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ESSENTIALS OF DIAGNOSIS

  • Serum potassium level greater than 5.0 mEq/L (5.0 mmol/L).

  • Hyperkalemia may develop in patients taking angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers, potassium-sparing diuretics, or their combination, even with no or only mild kidney dysfunction.

  • The ECG may be normal despite life-threatening hyperkalemia.

  • Measurement of plasma potassium level differentiates potassium leak from blood cells from truly elevated serum potassium.

  • Rule out extracellular potassium shift from the cells in acidosis and assess renal potassium excretion.

GENERAL CONSIDERATIONS

Hyperkalemia usually occurs in patients with advanced kidney disease but can also develop with normal kidney function (Table 21–6). Acidosis causes intracellular potassium to shift extracellularly. Serum potassium concentration rises about 0.7 mEq/L for every decrease of 0.1 pH unit during acidosis. Fist clenching during venipuncture may raise the potassium concentration by 1–2 mEq/L by causing acidosis and potassium shift from cells. In the absence of acidosis, serum potassium concentration rises about 1 mEq/L when there is a total body potassium excess of 1–4 mEq/kg. However, the higher the serum potassium concentration, the smaller the excess necessary to raise the potassium levels further.

Table 21–6.Causes of hyperkalemia.

Mineralocorticoid deficiency from Addison disease or CKD is another cause of hyperkalemia with decreased renal excretion of potassium. Mineralocorticoid resistance due to genetic disorders, interstitial kidney disease, or urinary tract obstruction also leads to hyperkalemia.

ACE inhibitors or angiotensin-receptor blockers (ARBs) may cause hyperkalemia. The concomitant use of spironolactone, eplerenone, or beta-blockers further increases the risk of hyperkalemia. Thiazide or loop diuretics and ...

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