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ALDU<br />

8556<br />

regulator of the synthesis and secretion of aldosterone. Likewise, increased concentrations of potassium in<br />

the plasma may directly stimulate adrenal production of the hormone. Under physiologic conditions,<br />

pituitary adrenocorticotropic hormone is not a major factor in regulating aldosterone secretion. See<br />

Steroid Pathways in Special Instructions.<br />

Useful For: Investigation of primary aldosteronism (eg, adrenal adenoma/carcinoma and adrenal<br />

cortical hyperplasia) and secondary aldosteronism (renovascular disease, salt depletion, potassium<br />

loading, cardiac failure with ascites, pregnancy, Bartter syndrome)<br />

Interpretation: A high ratio of serum aldosterone (SA) in ng/dL to plasma renin activity (PRA) in<br />

ng/mL per hour, is a positive screening test result, a finding that warrants further testing. A SA/PRA ratio<br />

> or =20 is only interpretable with a SA > or =15 ng/dL and indicates probable primary aldosteronism.<br />

Renal disease, such as unilateral renal artery stenosis, results in elevated renin and aldosterone levels.<br />

Renal venous catheterization may be helpful. A positive test is a renal venous renin ratio<br />

(affected/normal) >1.5. See Renin-Aldosterone Studies and Steroid Pathways in Special Instructions.<br />

Note: Advice on stimulation or suppression tests is available from <strong>Mayo</strong> Clinic's Division of<br />

Endocrinology and may be obtained by calling <strong>Mayo</strong> <strong>Medical</strong> <strong>Laboratories</strong>.<br />

Reference Values:<br />

0-30 days: 17-154 ng/dL*<br />

1-11 months: 6.5-86 ng/dL*<br />

1-10 years: < or =40 ng/dL (supine)*<br />

< or =124 ng/dL (upright)*<br />

> or =11 years: < or =21 ng/dL (a.m. peripheral vein specimen)<br />

Reference range based on upright a.m. collection from subjects on ad lib sodium intake.<br />

*Loeuille GA, Racadot A, Vasseur P, Vandewalle B: Blood and urinary aldosterone levels in normal<br />

neonates, infants and children. Pediatrie 1981;36:335-344<br />

Clinical References: 1. Young WF Jr: Primary aldosteronism: A common and curable form of<br />

hypertension. Cardiol Rev 1999;7:207-214 2. Young WF Jr: Pheochromocytoma and primary<br />

aldosteronism: diagnostic approaches. Endocrinol Metab Clin North Am. 1997;26:801-827 3. Hurwitz S,<br />

Cohen RJ, Williams GH: Diurnal variation of aldosterone and plasma renin activity: timing relation to<br />

melatonin and cortisol and consistency after prolonged bed rest. J Appl Physiol 2004;96:1406-1414<br />

Aldosterone, Urine<br />

Clinical Information: Aldosterone stimulates sodium transport across cell membranes, particularly in<br />

the distal renal tubule where sodium is exchanged for hydrogen and potassium. Secondarily, aldosterone<br />

is important in the maintenance of blood pressure and blood volume. Aldosterone is the major<br />

mineralocorticoid and is produced by the adrenal cortex. The renin-angiotensin system is the primary<br />

regulator of the synthesis and secretion of aldosterone. Likewise, increased concentrations of potassium in<br />

the plasma may directly stimulate adrenal production of the hormone. Under physiologic conditions,<br />

pituitary adrenocorticotropic hormone can stimulate aldosterone secretion. Urinary aldosterone levels are<br />

inversely correlated with urinary sodium excretion. Normal subjects will show a suppression of urinary<br />

aldosterone with adequate sodium repletion. Primary hyperaldosteronism, which may be caused by<br />

aldosterone-secreting adrenal adenoma/carcinomas or adrenal cortical hyperplasia, is characterized by<br />

hypertension accompanied by increased aldosterone levels, hypernatremia, and hypokalemia. Secondary<br />

hyperaldosteronism (eg, in response to renovascular disease, salt depletion, potassium loading, cardiac<br />

failure with ascites, pregnancy, Bartterâ€s syndrome) is characterized by increased aldosterone levels<br />

and increased plasma rennin activity.<br />

Useful For: Investigation of primary aldosteronism (eg, adrenal adenoma/carcinoma and adrenal<br />

cortical hyperplasia) and secondary aldosteronism (renovascular disease, salt depletion, potassium<br />

loading, cardiac failure with ascites, pregnancy, Bartter's syndrome)<br />

Interpretation: Under normal circumstances, if the 24-hour urinary sodium excretion is >200 mEq,<br />

the urinary aldosterone excretion should be 12 mcg/24<br />

hours as part of an aldosterone suppression test is consistent with hyperaldosteronism. 24-Hour urinary<br />

Current as of January 4, 2013 7:15 pm CST 800-533-1710 or 507-266-5700 or <strong>Mayo</strong><strong>Medical</strong><strong>Laboratories</strong>.com Page 70

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