Friday, November 3, 2017

Laboratory Findings in Primary Aldosteronism



Primary aldosteronism encompasses disorders caused by excessive aldosterone secretion independent of the renin-angiotensin system. These disorders are characterized by hypertension, hypokalemia,and suppression of the renin-angiotensin system
  • Hypokalemia occurs frequently.
  • Serum pH and the carbon dioxide and sodium concentrations may be elevated and 
  • the serum chloride and magnesium levels decreased. 
  • Serum levels of calcium are normal, even in children who manifest tetany. 
  • The urine is neutral or alkaline, and urinary potassium excretion is high. 
  • Plasma levels of aldosterone may be normal or elevated. 
  • Aldosterone concentrations in 24-hr urine collections are always increased. 
  • Plasma levels of renin are persistently low.
The diagnostic test of choice for primary aldosteronism is controversial. Both renin and aldosterone levels may vary by time of day, posture, and sodium intake, making it difficult to establish consistent reference ranges. It is desirable to establish a consistent sampling protocol, for example, mid-morning after the patient has been sitting for 15 min. If possible, antihypertensive drugs or other medications that can affect aldosterone or renin secretion should be avoided for several weeks prior to testing,
including diuretics, B-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, clonidine and nonsteroidal anti-inflammatory agents. Patients taking these agents may need to be changed to alpha-adrenergic blockers or calcium channel blockers that have smaller effects on the biochemical measurements. The ratio of plasma aldosterone concentration to renin activity is always high, and this represents a cost-effective screening test for primary aldosteronism. Aldosterone does not decrease with administration of saline solution or fludrocortisone, and renin does not respond to salt and fluid restriction. Urinary and plasma levels of 18-oxocortisol and 18-hydroxycortisol may be increased but not to the extent seen in glucocorticoid-suppressible hyperaldosteronism.

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