A physiologic-based approach to the evaluation of a patient with hyperkalemia

Am J Kidney Dis. 2010 Aug;56(2):387-93. doi: 10.1053/j.ajkd.2010.01.020. Epub 2010 May 20.


Hyperkalemia generally is attributable to cell shifts or abnormal renal potassium excretion. Cell shifts account for transient increases in serum potassium levels, whereas sustained hyperkalemia generally is caused by decreased renal potassium excretion. Impaired renal potassium excretion can be caused by a primary decrease in distal sodium delivery, a primary decrease in mineralocorticoid level or activity, or abnormal cortical collecting duct function. Excessive potassium intake is an infrequent cause of hyperkalemia by itself, but can worsen the severity of hyperkalemia when renal excretion is impaired. Before concluding that a cell shift or renal defect in potassium excretion is present, pseudohyperkalemia should be excluded.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Aldosterone / blood
  • Chronic Disease
  • Diabetes Mellitus, Type 1 / epidemiology
  • Diabetes Mellitus, Type 1 / physiopathology
  • Diabetic Ketoacidosis / physiopathology
  • Glomerular Filtration Rate / physiology
  • Humans
  • Hyperkalemia / blood
  • Hyperkalemia / epidemiology
  • Hyperkalemia / physiopathology*
  • Kidney / physiopathology*
  • Kidney Tubules / physiopathology
  • Liddle Syndrome / metabolism
  • Liddle Syndrome / physiopathology
  • Male
  • Potassium, Dietary / administration & dosage
  • Renin-Angiotensin System / drug effects
  • Renin-Angiotensin System / physiology
  • Sodium Bicarbonate / therapeutic use


  • Potassium, Dietary
  • Aldosterone
  • Sodium Bicarbonate