Hypoaldosteronism

In medicine (endocrinology), hypoaldosteronism refers to decreased levels of the hormone aldosterone.

The term "isolated hypoaldosteronism" is used to describe lowered aldosterone without corresponding changes in cortisol. (The two hormones are both produced by the adrenals.)

Causes
There are several causes for this condition, including primary adrenal insufficiency, congenital adrenal hyperplasia, and medications (certain diuretics, NSAIDs, and ACE inhibitors).


 * Aldosterone deficiency-Primary (rare)
 * 1) Primary adrenal insufficiency
 * 2) Congenital adrenal hyperplasia (21 and 11β but not 17)
 * 3) Aldosterone synthase deficiency


 * Hyporeninemic hypoaldosteronism (due to decreased angiotensin 2 production as well as intra-adrenal dysfunction)
 * 1) Renal dysfunction-most commonly diabetic nephropathy


 * 1) ACE inhibitors
 * 2) NSAIDs
 * 3) Cyclosporine

Treatment

 * Aldosterone deficiency should be treated with a mineralocorticoid (such as fludrocortisone), as well as possibly a glucocorticoid for cortisol deficiency, if present.
 * Hyporeninemic hypoaldosteronism is amenable to fludrocortisone treatment, but the accompanying hypertension and edema can prove a problem in these patients, so often a diuretic (such as the thiazide diuretic, bendrofluazide,or a loop diuretic, such as furosemide) is used to control the hyperkalemia.

Effects
This condition may result in hyperkalemia, when it is sometimes termed 'type 4 renal tubular acidosis' even though it doesn't actually cause acidosis. It can also cause urinary sodium wasting, leading to volume depletion and hypotension.

Na+ is lost in the urine. K+ is retained, and the plasma K+ rises.

When adrenal insufficiency develops rapidly, the amount of Na+ lost from the extracellular fluid exceeds the amount excreted in the urine, indicating that Na+ also must be entering cells. When the posterior pituitary is intact, salt loss exceeds water loss, and the plasma Na+ falls. However, the plasma volume also is reduced, resulting in hypotension, circulatory insufficiency, and, eventually, fatal shock. These changes can be prevented to a degree by increasing the dietary NaCl intake. Rats survive indefinitely on extra salt alone, but in dogs and most humans, the amount of supplementary salt needed is so large that it is almost impossible to prevent eventual collapse and death unless mineralocorticoid treatment is also instituted