II. Causes: Decreased Renal Excretion

  1. Hypoaldosteronism
    1. Hyporeninemic hypoaldosteronism
      1. Intrinsic renal disease (provoked by Dehydration)
        1. Type IV Renal Tubular Acidosis
        2. Diabetes Mellitus (esp. Diabetic Nephropathy)
        3. Interstitial Nephritis
      2. Prostaglandin synthetase inhibitors
    2. Primary Hypoaldosteronism
    3. Medication-induced hypoaldosteronism
      1. See medications below
    4. Adrenal Insufficiency (volume low, decreased GFR)
  2. Decreased distal renal flow
    1. Hypovolemia
    2. Renal Insufficiency or Renal Failure
      1. Acute Kidney Injury
      2. Chronic Kidney Disease
    3. Congestive Heart Failure
    4. Congestive Heart Failure
      1. Decreased distal nephron Sodium delivery
  3. Primary tubular defects
    1. Renal Tubular Acidosis (Type 4)
    2. Obstructive uropathy
    3. Tubular unresponsiveness to Aldosterone
      1. Systemic Lupus Erythematosus
      2. Multiple Myeloma
      3. Sickle Cell Anemia
  4. Medications
    1. See BRASH Syndrome
    2. Medication-induced hypoaldosteronism
      1. Heparin
      2. Cyclosporine
      3. ACE Inhibitor or Angiotensin Receptor Blocker
        1. Responsible for 50% of medication induced Hyperkalemia
        2. Concurrent trimethoprim-sulfamethoxazole increases risk (especially age>66)
        3. Risk of Hyperkalemia within the first year of starting ACE/ARB: 10%
        4. Raebel (2012) Cardiovasc Ther 30(3): e156-66 +PMID:21883995 [PubMed]
      4. Aldosterone Antagonists
        1. Potassium sparing Diuretics (e.g. Spironolactone)
    3. Other medications
      1. NSAIDS
      2. Lithium
      3. Trimethoprim
      4. Calcineuron inhibitors (e.g. Tacrolimus)
      5. Heparin
      6. Beta Blockers

III. Causes: Transcellular Shift or Redistribution (ICF to ECF)

  1. Metabolic Acidosis (more likely with mineral acids NH4, HCl)
  2. Hyperkalemic periodic paralysis
  3. Insulin deficiency or resistance (Diabetes Mellitus)
  4. Rapid ECF rise
    1. Hypertonic Glucose or Mannitol infused
  5. Hemodialysis
  6. Coronary bypass
  7. Cell lysis
    1. Any significant cause of cell turnover releases significant Potassium
      1. 98% of body Potassium is intracellular
    2. Rhabdomyolysis
    3. Tissue necrosis, severe Burn Injury or crush injury
    4. Tumor Lysis Syndrome (e.g. severe Hemolytic Anemia)
    5. Massive Hemolysis
    6. Surgery
    7. Gastrointestinal Bleeding
    8. Red Blood Cell Transfusion
  8. Hypertonicity
    1. Hyperglycemia
    2. Mannitol
  9. Medications
    1. Succinylcholine (if concurrent tissue damage)
    2. Beta Blockers
    3. Digitalis Intoxication (Digoxin Toxicity)
    4. Arginine
    5. Somatostatin

IV. Causes: Potassium Load

  1. Oral or IV Potassium Supplementation
    1. High Dietary Potassium intake rarely causes Hyperkalemia in patients with normal Renal Function
    2. See Foods with High Potassium Content
    3. Salt substitute
    4. Protein calorie supplements
    5. Total Parenteral Nutrition
    6. Enteral feeding with high Potassium load
  2. Blood Transfusion (pRBC transfusion)
  3. High dose Penicillin G (1.7 meq K+ per 1 Million Units)

V. Causes: Pseudohyperkalemia (actual Serum Potassium less than lab reported value)

  1. Blood sample clotted or cooled
  2. Delayed analysis or other lab error
  3. Familial Pseudohyperkalemia
  4. Hemolysis
    1. Excessive Tourniquet or fist clenched repeatedly
    2. Hemolysis via small needle or Traumatic venipuncture
  5. Severe blood cell hyperplasia
    1. Severe Thrombocytosis (>500,000/mm3)
    2. Severe Leukocytosis (>75,000/mm3)

VI. References

  1. Gibbs in Marx (2002) Rosen's Emerg Med, p. 1730-1
  2. Klahr (2001) in Noble (2001) Primary Care p. 1359-62
  3. Kim (2023) Am Fam Physician 107(1): 59-70 [PubMed]
  4. Viera (2015) Am Fam Physician 92(6): 487-95 [PubMed]

Images: Related links to external sites (from Bing)

Related Studies