Serum, Urine, Cerebrospinal fluid, Bronchoalveolar lavage, Amniotic fluid, Plasma
Store the kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).
0.313 – 20 ng/ml
Limit of Detection
n=8, CV = 4.9%
n=6, CV = 6%
- It is intended for research use only
- The total assay time is less than 2.5 hours
- The kit measures angiotensinogen in serum, plasma (EDTA, citrate, heparin), urine, cerebrospinal fluid (CSF), bronchoalveolar lavage fluid (BALF) and amniotic fluid
- Assay format is 96 wells
- Standard is recombinant protein
- Components of the kit are provided ready to use, concentrated or lyophilized
Cardiovascular disease, Renal disease
Human angiotensinogen (AGT), also known as serpin peptidase inhibitor, clade A or member 8, is a component of the renin-angiotensin system (RAS), a hormone system that regulates blood pressure and fluid balance. AGT is the only defined substrate for renin which catalytically cleaves the 10 N-terminal amino acids of AGT to produce angiotensin I in response to lowered blood pressure. Angiotensin I is subsequently converted to the physiologically active peptide Angiotensin I through the removal of two C-terminal residues by the Angiotensin converting enzyme (ACE). Angiotensin I functions in the regulation of volume and mineral balance of body fluids. Both angiotensin I and angiotensin II can be further processed to generate angiotensin III, which stimulates aldosterone release, and angiotensin IV. AGT is the only precursor of all the angiotensin peptides and the cleavage of AGT by renin is the rate-limiting step of RAS. Angiotensinogen is mainly produced in the liver and secreted in plasma but also is synthesized in adipocytes, proximal tubule epithelial cells, and astrocytes. AGT identified in urine (UAGT) is produced and secreted by the kidney proximal tubules and does not come from plasma. UAGT is involved in the intrarenal RAS and reflects intrarenal angiotensin II activity associated with increased risk for deterioration of renal function in patients with chronic kidney disease such as diabetic nephropathy and membranous nephropathy as well as in patients with acute kidney injury. Urinary AGT is increased in hypertensive patients and treatment with RAS blockers suppresses UAGT levels which indicate that the efficacy of RAS blockade to reduce the intrarenal RAS activity can be assessed by measurement of UAGT.