Select country change
Shopping cart (0 , 0,00 ) Menu Search
Manufactured by BioVendor

Active Renin Human ELISA

  • Regulatory status:RUO
  • Type:Sandwich ELISA, Biotin-labelled antibody
  • Other names:Angiotensinogenase, REN
  • Species:Human
Please select your region to see available products and prices.
Cat. No. Size Price


RD194169200R 96 wells (1 kit)
PubMed Product Details
Technical Data

Type

Sandwich ELISA, Biotin-labelled antibody

Applications

Serum, Urine, Amniotic fluid, Plasma (EDTA, citrate, heparin)

Sample Requirements

35 µl

Shipping

At ambient temperature. Upon receipt, store the product at the temperature recommended below.

Storage/Expiration

Store the complete kit at 2 8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Curve

Calibration Range

4.5 – 144 µIU/ml

Limit of Detection

0.64 µIU/ml

Intra-assay (Within-Run)

n = 8; CV = 5.4 %

Inter-assay (Run-to-Run)

n = 6; CV = 4.8 %

Spiking Recovery

100.0 %

Dilutation Linearity

101.2 %

Summary

Features

  • It is intended for research use only
  • The total assay time is less than 3.5 hours
  • The kit measures active renin in serum, plasma (EDTA, citrate, heparin), urine and amniotic fluid
  • Assay format is 96 wells
  • Calibrator is recombinant protein based
  • Components of the kit are provided ready to use, concentrated or lyophilized

Research topic

Blood pressure regulation and NO metabolism, Cardiovascular disease, Diabetology - Other Relevant Products, Renal disease

Summary

Renin is the rate-limiting enzyme in the renin-angiotensin-aldosterone system (RAAS), which primarily acts to control blood pressure and sodium balance. RAAS activity is also involved in angiogenesis, cellular growth, fibrosis, reproduction, inflammation, immunity, intracellular redox balance and antidiuretic hormone production. The active enzyme renin is a specific aspartyl protease with molecular weight of 37 kDa and is responsible for the cleavage of angiotensinogen produced in the liver into angiotensin I which is further converted into active angiotensin II in the vascular epithelium of the lung.
Renin is produced in juxtaglomerular (JG) cells of the kidney as the inactive precursor prorenin in which the prosegment region with 43 amino acid residues covers the active site of renin. Cleavage of the prosegment converts prorenin to active (mature) renin, and JG cells are the only known sites where prorenin is converted to renin proteolytically. Non-proteolytic activation occurs when prosegment is unfolded from enzymatic cleft, thus allowing intact prorenin to become catalytically active. This process occurs under acidic pH and low temperature or after binding of prorenin to renin receptor. The (pro)renin receptor is expressed in many organs, thus, it may help to accumulate renin and prorenin locally and activate tissue-specific renin-angiotensin systems (RAS). Locally expressed RAS was found in a number of tissues, including the kidney, adrenal gland, heart, vasculature and nervous system, under different physiological and pathophysiological conditions. Local RAS has a variety of functions, including local cardiovascular regulation, in association with or independently of the systemic RAS, as well as non-cardiovascular functions and influences cell growth, differentiation, apoptosis, etc.
Active renin is stored in granules of the JG cells and is released by an exocytic process into the kidney and then into systemic circulation. Renin secretion is stimulated by a fall in perfusion pressure or in NaCl delivery to the distal tubules and by an increase in sympathetic activity, in contrast to prorenin which is secreted into blood constitutively. Prorenin level in the circulation is about 10 times higher than that of mature renin. Renin has also been identified in urine and amniotic fluid. Control of renin secretion is the key determinant of the RAAS and renin’s chronic activation is the major contributing factor to pathogenesis and progression of cardiovascular and renal disorders. RAAS directly affects vascular and cardiac remodeling through proliferative and inflammatory signaling. Blockers of systemic RAS play a prominent role in the treatment of arterial hypertension, heart failure, diabetes and nephropathy.
The clinical application of renin inhibitor therapy has stimulated new interest in the measurement of renin and its precursor prorenin. Measurement of plasma active renin is important for differential diagnosis of hypertension, clinical assessment of hypertensive patients and for diagnostics of insufficient response to antihypertensive treatment.
The ratio of aldosterone to renin concentration should be useful for screening patients suspected of primary aldosteronism. Study of the relationship of plasma renin levels to renal function in patients with primary aldosteronism indicated that the lack of suppression of renin by excess aldosterone is associated with more severe renal damage and predicts less favorable outcomes after treatment. Urine renin reflects the renal RAAS activity in the kidney and thus may reflect success of RAAS blockade in the kidney during RAAS blocker therapy in patients with diabetic as well as non-diabetic nephropathy.
Other clinical implications of active renin measurement involve diagnosis of isolated deficit in mineral corticoids, detection of renin producing tumor in kidney, or monitoring of glucocorticoid therapy.

