Peer-reviewed veterinary case report
Amino acid nutrition linked to ammonia issues in cat with liver
By Park, Jinyeong et al.·Published in Journal of the American Animal Hospital Association·2026·View original on PubMed →
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Original publication title: Effect of Parenteral Amino Acid Composition on Hyperammonemia in a Cat with Hepatic Lipidosis.
- Species:
- cat
Plain-English summary
An 8-year-old spayed female domestic shorthair cat was brought to the vet after showing signs of not eating and being unusually tired for a week. Tests revealed she had hepatic lipidosis, a serious liver condition. After being hospitalized and treated, her appetite and energy improved, but she still wasn't eating enough on her own, so she was given a special amino acid solution through a tube. Unfortunately, within a day, she developed serious neurological symptoms like vocalizing, panting, and even became comatose, likely due to a lack of arginine, an important amino acid. The vet adjusted her treatment, and this case highlights the need for careful selection of nutrients in cats with liver issues.
People also search for: cat not eating · hepatic lipidosis treatment in cats · cat liver disease symptoms
Abstract
An 8 yr old spayed female domestic shorthair presented with a 1 wk history of anorexia and lethargy. Cytological examination of the liver using fine-needle aspiration revealed numerous adipocytes, confirming hepatic lipidosis. The cat was hospitalized for treatment; subsequently, the clinical signs and blood analysis results improved. On day 17, the nasoesophageal tube was removed because of recovery of appetite and vitality. However, owing to insufficient voluntary food intake, partial parenteral nutrition (PPN) was initiated using an amino acid solution with a low branched-chain amino acid (BCAA)/aromatic amino acid (AAA) ratio and arginine deficiency. Within 24 hr of PPN administration, neurological signs were observed, including vocalization, panting, hyperactivity, and a subsequent comatose state. Although hepatic encephalopathy was considered, there was limited evidence of hepatic failure. The clinical course was most consistent with acute hyperammonemia secondary to arginine deficiency, although a contributing role of the low BCAA/AAA ratio cannot be excluded. This case suggests that amino acid PPN with arginine deficiency and a low BCAA/AAA ratio may contribute to neurological signs in cats, underscoring the importance of careful amino acid selection in nutritional formulations.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/41448592/