AKI Algorithm · Reasoning GP

1

Safety

Red Flags — Identify life-threatening AKI immediately

Done

Screen for these before anything else. AKI can be rapidly fatal — hyperkalaemia and pulmonary oedema kill within hours.

Hyperkalaemia ≥6.5 mmol/L ECG changes (peaked T, wide QRS, sine wave), weakness, palpitations → 999 cardiac arrest risk

Oliguria / Anuria Urine output <0.5 ml/kg/hr for 6+ hours or complete anuria → 999 severe AKI

Pulmonary oedema Breathlessness at rest, crackles, O₂ sats falling, pink frothy sputum → 999 fluid overload

Uraemic encephalopathy Confusion, drowsiness, asterixis (flapping tremor), pericardial rub → 999 dialysis urgency

Sepsis + AKI HR >90, RR >20, temp >38 or <36, BP <90 systolic + rising creatinine → 999 septic AKI

Haemodynamic collapse SBP <90 mmHg, cold peripheries, reduced GCS → 999 shock state

Rhabdomyolysis Dark cola-coloured urine, severe myalgia, CK markedly elevated → 999 myoglobin nephrotoxicity

Obstructive uropathy Bilateral flank pain, bladder distension, unable to pass urine despite urge → Same-day urology

Rapidly rising creatinine Creatinine doubled within 24–48 h or rise >354 µmol/L → Same-day medical

NSAID/nephrotoxin exposure + AKI Recent high-dose NSAID, contrast, aminoglycoside + rising creatinine, unwell → Same-day

AKI kills via three mechanisms: (1) Hyperkalaemia causes fatal arrhythmias — K⁺ ≥6.5 mmol/L warrants emergency ECG and IV treatment. (2) Fluid overload causes pulmonary oedema — loss of fluid excretion rapidly accumulates. (3) Uraemia accumulates toxins causing pericarditis, encephalopathy and coagulopathy. NICE NG148 mandates same-day specialist input for AKI stage 2–3. Missing severe AKI in primary care is a leading cause of preventable death and a frequent source of medico-legal claims. The "sick day rules" campaign exists because GPs historically underpowered this safety screen.

2

Diagnose

Confirm AKI — KDIGO staging criteria

Done

AKI is defined by KDIGO 2012 criteria. You need a baseline creatinine — use most recent value within 3 months if no acute result available.

AKI Stage 1

Creatinine rise 1.5–1.9× baseline OR rise ≥26.5 µmol/L within 48 h Moderate concern

AKI Stage 2

Creatinine rise 2.0–2.9× baseline High concern — same-day review

AKI Stage 3

Creatinine rise ≥3× baseline OR creatinine ≥354 µmol/L OR oliguria >12h OR dialysis Emergency — 999

Urine output

<0.5 ml/kg/hr for ≥6h = Stage 1 | <0.5 ml/kg/hr for ≥12h = Stage 2 | <0.3 ml/kg/hr for ≥24h or anuria ≥12h = Stage 3

Baseline creatinine

Use most recent stable value within 3 months. If unavailable, use CKD-EPI to estimate baseline from known eGFR. If no prior results: treat lowest result as baseline

eGFR caveat

eGFR can lag in rapidly changing AKI — use absolute creatinine values for staging, not eGFR alone

AKI alert

NHS Spine AKI algorithm generates automatic GP alerts. Check your lab results carefully for flagged AKI notifications

KDIGO staging is the global standard adopted by NICE NG148. Stage 1 AKI detected early can often be managed in primary care with reversal of precipitants. Stage 2–3 require hospital assessment. The NHS Spine AKI algorithm automatically flags AKI to GPs — studies show it reduces delayed diagnosis by ~40%. eGFR underestimates severity in rapidly rising creatinine because the CKD-EPI formula assumes steady-state — always reference absolute creatinine values against the individual's baseline.

3

Diagnose

Identify the Cause — Pre-renal, Intrinsic, Post-renal

Done

Classify cause rapidly — it directly drives management. History is the most powerful diagnostic tool here.

