Aldosterone

Aldosterone

Number
	004374
CPT
	82088
Related Information
	Endocrine Appendix
Special Instructions
	The patient's posture at the time of collection should be noted (see Patient Preparation). Instructions for suppression/stimulation tests that involve serum aldosterone measurement can be found in the Endocrine Appendix . Also refer to this appendix for instructions on multiple specimen testing.
Specimen
	Serum or plasma
Volume
	0.8 mL
Minimum Volume
	0.3 mL (Note: This volume does not allow for repeat testing.)
Container
	Red-top tube, gel-barrier tube, or lavender-top (EDTA) tube
Collection
	Specify if specimen is from peripheral vein, adrenal, etc. State whether the patient was supine or upright when the blood was drawn. If a red-top tube is used, transfer separated serum to a plastic transport tube.
Storage Instructions
	Refrigerate
Patient Preparation
	No isotopes administered 24 hours prior to venipuncture. In order to facilitate interpretation of test results, the patient should be taken off medications for at least 3 weeks prior to sample collection. Dietary sodium levels during the period prior to testing can affect aldosterone levels. Reference intervals are based on the clinician's verification that the patient has been on a normal sodium diet. Since patient posture prior to collection affects aldosterone levels, it is recommended that the patient be ambulatory for at least 30 minutes before blood collection. If inpatients are physically able, they should be asked to ambulate for 30 minutes before blood is drawn for aldosterone. Reference intervals are provided for patients who have ambulated for at least 30 minutes prior to collection (standing patients). Reference intervals are also provided for patients on a normal sodium diet who are unable to ambulate (recumbent patients).
Causes for Rejection
	Recently administered radioisotopes; gross hemolysis; gross lipemia
Reference Interval
	Pediatrics:^1,2 <1 year: 5.0-132.0 ng/dL 1-3 years: 5.0-60.0 ng/dL 4-7 years: 4.0-76.0 ng/dL 8-11 years: 3.0-28.0 ng/dL 12-16 years: 1.0-18.0 ng/dL Adults: average sodium diet: Recumbent: 1.0-16.0 ng/dL Standing: 4.0-31.0 ng/dL Adrenal vein: 200.0-800.0 ng/dL
Use
	Evaluate patients with hypertension and possible hyperaldosteronism
Limitations
	Decreased perfusion of the kidneys leads to increased aldosterone and renin.
Methodology
	Radioimmunoassay (RIA)
Additional Information
	Aldosterone is a mineralocorticoid hormone produced in the adrenal zona glomerulosa under complex control by the renin-angiotensin system. Its action is on the renal distal tubule where it increases resorption of sodium and water at the expense of increased potassium excretion. Thus, syndromes of primary aldosterone excess show hypokalemia. Conversely, increased serum potassium levels act to increase aldosterone output. Renin also acts to increase aldosterone secretion through a feedback loop including angiotensins I and II. The principal use for aldosterone measurements is in the diagnosis of primary hyperaldosteronism, which is most commonly caused by a specific type of adrenal adenoma, Conn syndrome. Secondary aldosteronism is more common. Work-up is especially indicated in younger patient with hypertension and hypokalemia not induced by diuretic agents. Beeler and Catrou use criteria of serum potassium <3.5 mmol/L, 24-hour urine potassium ≥50 mmol/L, to begin work-up of a hypertensive patient for aldosteronism.³ Low plasma renin activity suggests primary aldosteronism and provides indication for aldosterone measurement in a hypertensive subject with renal potassium wasting.⁴ High resolution CT is highly accurate for detection of aldosterone-producing adenoma but results must be correlated with endocrine studies.⁵ Secondary aldosteronism may occur in congestive heart failure, cirrhosis with ascites, nephrosis, potassium loading, sodium-depleted diet, toxemia of pregnancy and other states of contraction of plasma volume, and Bartter syndrome. Renin is high in secondary aldosteronism, low in primary aldosteronism.
Footnotes
	Meites S, Buffone GJ, Cheng MH, et al, Pediatric Clinical Chemistry, Reference (Normal Values), 3rd ed, Washington, DC: AACC Press, 1989, 45. Stark P, Beckerhoff R, Leumann EP, et al, “Control of Plasma Aldosterone in Infancy and Childhood. A Study of Plasma Renin Activity, Plasma Cortisol, and Plasma Aldosterone,” Helv Paediatr Acta, 1976, 30(4-5):349-56. Beeler MF and Catrou PG, “Interpretations in Clinical Chemistry. A Textbook Approach to Chemical Pathology,” Chicago, IL: American Society of Clinical Pathologists, 1983. Watts NB and Keffer JH, “Renin-Angiotensin-Aldosterone,” Practical Endocrinology, 4th ed, Philadelphia, PA: Lea & Febiger, 1989, 130-5. Radin DR, Manoogian C, and Nadler JL, “Diagnosis of Primary Hyperaldosteronism: Importance of Correlating CT Findings With Endocrinologic Studies,” Am J Roentgenol, 1992, 158(3):553-7
References
	Alpern RJ and Toto RD, “Hypokalemic Nephropathy - A Clue to Cystogenesis?” N Engl J Med, 1990, 322(6):398-9. Bravo EL, “Primary Aldosteronism,” Urol Clin North Am, 1989, 16(3):481-6. Cuche JL, “Dopaminergic Control of Aldosterone Secretion. State-of-the-Art Review,” Fundam Clin Pharmacol, 1988, 2(4):327-39 (review). Garcia-Robles R and Ruilope LM, “Pharmacological Influences on Aldosterone Secretion,” J Steroid Biochem, 1987, 27(4-6):947-51 (review). McKenna TJ, Sequeira SJ, Heffernan A, et al, “Diagnosis Under Random Conditions of All Disorders of the Renin-Angiotensin-Aldosterone Axis, Including Primary Hyperaldosteronism,” J Clin Endocrinol Metab, 1991, 73(5):952-7. Muller J, “Regulation of Aldosterone Biosynthesis. Physiological and Clinical Aspects,” Monogr Endocrinol, 1987, 29:1-364 (review). Quinn SJ and Williams GH, “Regulation of Aldosterone Secretion,” Annu Rev Physiol, 1988, 50:409-26 (review). Tait JF and Tait SA, “A Steroids Memoir. A Decade (or More) of Electrocortin (Aldosterone),” Steroids, 1988, 51(3-4):213-50 (review). Torres VE, Young WF Jr, Offord KP, et al, “Association of Hypokalemia, Aldosteronism, and Renal Cysts,” N Engl J Med, 1990, 322(6):345-51. Young DB, “Quantitative Analysis of Aldosterone's Role in Potassium Regulation,” Am J Physiol, 1988, 255(5 Pt 2):F811-22 (review). Young WF Jr, Hogan MJ, Klee GG, et al, “Primary Aldosteronism: Diagnosis and Treatment,” Mayo Clin Proc, 1990, 65(1):96-110.