What causes hypercalcaemia
HyperkalemiaIndications Hyperkalemia is an increase in the level of potassium in the blood serum. A mild increase is usually asymptomatic. In contrast, high concentrations are potentially life-threatening and manifest themselves in muscle weakness, paralysis and cardiac arrhythmias. Elderly people with kidney disease are particularly at risk. Numerous drugs can promote the metabolic disorder because they inhibit the renin-angiotensin system, which promotes the excretion of potassium in the kidneys.
synonymous: hyperkalemia, excess potassiumbackground
Potassium ions play an important role in many biological processes, especially in the development of membrane and action potentials and electrical conduction in nerve cells and on the heart. 98% of potassium is localized intracellularly. The primary active transporter Na+/ K+-ATPase ensures the transport into the cells. Two hormones maintain the low levels of extracellular potassium. First, the insulin produced in the pancreas, which promotes the uptake of potassium by the cells, and second, the renin produced in the cells of the juxtaglomerular apparatus of the kidney. Renin promotes the secretion of aldosterone in the zona glomerulosa of the adrenal gland, which in turn promotes the excretion of potassium in the kidney (Figure). A smaller proportion of potassium is also excreted via the large intestine.
Hyperkalaemia is when a potassium concentration in the blood serum of more than 5.0 mmol / L is measured. Mild hyperkalemia often remains asymptomatic. With a moderate to strong increase from 6-8 mmol / L, however, sometimes serious complaints such as muscle weakness, general weakness, sensory disturbances, acidosis, paralysis, intestinal obstruction, central nervous disorders, EKG changes, cardiac arrhythmias, cardiac arrest and, in the worst case, a fatal outcome possible.causes
Three processes favor the development of hyperkalaemia: an increased intake of potassium, an increased release of potassium from the cells and a reduced elimination. Aldosterone promotes the excretion of potassium ions from the kidneys. Since aldosterone is itself under the control of the renin angiotensin system (RAS), any inhibition of this system can lead to an increase in potassium levels. Aldosterone is produced in the adrenal gland, which is why diseases of the adrenal gland also trigger hyperkalemia.
- 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 like amiloride and triamterene hold potassium back in the kidney
- Beta blockers inhibit the RAS by inhibiting the formation of renin
- NSAIDs decrease renin secretion and renal blood flow
- Potassium chloride is used as a drug to increase the exogenous intake of potassium
- Many 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.
- A diet rich in potassium increases the exogenous intake of potassium. It is a component of sea salt that is often recommended instead of table salt for people with high blood pressure. Potassium is found in numerous fruits, for example in bananas, avocados, raisins, melons, dried dates and apricots as well as in dark green leafy vegetables. Medicinal drugs, food and nutritional supplements can also contain high amounts of potassium.
Reduced potassium excretion:
Increased release of potassium from the cells:Risk factors
Elderly people with kidney disease who take medication are particularly at risk. Acute hyperkalemia is most commonly observed in the hospital. Basic diseases, a polymedication and drug interactions promote the development of the metabolic disorder.diagnosis
The diagnosis is made during medical treatment based on, among other things, the blood analysis, the patient's history, the physical examination and the ECG. Conditions that cause similar complaints must be excluded. In the case of so-called pseudohyperkalemia, laboratory results are available that incorrectly indicate elevated potassium levels. A common cause is the release of potassium from destroyed cells, e.g. from red blood cells.Non-drug treatment
The primary aim of non-drug therapy is to lower the exogenous intake of potassium through food and medication. Triggering drugs should be discontinued and switched if possible. For acute treatment, hemodialysis is also used in the case of a severe course that cannot be adequately treated with medication.Medication
Hyperkalemia is treated by a doctor. Acute deterioration, EKG changes, and severe symptoms are considered a medical emergency. For the exact therapy guidelines and the details on the use of the drugs, we refer to the specialist literature.
- Parenteral calcium briefly stabilizes the myocardium during acute treatment by antagonizing the effects of potassium on the cell membrane. However, it has no effect on the increased potassium concentration.
- Insulin promotes the absorption of potassium into the cells. It is usually given together with glucose to prevent hypoglycaemia.
- β2-Sympathomimetics such as salbutamol promote the endogenous release of insulin and the absorption of potassium into the cells. On the other hand, sympathomimetics stimulate the secretion of renin and thus its excretion from the kidneys (β1). They are administered by inhalation or parenterally.
- Sodium polystyrene sulfonate (Resonium® A) is a cation exchanger with a high affinity for potassium, which exchanges potassium ions in the intestinal lumen for sodium ions. It can be administered orally or rectally and is combined with laxatives such as sorbitol, which accelerate the bowel movement and thus lead to a rapid export of the bound potassium from the body. A common adverse effect is diarrhea. In hypernatremia, the drug is contraindicated due to the sodium content.
- Patiromer (Veltassa®) is an active ingredient from the group of cation exchangers that is used in adults. It binds potassium in the lumen of the gastrointestinal tract and directs 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.
Renin-angiotensin system, hypokalemialiterature
- Medicinal product information (CH)
- Burger C.M. Hyperkalemia. Am J Nurs, 2004, 104 (10), 66-70 Pubmed
- Elliott M.J., Ronksley P.E., Clase C.M., Ahmed S.B., Hemmelgarn B.R. Management of patients with acute hyperkalemia. CMAJ, 2010, 182 (15), 1631-5 Pubmed
- Gennari F.J. Disorders of potassium homeostasis. Hypokalemia and hyperkalemia. Crit Care Clin, 2002, 18 (2), 273-88, vi Pubmed
- Hollander-Rodriguez J.C., Calvert J.F. Jr. Hyperkalemia. Am Fam Physician, 2006, 73 (2), 283-90 Pubmed
- Khanna A., White W.B. The management of hyperkalemia in patients with cardiovascular disease. Am J Med, 2009, 122 (3), 215-21 Pubmed
- Sood M.M., Sood A.R., Richardson R. Emergency management and commonly encountered outpatient scenarios in patients with hyperkalemia. Mayo Clin Proc, 2007, 82 (12), 1553-61 Pubmed
- Palmer B.F. Managing hyperkalemia caused by inhibitors of the renin-angiotensin-aldosterone system. N Engl J Med, 2004, 351 (6), 585-92 Pubmed
- Parham W.A., Mehdirad A.A., Biermann K.M., Fredman C.S. Hyperkalemia revisited. Tex Heart Inst J, 2006, 33 (1), 40-7 Pubmed
- Perazella M.A. Drug-induced hyperkalemia: old culprits and new offenders. Am J Med, 2000, 109 (4), 307-14 Pubmed
- Rastergar A., Soleimani M. Hypokalaemia and hyperkalaemia. Postgrad Med J, 2001, 77, 759-764 Pubmed
- Weiner I.D., Wingo C.S. Hyperkalemia: a potential silent killer. J Am Soc Nephrol, 1998, 9 (8), 1535-43 Pubmed
- Weisberg L.S. Management of severe hyperkalemia. Crit Care Med, 2008, 36 (12), 3246-51 Pubmed
Author: PharmaWiki. Conflicts of Interest: None / Independent. The author has no relationships with the manufacturers and is not involved in the sale of the products mentioned. With many thanks to Matthias Vogelsgesang, pharmacist, Institute for Molecular Pharmacy at the University of Basel, for reading this critically. Illustration: © PharmaWiki.
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This article was last changed on 4.1.2018.
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