Addison’s disease is a rare endocrine disorder characterized by the adrenal glands’ insufficient hormone production. This leads to notable electrolyte imbalances: low sodium (hyponatremia) and elevated potassium (hyperkalemia). Understanding these hormonal deficiencies explains why these disturbances occur.
Addison’s Disease: A Hormonal Deficiency
Addison’s disease is a primary adrenal insufficiency where the adrenal glands are damaged and cannot produce enough steroid hormones. These small, triangle-shaped glands sit atop each kidney. The adrenal cortex produces glucocorticoids like cortisol and mineralocorticoids, primarily aldosterone.
While cortisol deficiency contributes to various symptoms, insufficient aldosterone production primarily drives the electrolyte disturbances of hyponatremia and hyperkalemia. Autoimmune destruction of the adrenal cortex is the most common cause (70% to 90% of cases), leading to a significant reduction in both cortisol and aldosterone. Symptoms typically do not appear until about 90% of the adrenal cortex has been damaged.
Aldosterone’s Role in Electrolyte Regulation
Aldosterone is a mineralocorticoid hormone synthesized in the adrenal cortex. Its main function is regulating the body’s salt and water balance, blood pressure, and sodium and potassium concentrations. This hormone acts primarily on the kidneys, targeting the late distal tubules and collecting ducts of the nephrons.
Within these kidney tubules, aldosterone promotes sodium reabsorption into the bloodstream. This process involves activating specific channels and pumps on cell membranes. As sodium is reabsorbed, potassium is simultaneously secreted into the urine, maintaining electrolyte balance. Water also follows sodium passively into the bloodstream, which helps regulate blood volume and blood pressure.
The Mechanism of Hyponatremia in Addison’s Disease
In Addison’s disease, aldosterone deficiency directly impairs the kidneys’ ability to reabsorb sodium. Without sufficient aldosterone, sodium is excessively lost in the urine, causing a decrease in blood sodium concentration, known as hyponatremia.
Reduced sodium levels impact fluid balance, as water often follows sodium. This can decrease overall blood volume, exacerbating the electrolyte imbalance and potentially affecting blood pressure. The body’s attempt to compensate for volume depletion can also lead to increased antidiuretic hormone (ADH) secretion, promoting water retention and further diluting blood sodium levels.
The Mechanism of Hyperkalemia in Addison’s Disease
Conversely, aldosterone deficiency in Addison’s disease explains the development of hyperkalemia, or high potassium levels. Aldosterone’s normal function includes stimulating potassium excretion into the urine through the renal tubules. Without adequate aldosterone, this primary mechanism for potassium removal is impaired.
As a result, potassium accumulates in the bloodstream because the kidneys cannot effectively excrete it. This retention leads to elevated potassium concentrations, contributing to the characteristic electrolyte imbalance seen in Addison’s disease. The absence of aldosterone directly links to both excessive sodium loss and potassium retention observed in this condition.