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About This Item
UNSPSC Code:
12161503
NACRES:
NA.84
usage
sufficient for 100 colorimetric tests
storage condition
dry at room temperature
technique(s)
activity assay: suitable
input
urine
serum
plasma
detection method
colorimetric
storage temp.
−20°C
General description
The new Urea Assay Kit, MAK471, is now available! Urea is the major end product of nitrogen metabolism in most animals and is produced in a series of reactions in the liver called the urea cycle. In the urea cycle, ammonia is converted to urea, which is carried by blood to the kidneys for elimination from the body. High levels of urea in the blood may indicate renal failure. Urea levels may also be elevated in response to treatment with certain drugs such as corticosteroids or in response to decreased kidney filtration due to dehydration or congestive heart failure. Decreased blood urea levels can occur in response to liver disease or malnutrition.
Application
Suitable for the measurement of urea concentration in a variety of samples such as serum, plasma, and urine, etc.
Urea assay kit has been used to measure the concentration of urea.
Biochem/physiol Actions
In this assay, Urea concentration is determined by a coupled enzyme reaction, which results in a colorimetric (570 nm) product, proportional to the Urea present.
Features and Benefits
Compatible with high-throughput handling systems.
Signal Word
Danger
Hazard Statements
Precautionary Statements
Hazard Classifications
Eye Irrit. 2 - Resp. Sens. 1 - Skin Irrit. 2 - Skin Sens. 1 - STOT SE 3
Target Organs
Respiratory system
Storage Class Code
10 - Combustible liquids
Flash Point(F)
188.6 °F - closed cup
Flash Point(C)
87 °C - closed cup
Regulatory Information
低风险生物材料
常规特殊物品
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Ito Y, et al.
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Urea and ammonia metabolism and the control of renal nitrogen excretion.
Weiner I D, et al.
Journal of the American Society of Nephrology, 10(8), 1444-1458 (2015)
Markers of renal function tests.
Gowda S, et al.
North American Journal of Medical Sciences, 2(4), 170-170 (2010)
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Atypical hemolytic uremic syndrome (aHUS) is frequently associated in humans with loss-of-function mutations in complement-regulating proteins or gain-of-function mutations in complement-activating proteins. Thus, aHUS provides an archetypal complement-mediated disease with which to model new therapeutic strategies and treatments. Herein, we
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