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Hyperkalemia

For further information, see CMDT Part 21-05: Hyperkalemia

Key Features

Essentials of Diagnosis

  • Serum potassium > 5.2 mEq/L (> 5.2 mmol/L)

  • Hyperkalemia may develop from angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and potassium-sparing diuretics, most commonly in patients with kidney dysfunction

  • The ECG may be normal despite life-threatening hyperkalemia

  • Rule out pseudohyperkalemia and extracellular potassium shift from the cells

General Considerations

  • Persistent hyperkalemia is generally due to

    • Impaired renal potassium excretion from low aldosterone effect (either decreased secretion of aldosterone or decreased responsiveness) or

    • Impaired delivery of sodium and water to the distal nephron or

    • Kidney disease (acute or chronic)

    • See Table 21–4

  • Transient hyperkalemia

    • Shift of intracellular potassium to the extracellular fluid

    • Occurs with tissue damage (rhabdomyolysis, tumor lysis, massive hemolysis, and trauma) or metabolic acidosis

Table 21–4.Causes of hyperkalemia.
View Table||Download (.pdf)
Table 21–4. Causes of hyperkalemia.

Pseudohyperkalemia

 Marked thrombocytosis or leukocytosis with release of intracellular K+

 Repeated fist clenching during phlebotomy, tourniquet application, use of small-bore needles during lab draw

Extracellular shift of K+

 Metabolic acidosis

 Insulin deficiency

 Hyperglycemia

 Alpha-adrenergic stimulation

 Tissue injury (rhabdomyolysis, hemolysis, tumor lysis)

 Hyperkalemic periodic paralysis

 Drugs (digoxin overdose, succinylcholine)

Kidney disease, acute and chronic

 Renal secretory defects (may or may not have reduced kidney function): interstitial nephritis, SLE, sickle cell disease, amyloidosis, obstructive nephropathy, kidney transplant

Hypoaldosteronism

 Addison disease

 Type IV renal tubular acidosis

 Heparin

 Ketoconazole

Drugs that inhibit potassium excretion

 Spironolactone, eplerenone, drospirenone, NSAIDs, ACE inhibitors, angiotensin II receptor blockers, triamterene, amiloride, trimethoprim, pentamidine, cyclosporine, tacrolimus

Excessive intake of K+

 Especially in patients with diminished kidney excretion

Etiology

Increased potassium release from cells

  • Pseudohyperkalemia (Table 21–4)

    • Leakage from marked thrombocytosis (> 500,000/mcL [500 × 109/L]) or leukocytosis (>100,000/mcL [100 × 109/L]), particularly leukemic cells

    • During phlebotomy

      • Fist clenching, application of tourniquets, using small bore needles

      • Presence of hemolysis in the processed sample suggests these etiologies.

  • Tissue breakdown

    • Tissue damage results in release of intracellular potassium to the extracellular space (rhabdomyolysis, tumor lysis, massive hemolysis, and trauma)

    • Hyperkalemia is more common when there is concurrent renal impairment

  • Hyperglycemia

    • Hyperkalemia may occur with uncontrolled diabetes, even if total body potassium is low

    • Due to a combination of insulin deficiency and hyperosmolarity

  • Metabolic acidosis

    • Serum potassium concentration rises ~ 0.7 mEq/L for every decrease of 0.1 pH unit

    • This effect is not seen with organic acidosis, such as lactic acidosis or ketoacidosis

Impaired kidney excretion

  • Acute kidney injury

    • Poor renal excretion of potassium from rapid reduction of kidney function

    • Hyperkalemia occurs more commonly in oliguric patients

  • Chronic kidney disease

    • Normal serum potassium generally preserved until GFR declines to < 20–30 mL/min/1.73 m2

    • Hyperkalemia with more modest decline in GFR is often ...

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