Differentiation of Mineralocorticoid-induced Hypertension

The differential diagnosis of mineralocorticoid excess involves primary and secondary aldosteronism, adrenal hydroxylation defects with concurrent overproduction of deoxycorticosterone, administration of substances with mineralocorticoid activity, such as drugs and licorice, and overproduction of glucocorticoids, which have associated mineralocorticoid activity. More uncommon syndromes may include a predominantly deoxycorticosterone-producing adenoma and Liddle’s syndrome, a renal tubular disease that mimics mineralocorticoid excess. A postulated mechanism also includes conditions that increase the sensitivity of the tissue to otherwise normal levels of the steroids. These syndromes are generally characterized by the concurrence of hypokalemia and hypertension with or without associated clinical signs of glucocorticoid and androgen excess or deficiency. The differential diagnosis of mineralocorticoid excess can thus be summarized as follows: Primary and secondary aldosteronism 11β and 17α defects with deoxycorticosterone overproduction Mineralocorticoid administration (drugs and licorice) Cushing’s syndrome with marked Cortisol overproduction Predominantly deoxycorticosterone-producing adenoma Liddle’s syndrome Increased sensitivity to mineralocorticoids.