Published 23 October 2009, doi:10.1136/bmj.b4114
Cite this as: BMJ 2009;339:b4114

Clinical Review

Hyperkalaemia

Moffat J Nyirenda, MRC clinician scientist/honorary consultant physician1, Justin I Tang, research fellow1, Paul L Padfield, professor of hypertension2, Jonathan R Seckl, professor of molecular medicine1

1 Endocrinology Unit, Centre for Cardiovascular Science, Queen’s Medical Research Institute, University of Edinburgh, Edinburgh EH16 4TJ, 2 Metabolic Unit, Western General Hospital, Lothian University Hospitals NHS Trust, Edinburgh

Correspondence to: M Nyirenda m.nyirenda@ed.ac.uk

The first 150 words of the full text of this article appear below.

Hyperkalaemia is defined as serum potassium concentration greater than 5.5 mmol/l. Its prevalence in the general population is unknown, but it is thought to occur in 1-10% of patients admitted to hospital.1 The rate of morbidity and mortality associated with hyperkalaemia has risen greatly with the use of drugs that target the renin-angiotensin system, and since publication 10 years ago of a randomised trial that showed that adding an aldosterone receptor antagonist to usual treatment for congestive failure improved outcomes.2 3 4 5


We searched PubMed for articles whose titles included the terms "hyperkalaemia" or "potassium homoeostasis" and restricted the search to articles published in English in the past 15 years. We also searched contemporary textbooks.


Potassium is the most abundant cation in the human body and has key roles in the excitatory properties needed for conduction of nerve impulses and muscle contraction. Ninety eight per cent of the body’s potassium is in . . . [Full text of this article]

Potassium redistribution (intracellular to extracellular fluid)
Decreased excretion of potassium
Decreased urine flow rate or sodium delivery to distal nephron
Drugs that alter transmembrane potassium movement
Potassium containing agents
Drugs that reduce aldosterone secretion
Drugs that block aldosterone binding to mineralocorticoid receptor
Drugs that inhibit activity of epithelial sodium channel

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