an important part of proper patient care. This article discusses methods of urolith retrieval, proper sample submission, methods of urolith analysis, and interpretation of results.

Topics: Animals; Cat Diseases; Cats; Cystine; Oxalates; Phosphates; Uric Acid; Urinary Calculi; Urinary Catheterization

This paper reports the results of a cohort study and randomised clinical trial (RCT) in cross-over design. In the cohort study, the range of urinary oxalate (Uox) and calcium (Uca) excretion was determined within a sample of the Dutch population of dogs and cats, and dietary and animal-related factors associated with these urine parameters were identified. Spot urine samples were collected from privately owned dogs (n=141) and cats (n=50). The RCT determined the effect of a commercial raw meat diet versus a dry diet on Uox and Uca excretion rate in 23 dogs. In the cohort study, Uox excretion ranged from 21.1 to 170.6 mmol oxalate/mol creatinine in dogs and 27.5 to 161.6 in cats. Urinary calcium excretion ranged from 3.4 to 462.8 mmol calcium/mol creatinine in dogs and 10.1 to 128.0 in cats. In dogs, increased Uox and Uca excretion was associated with (1) the intake of a dry diet as the primary source of energy, (2) receiving no snacks and (3) breed. Increased Uox excretion was associated with males as well. In cats, urine collection in anaesthetised subjects was identified as a confounder. In the RCT, feeding the dry diet resulted in higher Uox (P<0.001) and Uca (P=0.021) excretion rates in dogs.

Topics: Animal Feed; Animals; Breeding; Calcium; Calcium Oxalate; Cat Diseases; Cats; Cohort Studies; Creatinine; Cross-Over Studies; Dog Diseases; Dogs; Female; Male; Oxalates; Sex Factors; Urinary Calculi

Urinary tract stones are an important clinical problem in human and veterinary medicine. Hyperoxaluria is the single strongest promoter of kidney stone formation. The aims of the present study were to (a) evaluate oxalate degradation by a range of Bifidobacteria species and Lactobacillus species isolated from the canine and feline gastrointestinal tract in vitro and (b) to determine the impact of oxalate degradation by selected strains in vivo. The bacteria were grown in oxalate-containing media and their ability to degrade oxalate in vitro was determined using reverse-phased HPLC. Bifidobacteria species and Lactobacillus species that degraded oxalate in vitro and survived gastric transit were selected for further examination. The selected probiotics were fed to rats for 4 weeks. Urine was collected at week's 0, 2 and 4 and oxalate levels determined by HPLC. In vitro degradation was detected for 11/18 of the Lactobacillus species. In contrast, the capacity to degrade oxalate was not detected for any of the 13 Bifidobacterium species tested. Lactobacillus animalis 223C, Lactobacillus murinus 1222, L. animalis 5323 and L. murinus 3133 were selected for further investigation in a rat model. Urinary oxalate levels were significantly reduced (p<0.05) in animals fed L. animalis 5323 and L. animalis 223C but were unaltered when fed L. murinus 1222, L. murinus 3133 or placebo. Probiotic organisms vary widely in their capacity to degrade oxalate. In vitro degradation does not uniformly translate to an impact in vivo. The results have therapeutic implications and may influence the choice of probiotic, particularly in the setting of enteric hyperoxaluria.

Topics: Animals; Bifidobacterium; Body Weight; Cat Diseases; Cats; Dog Diseases; Dogs; Female; Gastrointestinal Tract; Lactobacillus; Oxalates; Probiotics; Rats; Rats, Sprague-Dawley; Urinary Calculi

Two unrelated Ragdoll cat mothers in Norway were found dead from renal disease. The histopathology was consistent with oxalate nephrosis with chronic or acute-on-chronic underlying kidney disease. Both cats had offspring and relatives with signs of urinary tract disease, including a kitten dead with urethral gravel. Eleven living Ragdoll cats, including nine relatives of the dead cats and the male father of a litter with similarly affected animals, were tested for primary hyperoxaluria (PH) type 1 and 2 by urine oxalate and liver enzyme analysis. Renal ultrasound revealed abnormalities in five living cats. One of these was azotaemic at the time of examination and developed terminal kidney disease 9 months later. A diagnosis of PH was excluded in 11 cats tested. The inheritance and aetiological background of the renal disease present in the breed remains unresolved at this point in time.

Topics: Animals; Cat Diseases; Cats; Female; Hyperoxaluria, Primary; Kidney Failure, Chronic; Male; Nephrosis; Norway; Oxalates; Ultrasonography

Topics: Acute Kidney Injury; Animals; Cat Diseases; Cats; Diagnosis, Differential; Female; Hyperoxaluria, Primary; Oxalates

A 7-month-old, male European cat was examined because of weakness and inappetence. The cat was dehydrated, polypnoeic and severely weak. Severe, generalised muscle atrophy was present. Spinal reflexes were all decreased to absent. Blood analysis and urinalysis showed several abnormalities, including intermittent hyperoxaluria. The L-gliceric acid concentration was remarkably increased. Electrodiagnostic tests of the peripheral nervous system were abnormal. At necropsy, generalised muscle atrophy was observed. Microscopically, both kidneys showed intraluminal birefringent oxalate crystals. Motor neuron degeneration and accumulation of neurofilaments were observed in the axons of the spinal motor neurons.

