Hyperkalemia (High Potassium)

Background

Potassium ions play an important role in many biological processes, particularly in the generation of membrane and action potentials and electrical conduction in nerve cells and the heart. Potassium is 98% localized intracellularly. The primary active transporter Na+/K+-ATPase provides transport into cells. Two hormones maintain the deep extracellular potassium concentration. The first is insulin, produced in the pancreas, which promotes the uptake of potassium into cells, and the second is renin, produced in the cells of the juxtaglomerular apparatus of the kidney. Renin promotes the secretion of aldosterone at the zona glomerulosa of the adrenal gland, which in turn promotes potassium excretion at the kidney (Figure). Potassium is also excreted to a lesser extent via the colon.

Symptoms

Hyperkalemia is said to occur when a blood serum potassium concentration of more than 5.0 mmol/L is measured. Mild hyperkalemia often remains asymptomatic. However, moderate to severe increases of 6-8 mmol/L or more may cause symptoms, some of them severe, such as muscle weakness, general weakness, sensory disturbances, acidosis, paralysis, intestinal obstruction, central nervous disturbances, ECG changes, cardiac arrhythmias, cardiac arrest, and, in the worst case, a fatal outcome.

Causes

Three processes favor the development of hyperkalemia: increased potassium uptake, increased release of potassium from cells, and decreased elimination. Aldosterone promotes the excretion of potassium ions at the kidney. Since aldosterone itself is under the control of the renin-angiotensin system (RAS), any inhibition of this system can lead to an increase in potassium concentration. Aldosterone is produced in the adrenal gland, which is why diseases of the adrenal gland also cause hyperkalemia. 1. drugs:

  • Renin inhibitors, ACE inhibitors and sartans inhibit the renin-angiotensin system.
  • Aldosterone antagonists such as spironolactone and eplerenone inhibit the effects of aldosterone
  • Potassium-sparing diuretics such as amiloride and triamterene retain potassium at the kidney site
  • Beta-blockers inhibit the RAS by inhibiting renin formation.
  • NSAIDs decrease renin secretion and renal blood flow.
  • Potassium chloride, as a drug, increases the exogenous supply of potassium
  • Numerous other drugs have the potential to cause hyperkalemia. These include amino acids, azole antifungals, benzylpenicillin potassium (penicillin G), ciclosporin, digoxin, heparins, pentamidine, succinylcholine, tacrolimus, and trimethoprim.

2. diet:

  • A diet rich in potassium increases the exogenous intake of potassium. It is a component of sea salt, which is often recommended instead of table salt for high blood pressure. Potassium is found in numerous fruits, for example, bananas, avocados, raisins, melons, dried dates and apricots, and dark green leafy vegetables. Medicinal drugs, drinking foods and food supplements may also contain high amounts of potassium.

3. diseases:

  • Diabetic nephropathy, renal failure, renal failure, heart failure.
  • Decreased formation, secretion of, or resistance to aldosterone: hypoaldosteronism, pseudohypoaldosteronism, mineralocorticoid deficiency, Addison’s disease (adrenal insufficiency), hyporeninemia
  • Cell dissolution: hemolysis, rhabdomyolysis, burns, trauma, tumor dissolution (cytostatics), limb ischemia.
  • Acidosis
  • Diabetes mellitus, insulin resistance, hyperosmolar states, hyperglycemia.

Risk factors

Those most at risk are older people with kidney disease who are taking medications. Acute hyperkalemia is most commonly seen in the hospital setting. Underlying diseases, polymedication, and drug interactions promote the development of the metabolic disorder.

Diagnosis

Diagnosis is made by medical treatment based on blood analysis, patient history, physical examination, and ECG, among other factors. Conditions that cause similar complaints must be excluded. In so-called pseudohyperkalemia, laboratory results are present that falsely indicate elevated potassium levels. A common cause is the release of potassium from destroyed cells, e.g., red blood cells.

Non-drug treatment

Nonpharmacologic therapy is primarily aimed at decreasing the exogenous intake of potassium via foods and medications. Triggering medications should be discontinued and switched if possible. Furthermore, for acute treatment, hemodialysis is used for a severe course that cannot be adequately treated with medication.

Drug treatment

Hyperkalemia is treated medically. If there is an acute worsening, ECG changes, and severe symptoms, it is a medical emergency. Refer to the literature for specific treatment guidelines and details on drug use. Calcium salts:

  • Parenteral calcium briefly stabilizes the myocardium during acute treatment by antagonizing the effects of potassium at the cell membrane. However, it has no effect on the increased potassium concentration.

Diuretics:

Insulins:

Beta2-sympathomimetics:

  • Β2Sympathomimetics such as salbutamol, on the one hand, promote endogenous secretion of insulin and uptake of potassium into cells. On the other hand, sympathomimetics stimulate renin secretion and thus renal excretion (β1). They are administered by inhalation or parenterally.

Ion exchangers:

  • Sodium polystyrene sulfonate (Resonium A) is a cation exchanger with a high affinity for potassium, exchanging potassium ions for sodium ions in the intestinal lumen. It can be applied orally or rectally and is combined with laxatives such as sorbitol, which result in acceleration of intestinal transit and thus rapid export of the bound potassium from the body. A common adverse effect is diarrhea. In hypernatremia, the drug is contraindicated because of the sodium content.
  • Patiromer (Veltassa) is an agent of the cation exchange group used in adults. It binds potassium in the lumen of the gastrointestinal tract and delivers it to excretion in the stool.

Causal drug treatment:

  • In addition to symptomatic treatment, more or less causal drug therapy is possible, depending on the cause. For example, hypoaldosteronism can be treated with the mineralocorticoid fludrocortisone.