Hyperammonaemia in four cats with renal azotaemia

Adagra, Carl; Foster, Darren

doi:10.1177/1098612x14527083

Cited by 5 publications

(4 citation statements)

References 27 publications

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“…Marked hyperammonemia was reported in a case series of four severely azotaemic cats, and in two of these cats the hyperammonaemia was associated with neurological signs consistent with an encephalopathy. 15 However, in another study with azotaemic cats, plasma arginine concentrations were almost always within the normal range. 24 Therefore, azotaemia should not be considered as the only triggering factor for hyperammonaemia in cats with CKD.…”

Section: Discussionmentioning

confidence: 92%

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Acquired urea cycle amino acid deficiency and hyperammonaemic encephalopathy in a cat with inflammatory bowel disease and chronic kidney disease

Dor

Adamany

Kisielewicz

et al. 2018

Journal of Feline Medicine and Surgery Open Reports

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Case summaryA 5-year-old male neutered Persian cat was referred for investigation of a 4 week history of weight loss, inappetence and intermittent vomiting. Chronic kidney disease (CKD) and inflammatory bowel disease were diagnosed, and despite immunosuppressive therapy and assisted enteral nutrition, the cat experienced persistent anorexia, vomiting and severe weight loss. After 2 additional weeks of treatment, the cat developed acute-onset neurological signs associated with severe hyperammonaemia and was euthanased. Plasma amino acid assessment revealed deficiency of several amino acids involved in the urea cycle, including arginine.Relevance and novel informationTo our knowledge, this is the first reported case of an acquired urea cycle amino acid deficiency without nutritional deprivation in a cat. Several contributing factors were suspected, including intestinal malabsorption and CKD. This case demonstrates the importance of urea cycle amino acids in feline metabolism and possible necessity for parenteral supplementation, particularly in the context of persistent weight loss despite adequate enteral nutrition.

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Section: Discussionmentioning

confidence: 92%

“…Contributing factors such as decreased intestinal absorption due to inflammatory bowel disease (IBD) or decreased renal synthesis owing to chronic kidney disease (CKD) have been suggested. 12 – 15 …”

Section: Introductionmentioning

confidence: 99%

Acquired urea cycle amino acid deficiency and hyperammonaemic encephalopathy in a cat with inflammatory bowel disease and chronic kidney disease

Dor

Adamany

Kisielewicz

et al. 2018

Journal of Feline Medicine and Surgery Open Reports

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“…KBH'li 4 kedide yapılan bir vaka serisinde, alanin aminotransferaz ve aspartat transaminaz seviyeleri normal olmasına rağmen hiperamonyemi belirlendiği ve kedilerin 2'sinde üremik ensefalopati gözlendiği bildirilmiştir. 56 Üremik ensefalopati, nadir görülen ciddi bir KBH komplikasyondur. Böbrek yetersizliği ile ilişkili toksik metabolik ensefalopati, üremik toksinlerin (özellikle amonyak) beyinde birikmesi, polisinaptik yolaklar ve inhibitör/eksitatör amino asit dengesini etkilemesi ile ilişkilidir.…”

Section: Nöroloji̇k Kompli̇kasyonlarunclassified

An Overview to Complications of Chronic Kidney Disease in Dogs and Cats: Traditional Review

