References
Hyperammonaemia in cats

Abstract
Ammonia is an important nitrogen source required for amino acid, protein and nucleic acid synthesis. In addition, it plays an essential role in the kidney's maintenance of acid–base balance. However, high concentrations of ammonia are cytotoxic and clinical signs primarily reflect neurotoxicity. The body detoxifies ammonia through the urea cycle in the liver or by consuming ammonia in the conversion of glutamate to glutamine in the liver, brain and muscle tissue. The most common cause of hyperammonaemia in cats is congenital portosystemic shunting. Additional causes include cobalamin or arginine deficiency, disruption of the urea cycle by congenital enzyme deficiencies or acute liver failure, excessive muscle activity, infections with urease-producing bacteria, kidney disease and multiple acquired portosystemic shunts.
The metabolism of ammonia is complex, yet a vitally important process required to maintain physiological homeostasis. Ammonia production is a by-product of the catabolism of nitrogen sources, most notably ingested protein and amino acids. Since ammonia is neurotoxic at high systemic blood concentrations, efficient mechanisms exist to compartmentalise the production and elimination of ammonia to maintain safe levels. The liver is the major player in ammonia excretion, while the intestine and kidney are the main ammonia producers. The liver can also generate ammonia, and the intestines and kidney can aid in ammonia excretion. Muscle can serve as an ammonia sink and in some cases increase ammonia load, which adds to the complexity of this process.
Ammonia is a biologically important source of nitrogen required for amino acid, protein and nucleic acid synthesis (Walker, 2014; Häberle, 2020; Butterworth, 2021). Additionally, ammonia plays a pivotal role in the kidney's maintenance of acid–base balance. Most ammonia is generated in the gastrointestinal tract from the action of urease-producing microbes on dietary and endogenous proteins (Table 1). The generated ammonia freely diffuses across the intestinal epithelium and makes its way into the portal blood. Additional sources of ammonia production include enterocyte metabolism of glutamine to glutamate in the intestine and kidney which releases ammonia, skeletal muscle production through the purine nucleotide cycle following strenuous exercise and hydrolysis of urea by urease-producing microbes in the gastrointestinal tract (Table 1).
Register now to continue reading
Thank you for visiting UK-VET Companion Animal and reading some of our peer-reviewed content for veterinary professionals. To continue reading this article, please register today.