Hypoaldosteronism

Hypoaldosteronism is an endocrinological disorder characterized by decreased levels of the hormone aldosterone. Similarly, isolated hypoaldosteronism is the condition of having lowered aldosterone without corresponding changes in cortisol. (The two hormones are both produced by the adrenals.) 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. There are several causes for this condition, including adrenal insufficiency, congenital adrenal hyperplasia, and some medications such as certain diuretics, NSAIDs, and ACE inhibitors. Primary aldosterone deficiency Primary adrenal insufficiency Congenital adrenal hyperplasia (21 but not 11β and 17) Aldosterone synthase deficiency Secondary aldosterone deficiency Secondary adrenal insufficiency Diseases of the pituitary or hypothalamus Hyporeninemic hypoaldosteronism (due to decreased angiotensin 2 production as well as intra-adrenal dysfunction) Renal dysfunction-most commonly diabetic nephropathy NSAIDs Ciclosporin 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 dietary NaCl intake.