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 symptoms of this condition include low sodium (hyponatremia), too much potassium (hyperkalemia), and a condition where the body produces too much acid (metabolic acidosis). These symptoms may cause muscle weakness, nausea, heart palpitations, irregular heartbeat, and abnormal blood pressure.
Renin deficiency is the most common cause of hypoaldosteronism, occurring most often in older patients with mild, nonoliguric renal disease who often have insulin-dependent diabetes and potentially diabetic nephropathy.
Hypoaldosteronism (HA) is a condition marked by decreased synthesis or diminished release of aldosterone (ALD) from the zona glomerulosa of the adrenal glands, or resistance to its action on target tissues. In conditions of resistance, aldosterone levels are often elevated and termed pseudo-hypoaldosteronism.
Most patients with hyporeninemic hypoaldosteronism respond well to low-potassium diet and, if necessary, a loop or thiazide diuretic to enhance potassium excretion. Fludrocortisone is sometimes needed with dosing affected by the cause of hormone deficiency.
Primary hyperaldosteronism caused by an adrenal gland tumor is often treated with surgery. It can sometimes be treated with medicines. Removing the adrenal tumor may control the symptoms. Even after surgery, some people still have high blood pressure and need to take medicine.
Hypoaldosteronism can occur as part of the presentation of Addison's disease, resulting from destruction of both adrenal glands or due to selective injury to cells producing aldosterone. Addison's disease can be a medical emergency due to deficiency of cortisol, as well as of aldosterone and other mineralocorticoids.
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.
Common complications of hypoaldosteronism include hyperkalemia, metabolic acidosis, hypotension, hypovolemia and hyponatremia. Depending on the extent of the hyperkalemia and underlying renal or adrenal condition at the time of diagnosis, the prognosis of hypoaldosteronism may vary.
Sometimes the lack of aldosterone in Addison's disease can cause hyponatremia. This condition occurs when you don't have enough sodium in your blood. Hyponatremia can cause confusion, fatigue, and muscle twitches and seizures. The lack of aldosterone can also cause hyperkalemia, or too much potassium.
Addison's disease, also called adrenal insufficiency, is an uncommon illness that occurs when the body doesn't make enough of certain hormones. In Addison's disease, the adrenal glands make too little cortisol and, often, too little of another hormone, aldosterone.
Hyperaldosteronism is a disease in which the adrenal gland(s) make too much aldosterone which leads to hypertension (high blood pressure) and low blood potassium levels. Primary hyperaldosteronism can be caused by either hyperactivity in one adrenal gland (unilateral disease) or both (bilateral disease).
The most often recommended screening test for primary aldosteronism is the aldosterone-to-renin ratio (ARR). ARR testing can easily be performed in the ambulatory setting typically without any additional preparation.
Screening with aldosterone-to-renin ratio (ARR) is the most practical and informative initial test. Subsequent confirmatory tests are: (1) oral salt loading; (2) saline infusion; (3) captopril challenge and (4) fludrocortisone suppression test.
These symptoms include fatigue, anxiety, depression, headache, and memory difficulties. High blood pressure is also associated with excess production of aldosterone (Conn's Syndrome).
Therefore, the authors of this article believe that, after excluding other causes, the existence of significant hyperkalemia (potassium levels > 5.5-6.0 mEq/L) accompanied by low or inappropriately normal aldosterone levels is indicative of hypoaldosteronism.
The most common symptoms are fatigue, muscle weakness, loss of appetite, weight loss, and abdominal pain. Adrenal insufficiency can be caused by autoimmune disease or suddenly stopping steroid medicines used to treat other conditions, among other causes.
Without aldosterone (for example if the adrenal glands are not working properly), the kidney loses excessive amounts of salt (sodium) and, consequently, water, leading to severe dehydration and low blood pressure.
Only one study reported the mortality rates of idiopathic hyperaldosteronism, and were about 1.51% at 3, 5, and 7.5 years while 10.61% at 10 years (22).
A steroid hormone made by the adrenal cortex (the outer layer of the adrenal gland). It helps control the balance of water and salts in the kidney by keeping sodium in and releasing potassium from the body. Too much aldosterone can cause high blood pressure and a build-up of fluid in body tissues.
Less well known is the fact that Conn's syndrome (Primary hyperaldosteronism) also can cause weight gain. The link between aldosterone, obesity, and weight gain has been studied in detail. Aldosterone levels are already elevated in obese individuals (without and adrenal tumor). In fact, aldosterone protects fat.
Aldosterone is well known to increase sodium reabsorption and potassium secretion by the kidney. It exerts its main effects on sodium and potassium balance by binding to the mineralocorticoid receptor (MCR) located in the distal convoluted tubule, connecting segment and cortical collecting duct in the kidney.
Potassium directly increases aldosterone secretion by the adrenal cortex and aldosterone then lowers serum potassium by stimulating its excretion by the kidney. High dietary potassium intake increases plasma aldosterone and enhances the aldosterone response to a subsequent potassium or angiotensin II infusion (12).