Hyperammonemia in azotemic cats.

OBJECTIVES: Hyperammonemia occurs in cats with hepatobiliary and nutritional (cobalamin and arginine deficiency) disorders, and has also been documented in four cats with renal azotemia. We hypothesized that in cats with renal azotemia, fasting hyperammonemia would correlate with indices of worsening kidney function, and would be independent of cobalamin, potassium, systemic inflammation or urinary tract infection (UTI) with urease-producing bacteria. METHODS: A fasted blood sample was prospectively collected for ammonia and cobalamin analysis from 18 client-owned cats with renal azotemia (creatinine [Cr] ⩾1.6 mg/dl, urine specific gravity <1.030 or documentation of historical chronic kidney disease [CKD]). Correlations between blood ammonia and selected biochemical parameters were analyzed using Pearson's correlation coefficient. RESULTS: Seven castrated males and 11 spayed females with a median age of 12 years (range 4-19 years) were enrolled. Ten of 18 (56%) cats presented for acute kidney injury (AKI) or acute on chronic kidney disease (AoCKD), and 8/18 (44%) presented for progressive CKD. The median Cr was 5.9 mg/dl (range 1.9-24.7 mg/dl). Hyperammonemia was documented in 4/18 (22%) cats, with a median of 95 µmol/dl (range 85-98 µmol/dl), and all four of these cats were classified as AKI/AoCKD. Blood ammonia concentrations had a significant moderate positive correlation between blood urea nitrogen (BUN) (r = 0.645, P = 0.003), Cr (r = 0.578, P = 0.012) and serum phosphorus (r = 0.714, P = 0.0009) but not with cobalamin, potassium or white blood cell count. No cats had UTIs with urease-producing bacteria. CONCLUSIONS AND RELEVANCE: A correlation exists between blood ammonia and BUN, Cr and phosphorus in cats with renal azotemia. Future studies are warranted in a larger population of cats to determine the true prevalence, etiology and potential therapeutic effect of medical management of hyperammonemia on long-term prognosis in cats with kidney disease.

Psychophysical measurement of contrast sensitivity in the behaving mouse.

To understand how activity in mammalian neural circuits controls behavior, the mouse is a promising model system due to the convergence of genetic, optical, and physiological methods. The ability to control and quantify behavior precisely is also essential for these studies. We developed an operant visual detection paradigm to make visual psychophysical measurements: head-fixed mice make responses by pressing a lever. We designed this task to permit neurophysiological studies of behavior in cerebral cortex, where activity is variable from trial to trial and neurons encode many types of information simultaneously. To study neural responses in the face of this complexity, we trained mice to do a task where they perform hundreds of trials daily and perceptual thresholds can be measured. We used this task to measure both visual acuity and the minimum detectable contrast in behaving mice. We found that the mouse contrast response function is similar in shape to other species. They can detect low-contrast stimuli, with a peak contrast threshold of 2%, equivalent to ∼15° eccentric in human vision. Mouse acuity is modest, with an upper limit near 0.5 cycles/°, consistent with prior data.