Clinical Summary

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 is not a major factor in regulating aldosterone secretion.

CAUTIONS:

 
Late p.m. levels can be up to 30% lower than early a.m. levels. Supine values are on average 50% lower than upright collections. Sodium-deplete patients have significantly elevated serum aldosterone (SA) levels, potentially exceeding the upper limit of the salt replete upright reference range by several fold. To account for these variables, at least in part, it is recommended that PRA is measured concomitantly. In situations of physiological variability, PRA should be altered in the same direction as aldosterone. For more information see Renin-Aldosterone Studies.

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 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.