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Related Concept Videos

Urea Cycle01:23

Urea Cycle

48.5K
The urea cycle describes how liver cells convert ammonia to urea. Ammonia is a toxic waste product of protein catabolism. Land animals must convert ammonia into the less toxic urea which can be safely eliminated by the kidneys through urine. Marine animals excrete ammonia directly, and the surrounding water dilutes the ammonia to safe levels.
48.5K
Physical Properties of Amines01:26

Physical Properties of Amines

3.8K
Amines with low molecular weight are usually gaseous at room temperature, while those with high molecular weight are liquid or solids in nature. Usually, low molecular weight amines have a rotten fish-like smell. Diamines typically have a pungent smell. For instance, cadaverine and putrescine, depicted in Figure 1, are two molecules responsible for decaying tissue.
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Comparative Excretory Systems02:24

Comparative Excretory Systems

26.0K
Animals have evolved different strategies for excretion, the removal of waste from the body. Most waste must be dissolved in water to be excreted, so an animal’s excretory strategy directly affects its water balance.
26.0K
Preparation of 1° Amines: Azide Synthesis01:22

Preparation of 1° Amines: Azide Synthesis

4.3K
Direct alkylation of ammonia produces polyalkylated amines, along with a quaternary ammonium salt. To exclusively prepare primary amines, the azide synthesis method can be used.
Azide ions act as good nucleophiles and react with unhindered alkyl halides to form alkyl azides. Alkyl azides do not participate in further nucleophilic substitution reactions, thereby eliminating the chances of polyalkylated products. Alkyl azides are reduced by hydride-based reducing agents, like lithium aluminum...
4.3K
Basicity of Heterocyclic Aromatic Amines01:25

Basicity of Heterocyclic Aromatic Amines

6.6K
Heterocyclic amines, where the N atom is a part of an alicyclic system, are similar in basicity to alkylamines. Interestingly, the heterocyclic amine having a nitrogen atom as part of an aromatic ring has much less basicity than its corresponding alicyclic counterpart. For this reason, as presented in Figure 1, piperidine (pKb = 2.8) is significantly more basic than pyridine (pKb = 8.8).
6.6K
2° Amines to N-Nitrosamines: Reaction with NaNO201:20

2° Amines to N-Nitrosamines: Reaction with NaNO2

5.0K
Secondary amines react with nitrous acid to form N-nitrosamines, as depicted in Figure 1. Nitrous acid, a weak and unstable acid, is formed in situ from an aqueous solution of sodium nitrite and strong acids, such as hydrochloric acid or sulfuric acid, in cold conditions. In the presence of an acid, the nitrous acid gets protonated. The subsequent loss of water results in the formation of the electrophile known as nitrosonium ion.
5.0K

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Microdialysis of Excitatory Amino Acids During EEG Recordings in Freely Moving Rats
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Hyperammonemia in azotemic cats.

Lauren Carvalho1, Denise Kelley2, Mary Anna Labato1

  • 1Small Animal Internal Medicine, Cummings School of Veterinary Medicine at Tufts University, Grafton, MA, USA.

Journal of Feline Medicine and Surgery
|November 20, 2020
PubMed
Summary
This summary is machine-generated.

Fasting hyperammonemia in cats with renal azotemia correlates with worsening kidney function, specifically blood urea nitrogen, creatinine, and phosphorus levels. This finding is independent of cobalamin, potassium, or systemic inflammation.

Keywords:
Acute kidney injuryammoniaazotemiablood urea nitrogenchronic kidney diseasecobalamincreatininevitamin B12

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Screening Assay for Oxidative Stress in a Feline Astrocyte Cell Line, G355-5
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Area of Science:

  • Veterinary Medicine
  • Nephrology
  • Biochemistry

Background:

  • Hyperammonemia is observed in cats with various disorders, including hepatobiliary, nutritional deficiencies, and renal azotemia.
  • Previous documentation noted hyperammonemia in four cats with renal azotemia, prompting further investigation.

Purpose of the Study:

  • To investigate the correlation between fasting hyperammonemia and indicators of kidney function in cats with renal azotemia.
  • To determine if hyperammonemia in these cats is influenced by cobalamin, potassium, systemic inflammation, or urease-producing bacteria.

Main Methods:

  • Prospective collection of fasted blood samples from 18 cats with renal azotemia for ammonia and cobalamin analysis.
  • Analysis of correlations between blood ammonia and biochemical parameters using Pearson's correlation coefficient.

Main Results:

  • Hyperammonemia was present in 22% of cats, predominantly those with acute kidney injury or acute on chronic kidney disease.
  • Significant positive correlations were found between blood ammonia and blood urea nitrogen (BUN), creatinine (Cr), and serum phosphorus.
  • No correlation was observed with cobalamin, potassium, or white blood cell count; no urinary tract infections with urease-producing bacteria were detected.

Conclusions:

  • A correlation exists between blood ammonia levels and key kidney function markers (BUN, Cr, phosphorus) in cats with renal azotemia.
  • Further research in larger cat populations is needed to establish the prevalence, causes, and therapeutic implications of hyperammonemia in feline kidney disease.