Abstract
The purpose of the study was to quantify serum and fecal amino acids (AA) in cats with chronic kidney disease (CKD) and compare to healthy cats. Thirty-five cats with International Renal Interest Society Stage 1–4 CKD and 16 healthy mature adult and senior client-owned cats were included in this prospective cross-sectional study. Sera were analyzed for 25 AA concentrations using an ion exchange chromatography AA analyzer with post column ninhydrin derivatization. Voided fecal samples were analyzed for 22 AA concentrations using liquid chromatography with tandem mass spectrometry. CKD cats had lower serum concentrations of phenylalanine (mean difference ± standard error of the mean: 12.7 ± 4.3 µM; p = 0.03), threonine (29.6 ± 9.2 µM; p = 0.03), tryptophan (18.4 ± 5.4 µM; p = 0.005), serine (29.8 ± 12.6 µM; p = 0.03), and tyrosine (11.6 ± 3.8 µM; p = 0.01) and higher serum concentrations of aspartic acid (4.7 ± 2.0 µM; p = 0.01), β-alanine (3.4 ± 1.2 µM; p = 0.01), citrulline (5.7 ± 1.6 µM; p = 0.01), and taurine (109.9 ± 29.6 µM; p = 0.01) when compared to healthy cats. Fecal AA concentrations did not differ between healthy cats and CKD cats. 3-Methylhistidine-to-creatinine did not differ between healthy cats with and without muscle loss. Cats with CKD IRIS Stages 1–4 have a deranged serum amino acid profile compared to healthy cats.
Highlights
Muscle loss, with or without concurrent loss of fat stores, occurs in cats with chronic kidney disease (CKD) and can contribute to weight loss [1,2]
Serum amino acids (AA) were measured in 26 CKD cats, and fecal AAs were measured in 31 CKD cats
We found that CKD cats have a deranged serum AA profile; in particular, CKD cats had lower serum concentrations of three essential and two nonessential AAs when compared to healthy cats
Summary
With or without concurrent loss of fat stores, occurs in cats with chronic kidney disease (CKD) and can contribute to weight loss [1,2]. Cachexia is the loss of lean body mass in acute and chronic disease and is caused by the utilization of amino acids (AA) from muscle as a primary energy source [3]. According to studies in people and rat models, cachexia is the result of negative energy intake, and increased protein catabolism secondary to metabolic acidosis, systemic inflammation, and insulin resistance [4]. CKD may cause protein malassimilation as a result of a decrease in the efficiency of protein digestion and decreased AA absorption in the small intestine [5,6]. Impaired protein digestion increases the abundance of proteolytic bacteria and fermentation of AAs to precursors of uremic toxins [4,7,8]
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