Hypoaldosteronism
Aldosterone
Specialty	Endocrinology

Hypoaldosteronism is anendocrinological disorder characterized by decreased levels of thehormonealdosterone. Similarly,isolated hypoaldosteronism is the condition of having loweredaldosterone without corresponding changes incortisol.^[1] (The two hormones are both produced by theadrenals.)

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Hypoaldosteronism causes low sodium (hyponatremia), high potassium (hyperkalemia), and metabolic acidosis, a condition in which the body produces excess acid. These conditions are responsible for the symptoms of hypoaldosteronism, which include muscle weakness, nausea,palpitations, irregular heartbeat, and abnormal blood pressure.^[2]

There are several causes for this condition, includingadrenal insufficiency,congenital adrenal hyperplasia, and some medications such as certaindiuretics,NSAIDs, andACE inhibitors.^[3]

• Primaryaldosterone deficiency

1. Primaryadrenal insufficiency
2. Congenital adrenal hyperplasia (21 but not11β and 17)
3. Aldosterone synthase deficiency

• Secondary aldosterone deficiency

1. Secondaryadrenal insufficiency
2. Diseases of thepituitary orhypothalamus

• Hyporeninemic hypoaldosteronism (due to decreasedangiotensin 2 production as well as intra-adrenal dysfunction)^[4]

1. Renal dysfunction-most commonlydiabetic nephropathy
2. NSAIDs
3. Ciclosporin

Hypoaldosteronism may result inhigh blood potassium and is the cause of 'type 4renal tubular acidosis', sometimes referred to as hyperkalemic RTA or tubular hyperkalemia. However, theacidosis, if present, is often mild. It can also cause urinarysodium wasting, leading to volume depletion andhypotension.^{[citation needed]}

When adrenal insufficiency develops rapidly, the amount of Na+ lost from theextracellular fluid exceeds the amount excreted in the urine, indicating that Na+ also must be entering cells. When theposterior 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, fatalshock. These changes can be prevented to a degree by increasing the dietaryNaCl 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.^{[citation needed]}

Patients with a suspected diagnosis of hypoaldosteronism are often screened with simple blood tests. Potassium levels, plasma aldosterone concentration and plasma renin activity are the three most useful in the first instance. Low aldosterone levels in the presence of high renin activity, often with low sodium, high potassium, is associated with primary hypoaldosteronism. Secondary hypoaldersteronism may be suspected if renin activity is low with low aldosterone concentrations. The plasmaaldosterone-to-renin ratio is calculated to determine if levels are sufficiently deranged to consider a diagnosis of hypoaldosteronism.^{[citation needed]}

If screening test is suggestive, a more definitive diagnosis is made by performing a saline suppression test, ambulatory salt loading test, or fludrocortisone suppression test. Imaging to detect anAdrenocortical adenoma may also be considered.^{[citation needed]}

• Aldosterone deficiency should be treated with amineralocorticoid (such as fludrocortisone), as well as possibly aglucocorticoid forcortisol deficiency if present.^{[citation needed]}
• Hyporeninemic hypoaldosteronism is amenable tofludrocortisone treatment,^[4] but the accompanyinghypertension andedema can prove a problem in these patients, so often adiuretic (such as thethiazide diuretic,bendrofluazide, or aloop diuretic, such asfurosemide) is used to control thehyperkalemia.^[5]

• Addison's disease
• Adrenal gland
• Hyperaldosteronism
• Pseudohypoaldosteronism

• Adrenal gland disorders

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