A Case of Renal Oxalosis in a 3-Month-Old Cat Raised under Controlled Conditions

Abstract

ABSTRACT. The kidneys of a 3-month-old female cat were examined. The cat which had been raised under controlled conditions with no history of any poisoning showed progressive weight loss with increases in blood BUN and creatinine concentrations. At necropsy, both kidneys were firm in consistency with formation of focal scars. Histopathologically, widespread deposition of crystals was observed in the renal tubules (in both dilated lumina and degenerative epithelia) accompanying mild interstitial fibrosis with lymphocyte infiltration. The crystals were colorless or basophilic on the hematoxilin and eosin-stained section and could be visualized with polarized light as doubly fractile crystals. The crystals were identified as calcium oxalate crystals by histochemical examinations using von Kossa stain and alizarin red S stain under different conditions and by ultrastructural examination. Judging from the above-mentioned findings, the present renal lesion detected in an infant cat was diagnosed as renal oxalosis which was suspected to be hereditary in nature. Oxalosis is characterized by widespread deposition of calcium oxalate crystals in the kidneys, bones, arterial media and myocardium, following increased concentrations of oxalate in body fluids, including the urine (hyperoxaluria) [4-8, 14, 16]. Deposition of calcium oxalate crystals most frequently occurs in the kidneys, resulting in renal failure and/or urolithiasis in severe cases. This renal disorder is called renal oxalosis. This paper describes the results of histopathological, histochemical, and ultrastructural examinations on the kidneys of an infant cat with renal oxalosis.A female mixed-breed cat which had been raised in a laboratory under controlled conditions with no history of any poisoning showed progressive weight loss with increases in BUN (from 140.1 to 388.5 mg/dl in 1 week -reference range 10-30 mg/dl) and creatinine (from 3.56 to 7.94 mg/dl in 1 week -reference range 0.8-1.4 mg/dl) concentrations, indicators of renal tubule disorder. At 3 months of age, the cat was euthanized and subjected to postmortem examination in the laboratory. At necropsy, both kidneys were firm in consistency with formation of focal scars. In the other organs, there were no gross abnormalities observed.The kidneys were sent to the authors' laboratory for histopathological, histochemical and ultrastructural examinations. Renal tissues were fixed in 4% phosphate-buffered paraformaldehyde (PFA) solution, embedded in paraffin, sectioned at 4 μm, and stained with hematoxylin and eosin (HE). Some sections were also subjected to von Kossa stain, alizarin red S stain with a modification of the previously published procedure [6,17], periodic acid-Schiff (PAS) reaction, periodic acid-methenamine-silver (PAM) stain, masson trichrome stain or phosphotungstic acid hematoxylin (PTAH) stain.For ultrastructural examination, small pieces of the PFAfixed tissues were post-fixed in 1% osmium tetroxide and embedded in epoxy resin. Ultrathin sections were doublestained with uranyl acetate...

Pathology and Epidemiology of Oxalate Nephrosis in Cheetahs

“…In humans and cats with inherited oxalate nephrosis, the disease is seen in juveniles. 6,15,16,27,49,78 In this study, although cheetahs < 1.5 years old had significantly more crystals than older cheetahs, which might indicate an inherited predisposition, relatively large numbers of crystals were seen in cheetahs of all ages. Lesions that are characteristic of primary disease in humans and cats, including granulomatous nephritis associated with interstitial oxalates, widespread tissue oxalate deposition, 10,12,45,66,80 and neurological disease, 30,52 were not seen in the cheetahs in this study.…”

“…This effect of oxalate crystals on tubular epithelium is well documented in humans and animals. 11,16,29,44,49,66,78,83 Raman spectroscopy confirmed that the majority of crystals were calcium oxalate. Melamine and other renal crystals were ruled out because the Raman spectral fingerprints did not match these compounds.…”

“…This effect of oxalate crystals on tubular epithelium is well documented in humans and animals. 11,16,29,44,49,66,78,83…”

Pulmonary Dystrophic Oxalosis and its Possible Relation to Fibrosis in an Aged Gentoo Penguin (<i>Pygoscelis papua</i>)

“…In humans, the hereditary oxalosis occurs as a result of autosomal recessive disorder in which there is abnormality of glycoxylate metabolism resulting in excess production of oxalate ions and increased absorption of oxalate ions by the gastrointestinal tract [3]. In veterinary medicine, there are a few reports on hereditary renal oxalosis in cats [26]. In humans, on the other hand, the acquired oxalosis includes 5 categories; due to excess ingestion of oxalate or oxalate producing compounds (exogenous oxalosis): increased absorption of normal dietary oxalate in enteric diseases (enteric oxalosis): oxalosis associated with chronic renal insufficiency (uremic oxalosis): excessive intake of vitamin C, and dietary insufficiency of pyridoxine and thiamine pyrophosphate (deficiency oxalosis) [3,6,22].…”