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Aldosterone w/Sodium, U Aldosterone with Sodium, Urine
Aldosterone 24 Hour Urine (ALDU)
Patient Prepartion: Spironolactone (Aldactone) should be discontinued for 4 to 6 weeks before testing.
1. Collect urine for 24 hours.
The plasma renin activity (PRA) cannot be interpreted if the patient is being treated with spironolactone (Aldactone). Spironolactone (Aldactone) should be discontinued for 4 to 6 weeks before testing.
Angiotensin converting enzyme (ACE) inhibitors have the potential to "falsely elevate" PRA. Therefore, in a patient treated with an ACE-inhibitor, the findings of a detectable PRA level or a low sodium aldosterone (SA)/PRA ratio do not exclude the diagnosis of primary aldosteronism. In addition, a strong predictor for primary aldosteronism is a PRA level undetectably low in a patient taking an ACE-inhibitor.
Aldosterone stimulates sodium transport across cell membranes, particularly in the distal renal tubule where sodium is exchanged for hydrogen and potassium. Secondarily, aldosterone is important in the maintenance of blood pressure and blood volume.
Aldosterone is the major mineralocorticoid and is produced by the adrenal cortex. The renin-angiotensin system is the primary regulator of the synthesis and secretion of aldosterone. Likewise, increased concentrations of potassium in the plasma may directly stimulate adrenal production of the hormone. Under physiologic conditions, pituitary adrenocorticotropic hormone can stimulate aldosterone secretion.
Urinary aldosterone levels are inversely correlated with urinary sodium excretion. Normal subjects will show a suppression of urinary aldosterone with adequate sodium repletion.
Primary hyperaldosteronism, which may be caused by aldosterone-secreting adrenal adenoma/carcinomas or adrenal cortical hyperplasia, is characterized by hypertension accompanied by increased aldosterone levels, hypernatremia, and hypokalemia. Secondary hyperaldosteronism (eg, in response to renovascular disease, salt depletion, potassium loading, cardiac failure with ascites, pregnancy, Bartterâ€™s syndrome) is characterized by increased aldosterone levels and increased plasma rennin activity.