MADEN¹,

KILIÇKAYA²,

İYİGÜN³

2022

Turkiye Klinikleri J Vet Sci

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ÖZET Kronik böbrek hastalıgȋ (KBH); böbreklerde önemli nefron kayıpları ile seyreden, geri dönüsümsüz (irreversibl) ve tipik olarak ilerleyici (progressive), yapısal ve/veya isļevsel bozukluk olarak tanımlanmaktadır. Basţa orta ve ileri yasļı kedi ve köpekler olmak üzere, her yasţaki evcil hayvanlarda görülen böbrek hastalıklarının en yaygın türüdür. KBH insidansı, köpek ve kedilerde sırasıyla %0,5-1,5 ve %1-3 arasında görülmektedir. Geriatrik kedilerde KBH prevalansının, geriatrik köpeklerden daha yüksek oldugȗ ve %35-81 gibi yüksek oranlarda seyrettigȋ bildirilmektedir. Tubulointerstisyel yangı ve fibrozis ile karakterize olan KBH; genetik, çevresel ve bireysel faktörlerin etkin oldugȗ karmasik ve ilerleyici bir hastalık tablosu ile seyreder. Böbrek hasarına cevap olarak; hemodinamik adaptasyonlar, sistemik hipertansiyon, renin-anjiyotensin aldosteron sisteminin aktivasyonu, proteinüri, hiperfosfatemi, hipoksi ve oksidatif stres gelisir. Basļangıç nedeni ne olursa olsun, yangı ve fibrozise ilerleyen, yavaş seyirli böbrek hasarı olusur. Hastalıgȋn ilerlemesi ile ilisķili faktörlerin anlasilması, hastalıgȋn ilerlemesini yavasļatabilen terapötik müdahale potansiyeli saglar. Bu çerçevede böbrek fonksiyonu, homeostatik adaptasyonlar ve böbrek hasarının sonuçlarının değerlendirilmesi, komplikasyonların belirlenmesi ve yönetimi, KBH tedavisinin en önemli unsurlarını oluşturmaktadır. KBH olgularında böbrek fonksiyon kaybına paralel olarak; anemi, sistemik hipertansiyon, kardiyovasküler ve gastrointestinal bozukluklar, asit-baz dengesi ve elektrolit bozuklukları, hormonal degȋsiklikler, lipid metabolizması bozuklukları ve üremik ensefalopati gibi komplikasyonlar gelismektedir. KBH'li hastaların böbrek fonksiyonlarının korunması ve yasam kalitesinin iyilesţirilmesinde bu komplikasyonların bilinmesi, destekleyici ve semptomatik tedavi uygulamalarıyla iyi yönetilebilmesi önemlidir. Bu anlamda KBH yönetimi, bir komplikasyon yönetimi olarak degȇrlendirilmelidir. Bu derlemede, KBH olgularında gelisȩn anemi, sistemik hipertansiyon, kardiyovasküler ve gastrointestinal bozukluklar, asit-baz dengesi, elektrolitler ve hormonlarla ilgili degȋsiklikler, lipid metabolizması bozuklukları ve nörolojik komplikasyonlar özetlenmisţir. Anah tar Ke li me ler: Kronik böbrek hastalığı; komplikasyon;köpek; kedi ABS TRACT Chronic kidney disease (CKD); It is defined as an irreversible and typically progressive structural and/or functional disorder with significant loss of nephrons in the kidneys. It is the most common type of kidney disease seen in pets of all ages, especially middle and older cats and dogs. The incidence of CKD is seen between 0.5-1.5% and 1-3% in dogs and cats, respectively. It has been reported that the prevalence of CKD in geriatric cats is higher than that of geriatric dogs, with a high rate of 35-81%. CKD characterized by tubulointerstitial inflammation and fibrosis; It progresses with a complex and progressive disease in which genetic, environmental and individual factors are effective. In response to kidney damage; hemo...

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“…15 Fasting hyperammonemia was reported in four cats with renal azotemia, though an underlying mechanism was not identified. 16 We speculated that hyperammonemia may be an underreported phenomenon in cats with kidney disease. Thus, the objective of the current study was to document blood ammonia concentrations in cats that presented for evaluation of renal azotemia.…”

Section: Introductionmentioning

confidence: 99%

Hyperammonemia in azotemic cats

Carvalho

Kelley²,

Labato

et al. 2020

Journal of Feline Medicine and Surgery

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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.

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Hyperammonaemia in four cats with renal azotaemia

Cited by 5 publications

References 27 publications

Acquired urea cycle amino acid deficiency and hyperammonaemic encephalopathy in a cat with inflammatory bowel disease and chronic kidney disease

Acquired urea cycle amino acid deficiency and hyperammonaemic encephalopathy in a cat with inflammatory bowel disease and chronic kidney disease

An Overview to Complications of Chronic Kidney Disease in Dogs and Cats: Traditional Review

Hyperammonemia in azotemic cats

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