What to do if you have hyperthyroidism and potassium deficiency

Potassium plays a vital role in the balance of body fluids in the human body. If the body lacks potassium, it will cause nausea and vomiting, so we should carry out potassium supplementation treatment in time. Hyperthyroidism patients will suffer from rapid loss of potassium due to their body metabolism, so we should pay attention to our daily diet and eat more fruits and vegetables, which can alleviate the loss of potassium to a certain extent. So, what should patients with hyperthyroidism do if they are deficient in potassium?

① Long-term continuous use or excessive dosage of diuretics: for example, diuretics that inhibit the reabsorption of sodium and water in the proximal tubule (carbonic anhydrase inhibitor acetazolamide) and diuretics that inhibit the reabsorption of Cl- and Na+ in the thick ascending limb of the loop of Henle (furosemide, uric acid, thiazide, etc.) can increase the original urine flow reaching the distal renal tubule, and the increase in flow here is an important reason for promoting increased tubular potassium secretion. The above-mentioned diuretics can also increase the amount of Na+ reaching the distal convoluted tubule, thereby leading to potassium loss through enhanced Na+-K+ exchange. Many diuretics share a common mechanism for increasing renal potassium excretion: increased aldosterone secretion through a reduction in blood volume. The action of furosemide, uric acid, and thiazides is to inhibit the reabsorption of Cl- by the thick ascending limb of the loop of Henle, thereby also inhibiting the reabsorption of Na+. Therefore, long-term use of these drugs can lead to both hyponatremia and hypochloremia. It has been shown that hypochloremia caused by any reason can increase renal potassium excretion. One of the possible mechanisms is that hypochloremia seems to directly stimulate the potassium secretion function of the distal renal tubules.

② Certain kidney diseases: such as distal renal tubular acidosis, due to the dysfunction of distal tubular hydrogen secretion, H+-Na+ exchange is reduced and K+-Na+ exchange is increased, leading to potassium loss. In proximal renal tubular acidosis, the reabsorption of HCO3- in the proximal tubule is reduced, and the increase in HCO3- reaching the distal tubule is an important reason for promoting increased potassium excretion in the distal tubule (details later). During the polyuria phase of acute tubular necrosis, increased potassium excretion may occur due to osmotic diuresis caused by increased urea in the tubular fluid and insufficient water and electrolyte reabsorption by the newly formed tubular epithelium.

③ Excessive adrenal cortical hormones: When primary and secondary aldosterone increases, the Na+-K+ exchange in the distal renal tubules and collecting ducts increases, thereby excreting potassium and retaining sodium. In Cushing's syndrome, secretion of the glucocorticoid cortisol increases dramatically. Cortisol also has certain mineralocorticoid-like effects. Large amounts of long-term cortisol can also promote Na+-K+ exchange between the distal convoluted tubule and the collecting duct, leading to increased renal potassium excretion.

④ The amount of anions that are difficult to reabsorb in the distal convoluted tubule increases : HCO3-, SO42-, HPO42-, NO3-, β-hydroxybutyric acid, acetoacetic acid, penicillin, etc. When they increase in the distal tubular fluid, the negative charge of the primary urine increases because they cannot be reabsorbed. Therefore, K+ easily enters the tubular fluid from the renal tubular epithelial cells and is lost in the urine.

⑤Magnesium deficiency: Magnesium deficiency often causes hypokalemia. Potassium reabsorption in the ascending limb of the loop of Henle depends on the Na+-K+-ATR enzyme in the renal tubular epithelial cells, which in turn requires Mg2+ activation. When magnesium is deficient, this enzyme may be inactivated due to the lack of Mg2+ in the cell, resulting in impaired potassium reabsorption and potassium loss. Animal experiments have also shown that magnesium deficiency can also cause increased aldosterone, which may also be the cause of potassium loss.

⑥ Alkali poisoning: In alkali poisoning, the excretion of H+ by the renal tubular epithelial cells decreases, so the H+-Na+ exchange is enhanced, and the excretion of potassium in the urine increases.