A- Increased Potassium Intake
- Dietary excess (Banana, citrus fruits...)
- Intravenous load with K+ containing fluids
- Drugs containing K+ e.g. potassium penicillin
- Salt substitutes containing KCL rather than NaCL
B- Shift of Intracellular K+ to extracellular Compartment
- Acidosis
- Cell damage (cancer chemotherapy, crush injury, incompatible
blood transfusion). - Muscle disease
- Convulsions, myositis, periodic paralysis, suxamethonium
anaesthesia.
C- Decreased excretion of K+ by the kidneys- Renal failure • mineralocorticoid deficiency
- drug interference as ACEI, cyclosporine, NSAIDS, Tacrolimus
and K+ sparing diuretics.
D- Factitious:
Haemolysis of blood sample, severe leucocytosis or
thrombocytosis.As a result of the strong defence mechanisms against
hyperkalaemia, usually more than one factor is present for hyperkalaemia
to occur. In practice, usually there is impaired renal excretion combined
with other factor as drug intake e.g. ACEI.
Normal K+ homeostasis involves about 100 mmol/day oral intake
and about 10 mmol/d faecal output and about 90 mmol/day being excreted
by the kidney. Hyperkalaemia usually occurs only when renal failure is