This is the most common cause of hyperkalaemia and may not always be obvious in the case of potassium EDTA, as sometimes the mistake may be realised upon collection and the sample transferred to another collection tube before arrival in the laboratory. In cases where the patient has no history of other disease and no clinical symptoms, a repeated measurement on a new sample may be advisable to rule out artefact.
As the potassium is mainly intracellular, anything which causes the movement of potassium out, or prevents entry in, to cells will cause hyperkalaemia. Factors that cause the movement of potassium out of cells are hypertonicity, acidosis, severe cell damage and cell death. Cell damage and death will release potassium out of the cell due to cell lysis. In hypertonic states, the decreased ICF volume causes increased cell potassium concentration, causing potassium to move out of the cell into the ECF. In all cases of acidosis, the hydrogen ion concentration in the blood increases. The buffering of hydrogen ions that takes place leads to a displacement of potassium ions from the ICF to the ECF. In both acidosis and diabetes, the increased potassium loss in the urine due to osmotic diuresis may lead to reduced total body potassium although the plasma potassium levels are increased. Cell damage may also prevent the uptake of potassium as will a lack of insulin. A membrane bound, ATPase dependent sodium pump actively excludes sodium from cells causing passive movement of potassium into the cell. Any cell membrane damage or impaired activity of the sodium pump will decrease the potassium uptake into cells. Insulin stimulates the cellular uptake of potassium; therefore a lack of insulin, which may occur in untreated diabetes mellitus, will prevent potassium from entering the cells. Another cause of serum potassium above normal levels may be due to digoxin poisoning, as any doses above the upper therapeutic dose also prevents potassium entering cells.