Topics: Acute Kidney Injury; Animals; Cat Diseases; Cats; Electromyography; Female; Hyperoxaluria, Primary; Muscle Weakness; Muscular Atrophy; Oxalates

A pathological study on 5 of 21 cats affected naturally with systemic calcinosis was performed. The animals ranged in age from 1 to 9 years. Hematology and serum chemistry analyses showed the elevated values of phosphorus, blood urea nitrogen and serum creatinine. X-ray examination disclosed the increased density of systemic bones. Histologically, marked calcification was present at the vascular walls of almost all the organs including the lungs, trachea, kidneys, heart, aorta, alimentary tracts, choroid plexus and bones. In the lungs, kidneys and stomach, the calcified lesions were associated with deposition of oxalate crystals. Serum chemistry showed more elevated values of 25-hydroxycholecalciferol (vitamin D) of the affected cats than the normal level. Retrospective examination revealed that these cats had been fed the commercial pet foods containing a large amount of vitamin D (6,370 IU/100 g diet) from their young age, and its value was about ten times as much as that of the control food (680 IU/100 g diet). Pathological changes found in the cats from the experimental vitamin D3 toxicosis were similar to those in the natural cases. In addition, tissue levels of calcium, phosphorous and zinc in the lungs and kidneys were markedly elevated in both natural and vitamin D-intoxicated cases. These findings suggest that long-term feeding of the pet food containing excessive vitamin D was responsible for the outbreak of the systemic calcinosis in the cats.

Topics: Animals; Aorta; Blood Urea Nitrogen; Bone and Bones; Calcifediol; Calcinosis; Calcium; Cat Diseases; Cats; Choroid Plexus; Creatinine; Disease Outbreaks; Drug Overdose; Female; Japan; Kidney; Lung; Male; Oxalates; Phosphorus; Stomach; Trachea; Vitamin D; Zinc

Renal ultrasonographic findings in 12 dogs and 3 cats determined to have oxalate nephrosis presumed to be secondary to ethylene glycol intoxication were examined. Ultrasonographic changes varied from mild to marked increases in renal cortical echogenicity. A pattern of greater than normal cortical and medullary echogenicity with persistence of areas of lesser echo intensity at the corticomedullary junction and central medullary regions was observed. This pattern, termed the halo sign, was recognized in 7 dogs and 1 cat concurrent with the development of clinical anuria. Ultrasonographic patterns in these clinical cases were similar to those observed in a previous study of dogs with experimentally induced ethylene glycol nephrosis. Ultrasonographic findings were not considered pathognomonic of ethylene glycol nephrosis. Due to the high death rate reported in the cases surveyed, detection of ultrasonographic changes was considered to warrant a guarded to poor prognosis. Because of the association of the halo sign with anuria, its detection was considered to warrant a grave prognosis.

Topics: Animals; Cat Diseases; Cats; Dog Diseases; Dogs; Ethylene Glycols; Nephrosis; Oxalates; Prognosis; Retrospective Studies; Ultrasonography

The clinical features of a newly recognised inherited disease, primary hyperoxaluria in the cat, are reported. Affected cats developed acute renal failure between five and nine months old owing to the deposition of oxalate crystals in the tubules of the kidney. In addition to the signs attributable to kidney failure the affected animals became profoundly weak; there was evidence of denervation atrophy in skeletal muscle, and accumulations of neurofilaments were found in the proximal axons of the ventral horn cells and dorsal root ganglion cells of the spinal cord. Examination of urine from affected cats revealed L-glyceric aciduria and intermittent hyperoxaluria suggesting that the disease is a feline analogue of the human disorder, primary hyperoxaluria type 2. This supposition was confirmed by liver enzyme studies.

Topics: Acute Kidney Injury; Animals; Atrophy; Cat Diseases; Cats; Electromyography; Female; Hyperoxaluria; Hyperoxaluria, Primary; Kidney; Male; Muscles; Oxalates; Pedigree; Spinal Cord

Topics: Acute Kidney Injury; Animals; Cat Diseases; Cats; Disease Models, Animal; Female; Glyceric Acids; Hyperoxaluria; Male; Oxalates; Oxalic Acid

Topics: Animals; Cat Diseases; Cats; Oxalates; Urinary Calculi

Topics: Animals; Brain; Carnivora; Cat Diseases; Cats; Dog Diseases; Dogs; Ethylene Glycols; Glycols; Nephritis; Neurologic Manifestations; Oxalates; Pathology; Poisoning; Toxicology