Chapter 13 Hyperkalaemia

13.1 Causes of hyperkalaemia

  1. spurious
  2. distribution (ECF/ICF shifts)
  3. impaired renal K+ excretion

Renal excretion of K+ may be impaired if any of the following are limited (Hunter & Bailey, 2019):

  • GFR
  • tubular flow rate
  • delivery of Na+ to the distal nephron
  • aldosterone signalling in the distal nephron

Hyperkalaemia is often due to an inappropriate shift from electrogenic to electroneutral Na+ reabsorption:

Therefore the causes of hyperkalaemia are:

EXCESSIVE K LOAD diet high-K diet
drugs IV penicillin
TRANSCELLULAR SHIFTS cell injury rhabdomyolysis
beta-blockers
digoxin
anaesthetic agents
mannitol
RENAL IMPAIRMENT renal impairment AKI / CKD
DEFECTIVE ALDOSTERONE SIGNALLING impaired renin secretion DM
beta-blockers
NSAIDS
ACEi
ARBs
Addison’s
heparins
ketoconazole
PHAI
spironolactone / eplerenone
DEFECTIVE ELECTROGENIC NA TRANSPORT ENaC blockade PHAI
amiloride / triamterine
trimethoprim
pentamidine
lithium
PHAII
CNIs

Use FECl response to thiazides as functional test for PHAII (normal response is < 3% increment).

13.2 Causes of spurious hyper- and hypokalaemia

PseudohyperK from K-EDTA contamination.

PseudohyperK due to prolonged delay prior to centrifugation (blood cells leak K in cold weather).

PseudohypoK due to prolonged delay prior to centrifugation (blood cells take up K via Na-K-ATPase in the warm; “seasonal pseudohypoK” in summer).

PseudohyperK due to leucocytosis (WBC > 70) – K released from cells during clot formation (test by measuring serum and plasma K simultaneously).

Familial hyperK due to abnormalities in RBC membrane permeability.