Synopsis
Manage the interacting acid-base, potassium and volume consequences of advanced CKD while recognising emergencies and preserving beneficial therapy where safely possible.
- Declining ammonium and acid excretion causes a usually normal-anion-gap metabolic acidosis before advanced uraemia adds retained unmeasured acids; always look for diarrhoea, ketoacidosis, lactic acidosis and drugs as superimposed causes.
- NICE advises considering oral sodium bicarbonate in adults with G4 or G5 CKD and serum bicarbonate below 20 mmol/L, balancing correction against sodium load, blood pressure and oedema.
- Hyperkalaemia reflects reduced excretion plus medicines, acidosis, insulin deficiency, tissue breakdown, constipation and dietary sources; haemolysed samples require confirmation unless clinical or ECG danger makes treatment urgent.
Key red flags
Severe hyperkalaemia, any potassium-associated ECG change, weakness progressing to paralysis or a peri-arrest rhythm requires immediate monitored treatment and senior renal or critical-care help.
Investigation priorities
Confirm an unexpected result and track response while excluding collection-related pseudohyperkalaemia.
Management branches
Potassium is severely raised or compatible ECG change, weakness or instability is present.
- Use ABCDE, call senior help, place continuous monitoring and IV access, repeat a non-haemolysed sample if this does not delay treatment and contact renal services early.
- Give the UKKA calcium salt and setting-specific dose to stabilise myocardium when indicated, repeating ECG assessment because calcium does not reduce potassium.
Key medicines
IV calcium for hyperkalaemic ECG toxicityUse UKKA's setting-specific regimen: 10 mL 10% calcium chloride over 5 minutes in resuscitation, or 30 mL 10% calcium gluconate over 10 minutes otherwise.
Soluble insulin with IV glucoseFollow the current UKKA hospital algorithm using 10 units soluble insulin with 25 g glucose and the additional glucose-infusion branch for lower pretreatment glucose.