Hyperkalemia is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • Hyperkalemia is defined as a plasma [K+] >5.0 mEq/L.
  • Pseudohyperkalemia represents an artificially elevated plasma [K+] due to K+ movement out of cells immediately before or following venipuncture. Contributing factors include repeated fist clenching, hemolysis, and marked leukocytosis or thrombocytosis.
  • True hyperkalemia occurs as a result of (1) transcellular shift, (2) increased exposure to K+, and most commonly, (3) decreased renal K+ excretion. Combinations of these mechanisms often underlie cases of hyperkalemia in clinical practice, and decreased renal excretion is nearly always some component of the pathophysiology.
    • Transcellular shift. Insulin deficiency, hyperosmolality, nonselective β-blockers, digitalis, metabolic acidosis (excluding those from organic acids), and depolarizing muscle relaxants, such as succinylcholine, release K+ from predominate ICF stores into the ECF compartment. The release of intracellular K+ can also be seen after severe exercise, rhabdomyolysis, and tumor lysis syndrome. In the younger population, familial hyperkalemic periodic paralysis is a rare but important cause to consider as well.
    • Increased exposure to K+ is rarely the sole cause of hyperkalemia unless there is an impairment in renal excretion. Foods with a high content of K+ include salt substitutes, dried fruits, nuts, tomatoes, potatoes, spinach, bananas, and oranges. Juices derived from these foods may be especially rich sources.
    • Decreased renal K+ excretion. In the setting of hyperkalemia, the kidney is capable of generating a significant urinary excretion of K+. This process can be impaired by a number of processes, including intrinsic renal disease, decreased delivery of filtrate to the distal nephron, adrenal insufficiency, and hyporeninemic hypoaldosteronism (type 4 RTA).
  • Drugs may also be implicated in the genesis of hyperkalemia through a variety of mechanisms. Common culprits include angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, potassium-sparing diuretics, NSAIDs, and cyclosporine. Heparin and ketoconazole can also contribute to hyperkalemia through the decreased production of aldosterone, although these agents alone are typically insufficient to sustain a clinically significant hyperkalemia.

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