CKD acidosis, potassium and fluid management

01Purpose and principlesWhat the treatment does and how it fits into care.

Acid, potassium and sodium-water handling fail together as CKD advances. Acidosis promotes muscle loss, bone buffering and hyperkalaemia; constipation and insulin deficiency further impair potassium disposal; sodium retention increases blood pressure and pulmonary congestion. A treatment aimed at one axis can affect the others: bicarbonate adds sodium, a loop diuretic removes potassium and water, and a sodium-containing binder may worsen oedema.

Acute hyperkalaemia is a resuscitation problem. A normal ECG does not prove safety, and treatment has three distinct aims: stabilise cardiac membrane, move potassium temporarily into cells, and remove potassium from the body. Dialysis is the most reliable removal method in anuric or refractory kidney failure, so renal contact must occur early rather than after repeated shifting therapies wear off.

Chronic management should preserve cardiorenal benefit where possible. Before permanently stopping RAS blockade, identify NSAIDs, salt substitutes, constipation, acidosis, poor glycaemic control, excess supplements and inappropriate dose combinations. A renal dietitian can target highly concentrated potassium sources without dismantling an otherwise cardioprotective, fibre-rich diet.

Key points

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.

02Indications, selection and cautionsWho may benefit, who needs urgent treatment and important alternatives.

Chronic metabolic acidosis

Persistently low bicarbonate with compensatory low carbon dioxide and no acute high-gap process may accompany G4–G5 CKD and contribute to fatigue and muscle wasting.

Hyperkalaemia risk cluster

Advanced CKD, diabetes, RAS blockade, mineralocorticoid antagonists, trimethoprim, NSAIDs, constipation and potassium salt substitutes create additive risk.

Electrical toxicity

Peaked T waves, PR prolongation, P-wave loss, QRS widening, bradyarrhythmia or sine-wave change indicates dangerous myocardial potassium effect, but ECG can remain deceptively normal.

Fluid excess

Rising weight, oedema, elevated JVP, hypertension, crackles, orthopnoea or reduced oxygenation reflects sodium-water excess rather than a creatinine number alone.

Intravascular depletion

Postural symptoms, low pressure, dry mucosa, cramps and a rising creatinine can coexist with peripheral oedema when cardiac failure or low albumin reduces effective circulation.

Uraemic indication

Refractory acidosis, potassium or overload alongside pericarditis, encephalopathy, bleeding or severe symptoms strengthens the need for urgent kidney-replacement assessment.

Red flags requiring action

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.

03Assessment before treatmentTests and checks that guide safe selection.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Repeat plasma potassiumFirst step
Why
Confirm an unexpected result and track response while excluding collection-related pseudohyperkalaemia.
Interpretation and limitations
Review haemolysis, thrombocytosis, leucocytosis and sampling technique, but do not delay treatment when the value, ECG or clinical state is immediately dangerous.
02
Twelve-lead ECG and cardiac monitoring
Why
Detect electrical toxicity and guide immediate IV calcium treatment.
Interpretation and limitations
Any compatible conduction or repolarisation change increases urgency; a normal tracing cannot exclude malignant arrhythmia at a high potassium concentration.
03
Venous or arterial blood gas
Why
Quantify pH and bicarbonate and identify respiratory compensation, lactate or another acute process.
Interpretation and limitations
Calculate the anion gap with laboratory electrolytes and investigate ketoacidosis, lactic acidosis, toxins or diarrhoea rather than attributing every acidosis to CKD.
04
Capillary glucose and blood ketones
Why
Identify insulin deficiency and prevent or detect hypoglycaemia during potassium-shifting treatment.
Interpretation and limitations
Ketoacidosis can drive extracellular potassium despite total-body depletion; follow the UKKA six-hour glucose schedule after insulin–glucose and extend when clinically needed.
05
Fluid balance and serial weight
Why
Estimate sodium-water accumulation and response to diuresis or ultrafiltration.
Interpretation and limitations
Compare with an established euvolaemic or post-dialysis target; oedema alone does not measure intravascular volume and intake-output charts are prone to error.
06
Chest radiograph and bedside lung assessment
Why
Support diagnosis of pulmonary congestion and identify infection or pleural disease causing breathlessness.
Interpretation and limitations
B-lines or radiographic oedema support excess lung water but must be integrated with cardiac function, albumin, weight and response to treatment.
07
Medicine diet and bowel review
Why
Find reversible drivers of potassium, acidosis and fluid accumulation.
Interpretation and limitations
Include over-the-counter NSAIDs, effervescent sodium, potassium salt substitutes, supplements, constipation, adherence and processed-food sodium; target advice to the actual exposure.

