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Potassium (K+) is the chief cation found within the intracellular fluid of all cells. The total body content of K+ is around 3,500 mmol, of which 98% is contained in the intracellular fluid (ICF) and only 2% is found in the extracellular fluid (ECF). Potassium cations are involved in the energetic metabolism of cells as they are needed for the synthesis and breakdown of adenosine triphosphate (ATP). Increasing intracellular concentration of K+ is typical for anabolic states, while decreasing intracellular concentration of K+ is consistent with catabolic states. K+ is bound to proteins and glycogen within cells and therefore is released during their breakdown.

Serum concentration of K+ (S-K+), also called kalemia is closely associated with pH levels of both ICF and ECF. Acidemia is consistent with hyperkalemia (increasing S-K+), while alkalemia results in hypokalemia (decreasing S-K+). For every change of pH by 0.1 points, kalemia decreases by approximately 0.6 mmol/L. [1]

Reference values:

  • plasma: 3.8–5.4 mmol/l
  • urine: 45–90 mmol/day
  • daily intake and expenditure 50–100 mmol (2–4 g).[2]

Regulation[edit | edit source]

  • Normal serum potassium values must be strictly maintained between 3.8–5.4 mmol/L, pathological hypokalemia and hyperkalemia can lead to cardiac arrhythmias (changes in S-K+ influence the resting membrane potential and excitability of cardiomyocytes)
  • S-K+ is maintained by excretion and reabsorption of K+ in distal tubules and collecting ducts of the nephron in the kidney
  • S-K+ is influenced by:
    • intake of K+ in food;
    • sodium (Na+) levels and renal tubular flow;
    • acid-base balance (ABB);
    • mineralocorticoid (aldosterone) activity;
    • sensitivity of cells of the distal tubules to mineralocorticoids;
    • type and interchangeability of anions.
  • It is hypothesised that a rapid increase in concentration of K+ in the ECF may lead to increased glucagon secretion → hyperglycemia → increased insulin secretion → increased uptake of glucose into muscle and adipose cells → glucose-K+ cotransport into cells → normalisation of kalemia (in the ECF)[1]
  • The concentration gradient between ECF and ICT (cca 110–140 mmol/l) is maintained by a Na+/K+-ATPase pump in the cellular membrane

Hypokalemia[edit | edit source]

  • Causes:
  1. Losses in the GIT:
    • acute and chronic diarrhoea;
    • laxative overuse;
    • vomiting;
    • fistulas.
  2. Renal losses:
    • diuretic therapy;
    • polyuric phase of acute kidney injury (AKI) – also acute renal failure (ARF);
    • renal tubular acidosis;
    • hyperaldosteronism;
    • Cushing syndrome and/or exogenous glucocorticoid use.
  3. Alkalosis
  4. Infusion of IV fluid (without K+)
  5. Diet low in potassium
  • Signs & symptoms – weakness, ileus, renal disease, arrhythmias, EKG – flattening and inversion of T waves, visible U wave, QT interval prolongation
  • Therapeutic substitution (calculation)K [mmol] = ECF x (4.4 – measured K) x 3 + K substitute for losses
    • Therapeutic substitution of potassium is contraindicated in oliguria or anuria. [2]

Hyperkalemia[edit | edit source]

  • Causes:
  1. Decreased excretion (renal cause):
  2. Movement of K+ from ICF to ECF:
    • acidosis (acute);
    • increased catabolic processes in cells or necrosis.
  3. Increased intake
  4. Low levels of mineralocorticoids[1]
  • Signs & symptoms: bradycardia, malignant arrhythmias (ventricular tachycardia and fibrillation), changes in EKG – peaked T waves, PQ interval prolongation, wide QRS, ST wave depression.
  • The role of insulin in regulation of kalemia:
    • insulin activates H+/Na+ antiport → increased intracellular concentration of Na+ → increased activity of Na+/K+ATPase → Na+ is pumped out of the cell and K+ is pumped into the cell → extracellular concentration of K+ decreases

Pseudohyperkalemia[edit | edit source]

  • Increased S-K+ in significant thrombocytosis (K+ cations are released from the thrombocytes that break down during the blood clot formation in the test tube)[1];
  • Hemolysis (in vitro); disintegration of erythrocytes during a blood test – occurs due to improper specimen sample handling.

References[edit | edit source]

Related articles[edit | edit source]

External links[edit | edit source]

References[edit | edit source]

  1. a b c d MASOPUST, Jaroslav – PRŮŠA, Richard. Patobiochemie metabolických drah. 2. edition. Univerzita Karlova, 2004. 208 pp. pp. 174–175. 
  2. a b SCHNEIDERKA, Petr. Kapitoly z klinické biochemie. 2. edition. Karolinum, 2004. ISBN 80-246-0678-X.

Bibliography[edit | edit source]

  • MASOPUST, Jaroslav – PRŮŠA, Richard. Patobiochemie metabolických drah. 2. edition. Univerzita Karlova, 2004. 208 pp. pp. 174–175. 

  • SCHNEIDERKA, Petr. Kapitoly z klinické biochemie. 2. edition. Karolinum, 2004. ISBN 80-246-0678-X.