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BOX 5-1 Clinical Circumstances That May Result in Hyperkalemia

  • Impaired renal excretion of potassium

    • Severe reduction in glomerular filtration rate

      • Chronic kidney disease

      • Subacute-reversible

        • Volume depletion

        • Pharmacological inhibition by angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)

    • Effective hypoaldosteronism

      • Reduced synthesis due to

        • Addison’s disease

        • Heparin administration

      • Reduced secretion of aldosterone

        • Hyporeninemia

          • Diabetic nephropathy

          • Obstructive nephropathy

          • Nonsteroidal anti-inflammatory drugs (e.g., indomethacin)

          • Cyclo-oxygenase-2 inhibitors (COX-2, e.g., Vioxx, Celebrex)

        • Reduced activity of angiotensin-converting enzyme

      • Reduced renal tubular response to aldosterone

        • Aldosterone-receptor blockers (e.g., spironolactone)

        • Type 4 renal tubular acidosis

    • Pharmacological inhibitors of distal renal tubular Na+-K+ exchange (e.g., amilioride, triamterene)

  • Impaired systemic cellular accumulation of potassium

    • Hypoinsulinemia (type 1 diabetes)

    • Metabolic acidosis

    • β-andrenergic blockers (e.g., propanolol)

    • α-andrenergic agonists (e.g., phenylephrine)

  • Excessive cellular release of potassium

    • Rhabdomyolosis

    • Tumor lysis

    • Leukemia

Clinical conditions that commonly occur together and that amplify their hyperkalemic effects

  • Hyporeninemia/hypoaldosteronism and diabetic nephropathy

  • Chronic kidney disease with either ACE or ARB therapy

SOURCE: Fisch et al. (1966); Gennari and Segal (2002); Kamel et al. (1996); Oster et al. (1995); Schoolwerth et al. (2001); Tannen (1986); Textor et al. (1982).

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