Potassium

Marker Name: Potassium

REFERENCE RANGES FOR SERUM POTASSIUM:

Laboratory reference range: 3.5–5.2 nmol/L

Functional reference range: 4.0–4.5 nmol/L

DESCRIPTION:

Potassium (K) is an electrolyte that contributes to the resting membrane potential across all cell membranes, which is needed for nerve, muscle, and heart function.¹ Potassium is important for blood pressure control, gastrointestinal motility, acid-base homeostasis, glucose metabolism, renal function, and fluid and electrolyte balance.^2-4 Potassium homeostasis involves the intestines and kidneys and is regulated by aldosterone, which acts by enhancing urinary potassium secretion. Approximately 98 percent of potassium ions are inside cells; this chemical gradient is maintained by energy-intensive Na+/K+-ATPase pumps, insulin receptors, and beta-2-adrenergic receptors. Serum potassium concentration is a common test for evaluating potassium status.^5,6

High serum potassium concentration (hyperkalemia) is uncommon in patients with normal urinary potassium excretion due to a process called potassium adaptation: as potassium intake increases, the extent and efficiency of urinary excretion also increase. Reduced urinary potassium excretion can, however, be caused by several health conditions and drugs listed below. Increased potassium release from cells can also cause high serum potassium; in these cases, hyperkalemia typically only persists when renal insufficiency is also present. Often, high potassium indicates pseudohyperkalemia rather than true hyperkalemia, as repeated fist clenching or trauma during blood draw can cause increased potassium release from cells near the draw site.¹

Low serum potassium concentration (hypokalemia) is common. It can be caused by inadequate dietary intake, certain drugs, dialysis, plasmapheresis, increased potassium entry into the cells, decreased potassium exit from cells, and increased losses in the urine, gastrointestinal tract, or sweat. A specific list of conditions and drugs that cause these states is below.⁷

PATHOLOGICAL/CONVENTIONAL RANGE INDICATIONS:

High in:¹

• Reduced urinary potassium excretion
  • Acute and chronic kidney disease
  • Hypoaldosteronism
  • Voltage-dependent renal tubular acidosis, seen in:
    • Urinary tract obstruction
    • Lupus nephritis
    • Sickle cell disease
    • Renal amyloidosis
  • Effective arterial blood volume depletion
    • True blood volume depletion
    • Heart failure
    • Cirrhosis
  • Rare causes
    • Familial pseudohypoaldosteronism type 1
    • Familial pseudohypoaldosteronism type 2 (Gordon’s syndrome)
    • Ureterojejunostomy
  • Increased potassium release from cells, especially with concurrent renal insufficiency
    • Pseudohyperkalemia: potassium elevation in sample because of blood draw complication
      • Mechanical trauma
      • Repeated fist clenching
      • In patients with thrombocytosis
      • In patients with chronic lymphocytic leukemia
      • In patients with familial hyperkalemia
    • Fasting
    • Metabolic acidosis
    • Hyperglycemia
    • Insulin deficiency, especially in uncontrolled diabetes mellitus
    • Increased tissue catabolism, seen in:
      • Tumor lysis syndrome
      • Rhabdomyolysis
      • Trauma
      • Severe accidental hypothermia
    • Rare causes
      • Familial hyperkalemic periodic paralysis
      • Overdose of certain plants (digitalis, related digitalis glycosides)
      • Red cell transfusion, especially in infants with massive transfusions
      • Administration of succinylcholine, in patients with neuromuscular disease, burns, severe trauma, prolonged immobilization, or chronic infection
      • Administration of arginine hydrochloride
    • Drugs
      • Nonsteroidal anti-inflammatory drugs (aspirin, ibuprofen, naproxen)
      • Potassium-sparing diuretics (spironolactone, eplerenone, amiloride, triamterene)
      • Somatostatin or somatostatin agonist (octreotide)
      • Beta blockers, especially non-selective beta blockers (e.g., propranolol, labetalol)
      • Angiotensin-converting enzyme (ACE) inhibitors
      • Angiotensin II receptor blockers (ARBs)
      • Aminocaproic acid
      • Heparin
      • Activators of ATP-dependent potassium channels
        • Calcineurin inhibitors (e.g., cyclosporine, tacrolimus)
        • Diazoxide
        • Minoxidil
        • Some volatile anesthetics (e.g., isoflurane)

Low in:⁷

• Inadequate dietary intake
• Low-calorie diet
• Increased sweat losses
• Dialysis
• Plasmapheresis
• Increased potassium entry into cells
  • Elevated beta-adrenergic activity (e.g., from high stress)
  • Metabolic or respiratory alkalosis
  • Acute increase in blood cell production
  • Hypothermia
  • Hypokalemic periodic paralysis
• Decreased potassium exit from cells
  • Barium intoxication
  • Cesium intoxication
• Increased gastrointestinal potassium loss
  • Vomiting
  • Chronic diarrhea
  • Laxative abuse
  • Clay ingestion
  • Ogilvie’s syndrome
• Increased urinary potassium loss
  • Primary mineralocorticoid excess (e.g., primary aldosteronism)
  • Hypomagnesemia
  • Renal tubular acidosis
  • Polyuria
  • Liddle’s syndrome
  • Salt-wasting nephropathies
    • Bartter’s syndrome
    • Gitelman’s syndrome
    • Tubulointerstitial diseases (as seen in Sjögren’s syndrome)
    • Hypercalcemia
    • Tubular injury (as seen in leukemia)
  • Drugs
    • Diuretics (especially carbonic anhydrase inhibitors, loop diuretics, thiazide-type diuretics)
    • Amphotericin B
    • Cisplatin
    • Chloroquine
    • Certain antipsychotics (risperidone, quetiapine)
    • Theophylline
    • High-dose penicillin
    • Beta-adrenergic agonists
      • Albuterol
      • Terbutaline
      • Dobutamine
    • Sympathomimetics
      • Pseudoephedrine
      • Ephedrine
    • Heroin

FUNCTIONAL RANGE INDICATIONS:

High in:

• Functional dysglycemia
• HPA axis dysfunction
• Impaired kidney function
• Pseudohypoaldosteronism

Low in:

• Functional dysglycemia
• HPA axis dysfunction
• Malabsorption and malnutrition
• Alcoholism
• Medications such as antibiotics or diuretics
• Many other disease states

References:

1. http://www.uptodate.com/contents/causes-and-evaluation-of-hyperkalemia-in-adults
2. ID, Linus S, Wingo CS. Disorders of potassium metabolism. In: Freehally J, Johnson RJ, Floege J, eds. Comprehensive clinical nephrology. 5th ed.St. Louis: Saunders, 2014:118-118
3. Malnic G, Giebisch G, Muto S, Wang W, Bailey MA, Satlin LM. Regulation of K+ excretion. In: Alpern RJ, Caplan MJ, Moe OW, eds. Seldin and Giebisch’s the kidney: physiology and pathophysiology. 5th ed. London: Academic Press, 2013:1659-1716
4. Mount DB, Zandi-Nejad K. Disorders of potassium balance. In: Taal MW, Chertow GM, Marsden PA, Skorecki KL, Yu ASL, Brenner BM, eds. The kidney. 9th ed. Philadelphia: Elsevier, 2012:640-688
5. http://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults
6. http://www.uptodate.com/contents/clinical-manifestations-and-treatment-of-hypokalemia-in-adults
7. http://www.uptodate.com/contents/causes-of-hypokalemia-in-adults