**Areas of investigation: **

  • Atherosclerosis
  • Cardiovascular disease
  • Diabetes
  • Hypertension
  • Renal Disease
References to Summary

References to Renin

  • Atlas SA. The renin-angiotensin aldosterone system: pathophysiological role and pharmacologic inhibition. J Manag Care Pharm. 2007 Oct;13 (8 Suppl B):9-20
  • Brossaud J, Corcuff JB. Pre-analytical and analytical considerations for the determination of plasma renin activity. Clin Chim Acta. 2009 Dec;410 (1-2):90-2
  • Bystrom CE, Salameh W, Reitz R, Clarke NJ. Plasma renin activity by LC-MS/MS: development of a prototypical clinical assay reveals a subpopulation of human plasma samples with substantial peptidase activity. Clin Chem. 2010 Oct;56 (10):1561-9
  • Campbell DJ. Circulating and tissue angiotensin systems. J Clin Invest. 1987 Jan;79 (1):1-6
  • Campbell DJ, Nussberger J, Stowasser M, Danser AH, Morganti A, Frandsen E, Menard J. Activity assays and immunoassays for plasma Renin and prorenin: information provided and precautions necessary for accurate measurement. Clin Chem. 2009 May;55 (5):867-77
  • Cartledge S, Lawson N. Aldosterone and renin measurements. Ann Clin Biochem. 2000 May;37 ( Pt 3):262-78
  • Catena C, Colussi G, Nadalini E, Chiuch A, Baroselli S, Lapenna R, Sechi LA. Relationships of plasma renin levels with renal function in patients with primary aldosteronism. Clin J Am Soc Nephrol. 2007 Jul;2 (4):722-31
  • Chawla T, Sharma D, Singh A. Role of the renin angiotensin system in diabetic nephropathy. World J Diabetes. 2010 Nov 15;1 (5):141-5
  • Derkx FH, Schalekamp MP, Schalekamp MA. Two-step prorenin-renin conversion. Isolation of an intermediary form of activated prorenin. J Biol Chem. 1987 Feb 25;262 (6):2472-7
  • Distler A, Spies KP. Diagnostic procedure in renovascular hypertension. Clin Nephrol. 1991 Oct;36 (4):174-80
  • Doi SA, Abalkhail S, Al-Qudhaiby MM, Al-Humood K, Hafez MF, Al-Shoumer KA. Optimal use and interpretation of the aldosterone renin ratio to detect aldosterone excess in hypertension. J Hum Hypertens. 2006 Jul;20 (7):482-9
  • Glinicki P, Jeske W, Bednarek-Papierska L, Kruszynska A, Gietka-Czernel M, Roslonowska E, Slowinska-Srzednicka J, Kasperlik-Zaluska A, Zgliczynski W. The ratios of aldosterone / plasma renin activity (ARR) versus aldosterone / direct renin concentration (ADRR). J Renin Angiotensin Aldosteron. 2015 Dec;16 (4):1298-305
  • Hall JE. Control of glomerular filtration rate by rennin-angiotensin system . Am.J.Physiol. 1977;233(5) :F366-F372
  • Hardman JA, Hort YJ, Catanzaro DF, Tellam JT, Baxter JD, Morris BJ, Shine J. Primary structure of the human renin gene. DNA. 1984 Dec;3 (6):457-68
  • Hartman D, Sagnella GA, Chesters CA, Macgregor GA. Direct renin assay and plasma renin activity assay compared. Clin Chem. 2004 Nov;50 (11):2159-61
  • Ichihara A, Sakoda M, Kurauchi-Mito A, Kaneshiro Y, Itoh H. Renin, prorenin and the kidney: a new chapter in an old saga. J Nephrol. 2009 May-Jun;22 (3):306-11
  • Lim PO, Jung RT, MacDonald TM. Raised aldosterone to renin ratio predicts antihypertensive efficacy of spironolactone: a prospective cohort follow-up study. Br J Clin Pharmacol. 1999 Nov;48 (5):756-60
  • Montecucco F, Pende A, Mach F. The renin-angiotensin system modulates inflammatory processes in atherosclerosis: evidence from basic research and clinical studies. Mediators Inflamm. 2009;2009:752406
  • Mulatero P, Verhovez A, Morello F, Veglio F. Diagnosis and treatment of low-renin hypertension. Clin Endocrinol (Oxf). 2007 Sep;67 (3):324-34
  • Pacurari M, Kafoury R, Tchounwou PB, Ndebele K. The Renin-Angiotensin-aldosterone system in vascular inflammation and remodeling. Int J Inflam. 2014;2014:689360
  • Paul M, Poyan Mehr A, Kreutz R. Physiology of local renin-angiotensin systems. Physiol Rev. 2006 Jul;86 (3):747-803
  • Pratt RE, Carleton JE, Richie JP, Heusser C, Dzau VJ. Human renin biosynthesis and secretion in normal and ischemic kidneys. Proc Natl Acad Sci U S A. 1987 Nov;84 (22):7837-40
  • Reudelhuber TL. Prorenin, Renin, and their receptor: moving targets. Hypertension. 2010 May;55 (5):1071-4
  • Ruster C, Wolf G. Renin-angiotensin-aldosterone system and progression of r
Related Products Documents