MINERALOCORTICOID EXCESS
Hypersecretion of aldosterone by the adrenal cor-tex (primary
aldosteronism) can be due to a unilat-eral adenoma (aldosteronoma or Conn
syndrome), bilateral hyperplasia, or in very rare cases carcinoma of the
adrenal gland. Some disease states stimu-late aldosterone secretion by
affecting the renin– angiotensin system. For example, congestive heart failure,
hepatic cirrhosis with ascites, nephrotic syn-drome, and some forms of
hypertension (eg, renal artery stenosis) can cause secondary aldosteronism.
Although both primary and secondary aldosteron-ism are characterized by
increased levels of aldo-sterone, only the latter is associated with increased renin
activity. The usual clinical manifestations of mineralocorticoid excess include
hypokalemia and hypertension, and an increased ratio of aldosterone– plasma
renin activity has been noted in laboratory studies.
Fluid and electrolyte disturbances can be corrected preoperatively using
spironolactone. This aldoste-rone antagonist is a potassium-sparing diuretic
with antihypertensive properties. Intravascular volume can be assessed
preoperatively by testing for ortho-static hypotension.
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