Angiotensin II

CPT: 82163
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Special Instructions

Contact the LabCorp supply department for collection kit.


Expected Turnaround Time

4 – 14 days



Related Documents


Specimen Requirements


Specimen

Plasma, frozen


Volume

3 mL


Minimum Volume

1.5 mL (Note: This volume does not allow for repeat testing.)


Container

Lavender-top (EDTA) tube with Trasylol®


Collection

Trasylol® kits may be ordered through the PeopleSoft system (LabCorp N° 33328). Using a chilled 6-mL lavender-top (EDTA) tube taken from the kit, collect a whole blood specimen. Mix the specimen several times by inverting the EDTA collection tube. After removing the cap from the EDTA draw tube, take one of the sterile, Beral pipettes (from under the gray foam), and add 0.25 mL Trasylol® to the EDTA tube. Recap the EDTA tube and invert several times to mix well. Centrifuge the EDTA tube to separate the plasma from the cells, and immediately transfer the plasma into one of the brown screw-cap transfer tubes provided in the kit. There should be a "Trasylol® Added" label affixed to the brown transport tubes. Cap and freeze the labeled transport tube containing the EDTA plasma with Trasylol® added. To avoid delays in turnaround time when requesting multiple test on frozen samples, please submit separate frozen specimens for each test requested.


Storage Instructions

Freeze.


Stability Requirements

Temperature

Period

Room temperature

1 hour

Refrigerated

1 hour

Frozen

14 days

Freeze/thaw cycles

Stable x3


Patient Preparation

Patient must not have received radioactive substances 24 hours prior to test. Patient should be fasting.


Causes for Rejection

Sample not collected with Trasylol®; sample not submitted in tube with Trasylol label, gross hemolysis; recently administered radioisotopes; specimen not received frozen; serum, sodium citrate, or heparinized plasma specimen; lipemia


Test Details


Use

The renin-angiotensin aldosterone hormonal cascade that regulates blood pressure and water (fluid) balance begins with the biosynthesis of renin by the juxtaglomerular cells that line the afferent (and occasionally efferent) arteriole of the renal glomerulus.1,2 A drop in blood pressure decreases the perfusion of the juxtaglomerular apparatus, resulting in the release of the enzyme renin. Renin proceeds to cleave angiotensinogen to produce angiotensin I. Angiotensin I is in turn converted to angiotensin II by angiotensin-converting enzyme (ACE), which is found mainly in lung capillaries. Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular mesangial cells, causing these cells to contract along with the blood vessels surrounding them and causing the release of aldosterone from the adrenal cortex. Angiotensin II has multifaceted effects on aldosterone secretion, vasoconstriction, sodium reabsorption, and fluid volume, all of which serve to raise blood pressure. Laboratory studies with cultured cardiomyocytes have implicated angiotensin as a direct cause of left ventricular hypertrophy associated with hypertension. Angiotensin II also inhibits renin release by the kidney via a feedback mechanism.

Several investigators have found that a subgroup of patients with severe chronic heart failure has elevated plasma angiotensin II levels despite long-term ACE inhibitor use.3,4 This phenomenon has been referred to as ACE escape or angiotensin II reactivation and has been associated with increased mortality.4-7


Limitations

Results for this test are for research purposes only by the assay's manufacturer. The performance characteristics of this product have not been established. Results should not be used as a diagnostic procedure without confirmation of the diagnosis by another medically established diagnostic product or procedure.


Methodology

Radioimmunoassay (RIA)


Footnotes

1. Atlas SA. The renin-angiotensin system: Pathophysiological role and pharmacologic inhibition. J Manag Care Pharm. 2007; 13(8 Suppl B):9-20. 17970613
2. Reudelhuber TL, Bernstein KE, Delafontaine P. Is angiotensin II a direct mediator of left ventricular hypertrophy? Time for another look. Hypertension. 2007; 49(6):1196-1201. 17452509
3. Roig E, Pérez-Villa F, Morales M, et al. Clinical implications of increased plasma angiotensin II despite ACE inhibitor therapy in patients with congestive heart failure. Eur Heart J. 2000; 21(1):53-57. 10610744
4. van de Wal RM, Plokker HW, Lok DJ, et al. Determinants of increased angiotensin II levels in severe chronic heart failure patients despite ACE inhibition. Int J Cardiol. 2006; 106(3):367-372. 16337046
5. MacFadyen RJ, Lee AF, Morton JJ, et al. How often are angiotensin II and aldosterone concentrations raised during chronic ACE inhibitor treatment in cardiac failure? Heart. 1999; 82(1):57-61. 10377310
6. Athyros VG, Mikhailidis DP, Kakafika AI, et al. Angiotensin II reactivation and aldosterone escape phenomena in renin-angiotensin-aldosterone system blockage: is oral renin inhibition the solution? Expert Opin Pharmocother. 2007 Apr; 8(5):529-535. 17376010
7. Chinnaiyan KM, Alexander D, McCullough PA. Role of angiotensin II in the evolution of diastolic heart failure. J Clin Hypertens (Greenwich). 2005; 7(12)740-747. 16330897

LOINC® Map

Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
002180 Angiotensin II 1860-6 002181 Angiotensin II pg/mL 1860-6

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