04Treatment approachPreparation, options, escalation and aftercare.

01HYPERKAcute severe hyperkalaemiaFirst stepPotassium is severely raised or compatible ECG change, weakness or instability is present.

1Use 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.
2Give the UKKA calcium salt and setting-specific dose to stabilise myocardium when indicated, repeating ECG assessment because calcium does not reduce potassium.
3Give insulin–glucose plus adjunctive nebulised salbutamol where appropriate and implement the full baseline-dependent glucose support and six-hour surveillance protocol.
4Remove potassium with sodium zirconium cyclosilicate or another indicated route and urgent dialysis when anuric, refractory or clinically required; remeasure for rebound.

02CHRONIC-KRecurrent non-emergency hyperkalaemiaPotassium repeatedly limits useful RAS or mineralocorticoid treatment without acute electrical toxicity.

1Confirm persistence and review kidney trajectory, diabetes, acidosis, constipation, salt substitutes, NSAIDs, trimethoprim and combined potassium-raising medicines.
2Ask a renal dietitian for targeted modification that preserves fibre, energy and cardiovascular quality instead of banning all fruit and vegetables.
3Consider a loop or thiazide-type diuretic when volume and residual function support it, oral bicarbonate for qualifying acidosis, and a licensed binder under current NICE criteria.
4Reintroduce or optimise cardiorenal therapy only with an explicit potassium schedule and clear thresholds for urgent contact.

03ACIDOSISPersistent low bicarbonateA person with advanced CKD has confirmed bicarbonate below the reference range.

1Confirm the result and identify anion-gap disease, diarrhoea, drugs, ketoacidosis, lactic acidosis and respiratory disorder before assigning chronic renal acidosis.
2For adults with G4–G5 CKD and bicarbonate below 20 mmol/L, consider oral sodium bicarbonate under NICE after assessing blood pressure, oedema and tablet burden.
3Titrate to the renal service's safe target and monitor sodium, potassium, bicarbonate, weight and gastrointestinal tolerance.
4EscalationEscalate severe symptomatic acidaemia, refractory decline or concurrent uraemic indications for urgent kidney-replacement assessment.

04OVERLOADOedema and breathlessnessWeight gain, congestion or hypertension suggests sodium-water retention in CKD.

1Assess respiratory severity, oxygenation, heart failure, infection, albumin, urine output, salt intake and adherence; treat pulmonary oedema as an emergency.
2Agree a realistic target weight and sodium strategy and use an appropriately bioavailable loop-diuretic regimen when residual diuresis remains.
3Review response through urine output, weight, symptoms, blood pressure and renal function; avoid repeated blind dose increases in anuria.
4Arrange dialysis or ultrafiltration when fluid remains life-threatening or functionally disabling despite safe medical treatment.

05Regimens, contraindications and interactionsTreatment details and the circumstances that modify them.

Stabilise the myocardial membrane during severe hyperkalaemia with ECG toxicity while potassium-shifting and removal treatment is organised.

IV calcium for hyperkalaemic ECG toxicity

Use 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.

It does not lower potassium; monitor ECG, reassess effect and avoid extravasation, especially with calcium chloride. Seek toxicology advice when digoxin toxicity is suspected.

Temporarily shift extracellular potassium into cells during acute moderate or severe hyperkalaemia.

Soluble insulin with IV glucose

Follow the current UKKA hospital algorithm using 10 units soluble insulin with 25 g glucose and the additional glucose-infusion branch for lower pretreatment glucose.

Hypoglycaemia is common and delayed in kidney failure; monitor bedside glucose for at least the UKKA six-hour schedule, maintain IV access and do not mistake redistribution for potassium removal.

Activate beta-2-mediated intracellular potassium shift while definitive elimination is arranged.

Nebulised salbutamol

Use the UKKA high-dose nebulised adult regimen as an adjunct to insulin–glucose in acute severe hyperkalaemia, with cardiac monitoring.

Never use it alone for severe hyperkalaemia; response is variable and tremor, tachycardia, myocardial ischaemia and arrhythmia can occur.

Correct chronic metabolic acidosis, which may improve potassium control, muscle metabolism and kidney trajectory in selected adults.

Oral sodium bicarbonate

For qualifying G4–G5 CKD acidosis, start and titrate the local oral regimen to bicarbonate response while tracking sodium-related adverse effects.

