Abstract
The pathophysiology of hyponatremia in adrenal insufficiency has been a subject of intense controversy. The controversy centers on whether the inability of the kidney to maximally dilute the urine is secondary to increased levels of antidiuretic hormone (ADH) or is independent of ADH. Review of the pertinent studies allows us to conclude that (1) in prolonged glucocorticoid deficiency, plasma ADH levels are elevated because of decreased effective circulating blood volume; (2) in mineralocorticoid deficiency, plasma ADH levels may also be elevated, but in this case because of decreased absolute circulating blood volume; (3) in both instances the elevated ADH levels impair the ability to dilute the urine; and (4) in both glucocorticoid and mineralocorticoid deficiency hemodynamic changes may also contribute, independently of ADH, by limiting delivery of tubular fluid to the diluting site.
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