Assessment of urinary N-acetyl-beta-D-glucosaminidase activity in geriatric cats with variable plasma creatinine concentrations with and without azotemia
- PMID: 20113234
- DOI: 10.2460/ajvr.71.2.241
Assessment of urinary N-acetyl-beta-D-glucosaminidase activity in geriatric cats with variable plasma creatinine concentrations with and without azotemia
Abstract
Objective: To validate a non-automated technique for the measurement of urinary N-acetyl-beta-D-glucosaminidase (NAG) activity in cats and assess the correlation between NAG index, plasma creatinine concentration, and proteinuria.
Animals: 197 client-owned cats (> or = 9 years old; 119 neutered males and 78 neutered females) of which 103 had previously been determined to have chronic kidney disease (CKD).
Procedures: Preliminary assay validation was performed for a non-automated colorimetric technique for quantification of NAG activity. The effect of storage of samples was examined. A cross-sectional study was performed to assess urinary NAG index in cats with variable plasma creatinine concentrations and with proteinuria, as quantified by use of the urine protein-to-creatinine ratio (UP:C).
Results: Interassay coefficients of variance (CVs) in cats with low (mean, 0.64 U/L), medium (mean, 4.38.U/L), and high (mean, 8.48 U/L) urine NAG activity were 25.9%, 14.4%, and 25.1%, respectively, but intra-assay CVs were < 20%. Urine NAG activity was stable for 4 freeze-thaw cycles and for storage at -20 degrees C. There was no significant difference in log NAG index when cats (n = 197) were grouped according to plasma creatinine concentration, but a moderate positive correlation was found between log NAG index and log UP:C (r2 = 0.259).
Conclusions and clinical relevance: N-acetyl-beta-D-glucosaminidase activity can be quantified in feline urine by use of a non-automated colorimetric technique. However, data should be interpreted cautiously because of high interassay CVs. The NAG index in cats with CKD may be indicative of ongoing lysosomal activity rather than active proximal tubular cell damage.
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