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.
- ECG changes or severe hyperkalaemia require continuous monitoring and immediate membrane stabilisation with IV calcium, intracellular shift with insulin–glucose and potassium removal through the UKKA pathway.
- IV calcium protects the myocardium but does not lower serum potassium; repeat ECG and calcium assessment are required while definitive removal proceeds.
- Insulin–glucose can cause delayed severe hypoglycaemia, especially in kidney failure; follow the UKKA baseline-dependent glucose infusion and six-hour glucose-monitoring protocol.
- Nebulised salbutamol is an adjunct rather than sole treatment for severe hyperkalaemia, and sodium bicarbonate is not routinely used acutely unless the selected acid-base context supports it.
- Sodium zirconium cyclosilicate can contribute to acute potassium removal and chronic control; patiromer has delayed onset and must not replace emergency treatment.
- Treat oedema by establishing the cause and target weight, moderating sodium, using adequate loop-diuretic exposure when residual urine remains and arranging dialysis for refractory pulmonary congestion.
- Fluid restriction should be individualised to thirst, sodium, urine output and overload; over-restriction can cause hypotension, cramps, AKI and poor nutrition, while indiscriminate liberal intake worsens hypertension and breathlessness.
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.
Pulmonary oedema with hypoxaemia, exhaustion or poor response to diuretic requires emergency respiratory support and urgent dialysis consideration.
Severe acidaemia with shock, altered consciousness, respiratory fatigue or a high anion gap needs resuscitation and cause treatment rather than routine oral bicarbonate.
Anuria, rapidly rising creatinine or suspected obstruction changes chronic management into an acute kidney injury or urological emergency pathway.
Hypoglycaemia after insulin–glucose treatment can be delayed and neurological; scheduled bedside glucose monitoring must continue even after potassium improves.
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.
- Give insulin–glucose plus adjunctive nebulised salbutamol where appropriate and implement the full baseline-dependent glucose support and six-hour surveillance protocol.
- Remove potassium with sodium zirconium cyclosilicate or another indicated route and urgent dialysis when anuric, refractory or clinically required; remeasure for rebound.