Urinary orotic acid-to-creatinine ratios in cats with hepatic lipidosis

Jan L. VanSteenhouse From the Departments of Veterinary Pathology (VanSteenhouse), Veterinary Clinical Sciences (Dimski, Taboada), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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Donna S. Dimski From the Departments of Veterinary Pathology (VanSteenhouse), Veterinary Clinical Sciences (Dimski, Taboada), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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David H. Swenson From the Departments of Veterinary Pathology (VanSteenhouse), Veterinary Clinical Sciences (Dimski, Taboada), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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Joseph Taboada From the Departments of Veterinary Pathology (VanSteenhouse), Veterinary Clinical Sciences (Dimski, Taboada), and Veterinary Physiology, Pharmacology, and Toxicology (Swenson), School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803.

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Abstract

Objective

To determine urinary orotic acid (OA) conentration and evaluate the urinary OA-to-creatinine ratio (OACR) in cats with hepatic lipidosis (HL).

Animals

20 cats with HL and 20 clinically normal cats.

Procedure

Hepatic lipidosis was diagnosed on the basis of clinical signs, results of serum biochemical analyses, exclusion of other concurrent illness, and cytologic or histologic evaluation of liver biopsy specimens. Urine samples were collected from each cat and frozen at −20 C until assayed. Urine creatinine concentrations were determined, using an alkaline picrate method followed by spectrophotometric assay. Urine OA concentration was determined, using high-performance liquid chromatography. Minimum amount of detectable OA in feline urine was 1 µg/ml. Because of small interfering peaks near the base of the OA peak, the minimum quantifiable concentration of OA was determined to be 5 pg/ml. Urinary OACR was compared in both groups of cats.

Results

Differences in urinary OACR were not detected between clinically normal cats and cats with HL. Peaks were not detected for urinary OA in any of the 20 clinically normal cats. Of the 20 HL cats, 14 did not have detectable peaks for urinary OA. Of the 6 HL cats that had detectable urinary OA peaks, 3 had values of < 5 µg/ml.

Conclusions

Apparently, OACR does not increase significantly in cats with HL.

Clinical Relevance

Urinary OACR is not a useful diagnostic test for HL in cats. (Am J Vet Res 1999; 60:753–754)

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