Sodium can worsen hypertension, oedema and heart failure; tablet burden and gastric symptoms reduce adherence, and it is not routine resuscitation treatment for every acute acidosis.

Increase sodium, water and potassium excretion when functioning nephrons remain and treat CKD-associated congestion.

Loop diuretic

Use a renal-adjusted furosemide or equivalent regimen selected from residual urine output, gut absorption and congestion, escalating only with monitored response.

Hypovolaemia, hypotension, ototoxicity at high rapid IV exposure, hyponatraemia and worsening renal function require review; anuria will not respond meaningfully.

Remove potassium through gastrointestinal binding in adult hyperkalaemia and help maintain indicated RAS treatment in selected patients.

Sodium zirconium cyclosilicate

Use the SmPC oral correction regimen and subsequent potassium-guided maintenance dose when selected by the acute or chronic renal pathway.

It does not replace cardiac stabilisation or intracellular shift; monitor oedema and sodium burden, hypokalaemia and time separation from pH-dependent medicines including tacrolimus.

Provide chronic gastrointestinal potassium removal when recurrent hyperkalaemia limits beneficial cardiorenal therapy.

Patiromer

The adult SmPC starts 8.4 g once daily with weekly-or-longer titration, separated by at least 3 hours from specified oral medicines.

Delayed onset means it is not emergency treatment; monitor potassium, magnesium, calcium, constipation and medicine-binding interactions and do not stop without a recurrence plan.

06Complications, monitoring and follow-upAdverse effects, response and longer-term review.

During acute hyperkalaemia, repeat potassium after shifting and removal therapy at the local algorithm intervals and continue long enough to detect rebound as temporary intracellular effects fade.
Follow ECG continuously when severe hyperkalaemia or conduction change is present and reassess after IV calcium; biochemical improvement does not immediately prove electrical stability.
Measure bedside glucose for at least six hours after insulin–glucose under UKKA guidance, adding the recommended infusion for lower pretreatment glucose and extending surveillance if risk persists.
For chronic bicarbonate, record bicarbonate, potassium, sodium, blood pressure, weight and oedema after initiation and titration; stop chasing a number if sodium harm develops.
Track daily weights, symptoms, urine output, postural pressure and renal function during diuretic change, using a documented target weight rather than oedema alone.
With a chronic potassium binder, monitor potassium after dose or RAS changes and magnesium with patiromer or oedema with sodium zirconium cyclosilicate.
Reassess dietary adequacy, constipation and medicine reconciliation regularly so potassium control does not come at the cost of malnutrition or loss of essential cardiac therapy.

07Special situationsVariants, exceptions and circumstances that change the usual approach.

Calcium buys electrical time

The ECG may improve within minutes while serum potassium is unchanged, so stopping after calcium leaves the underlying threat intact.

Redistribution can rebound

Insulin and beta agonist move potassium into cells temporarily; without removal, the concentration can rise again after monitoring ends.

Normal ECG is not immunity

Severe hyperkalaemia can exist without classic peaked T waves, so urgency integrates concentration, trajectory and clinical state.

Acidosis links muscle and potassium

Chronic acid retention promotes catabolism and extracellular potassium, making bicarbonate a potentially multi-domain treatment when sodium tolerance permits.

Oedema can hide depletion

Heart failure or hypoalbuminaemia may produce swollen tissues but poor effective arterial volume, making uncritical diuresis hazardous.

Diet is more than bananas

Salt substitutes, processed food, supplements and constipation can matter more than a single fruit, and plant fibre supports bowel potassium excretion.

08Common pitfallsFrequent interpretation and management errors.

01
Do not delay treatment of severe or ECG-toxic hyperkalaemia while waiting for a repeat sample to exclude haemolysis.
02
Do not assume IV calcium lowers potassium or discharge after the ECG improves without elimination and rebound monitoring.
03
Do not omit scheduled glucose checks after insulin–glucose in kidney failure, where hypoglycaemia may be prolonged.
04
Do not use nebulised salbutamol alone for severe hyperkalaemia or patiromer as immediate rescue.
05
Do not give oral bicarbonate for every low value without confirming the acid-base disorder and assessing sodium-sensitive congestion.
06
Do not prescribe broad potassium restriction before correcting constipation, acidosis, hyperglycaemia, salt substitutes and culprit medicines.
07
Do not keep escalating a loop diuretic in an anuric patient with pulmonary oedema when dialysis is the definitive fluid-removal route.