Hypoaldosteronism is an endocrinological disorder characterized decreased levels of the hormonealdosterone. Similarly, isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol.
Hypoaldosteronism may result in high blood potassium and is the cause of 'type 4 renal tubular acidosis', sometimes referred to as hyperkalemic RTA or tubular hyperkalemia. However, the acidosis, if present, is often mild. It can also cause urinary sodium wasting, leading to volume depletion and hypotension. 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 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 mineralocorticoidtreatment is also instituted.
Diagnosis
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 plasma aldosterone-to-renin ratio is calculated to determine if levels are sufficiently deranged to consider a diagnosis of hypoaldosteronism. If screening test is suggestive, a more definitive diagnosis is made by performing either a saline suppression test, ambulatory salt loading test, or fludrocortisone suppression test. Imaging to detect an Adrenocortical adenoma may also be considered.
Treatment
Aldosterone deficiency should be treated with a mineralocorticoid, 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 is used to control the hyperkalemia.