Pre-renal (70%)

Reduced renal perfusion — dehydration, vomiting/diarrhoea, haemorrhage, sepsis, cardiac failure, hepatorenal, NSAID/ACEi/ARB-induced. Most reversible
Clue: concentrated urine, mucous membranes dry, low BP, tachycardia

Intrinsic renal (25%)

Tubular injury (ATN) — ischaemia, nephrotoxins (aminoglycosides, contrast, myoglobin, NSAIDs)
Glomerular — rapidly progressive GN (haematuria + proteinuria + casts)
Vascular — renal artery stenosis, TTP/HUS
Interstitial — AIN from drugs (penicillin, NSAIDs, PPIs) May need nephrology input

Post-renal (5%)

Obstruction — BPH, pelvic malignancy, retroperitoneal fibrosis, stones, urethral stricture
Clue: poor urine stream, nocturia, enlarged bladder, bilateral hydronephrosis on USS 2WW if malignancy suspected

Key history

Recent illness, fluid intake, medications (NSAIDs, ACEi/ARB, diuretics, antibiotics, contrast), prior CKD, urinary symptoms, systemic features (rash, arthralgia — vasculitis/AIN), BP medications

Sick day rules

Ask about recent dose changes or continuation of ACEI/ARB/diuretics/NSAIDs during acute illness — this is a common and preventable precipitant

Identifying cause is the pivot of AKI management. Pre-renal AKI (the vast majority in primary care) resolves with fluid resuscitation and nephrotoxin removal. Intrinsic renal causes (e.g. rapidly progressive GN) require urgent immunosuppression — delay causes irreversible nephron loss. Post-renal obstruction requires decompression (catheter or nephrostomy) — the longer obstruction persists, the greater the permanent damage. Sick day rules are validated: temporary cessation of ACEi/ARB/diuretics/NSAIDs/metformin during acute dehydrating illness prevents 20–30% of AKI hospital admissions.

4

Diagnose

Targeted Examination — Volume status and organ complications

Done

Examination guides fluid management and identifies life-threatening complications. Volume status is the critical assessment.

Vital signs

BP (both arms — discrepancy suggests vascular cause), HR, RR, temp, O₂ sats, GCS. Postural BP drop >20 mmHg = volume depletion confirmed

Volume status

Hypovolaemia: dry mucosae, reduced skin turgor, sunken eyes, tachycardia, low BP, reduced JVP
Hypervolaemia: raised JVP, peripheral oedema, crackles, ascites, S3 gallop → fluid overload

Cardiovascular

JVP (elevated = fluid overload or cardiac failure), heart sounds (pericardial rub = uraemia — emergency), peripheral oedema

Respiratory

Basal crackles (pulmonary oedema), reduced air entry, pleural effusion. O₂ sats <94% → same-day hospital

Abdomen

Palpable bladder (retention → catheterise), renal angle tenderness (pyelonephritis, obstruction), flank mass (tumour, PKD), liver size (hepatorenal syndrome)

Skin / rash

Purpuric rash → vasculitis/TTP; maculopapular rash → drug hypersensitivity (AIN); livedo reticularis → cholesterol emboli, vasculitis

Neurological

Asterixis (flapping tremor) = uraemia → emergency. Reduced GCS → 999. Check for Wernicke's if alcoholic/malnourished

Rectal exam

If post-renal obstruction suspected — enlarged, irregular prostate (BPH, malignancy)

Volume assessment fundamentally drives whether you give fluids (hypovolaemia → pre-renal AKI) or restrict them (fluid overload → intrinsic/post-renal AKI). Giving IV fluids to a fluid-overloaded patient causes pulmonary oedema. A pericardial rub indicates uraemic pericarditis — an absolute emergency requiring dialysis. Asterixis is a rapid bedside screen for uraemic encephalopathy. Examining for bladder distension takes 30 seconds and immediately identifies post-renal obstruction, which is fully reversible if decompressed quickly.

5

Diagnose

Investigations — Bloods, urine, and imaging

Done

Investigations confirm severity, identify cause, and guide treatment. Prioritise by urgency.

Urgent bloods

U&Es creatinine + potassium — K⁺ ≥6.0 mmol/L needs ECG immediately
FBC — anaemia (chronic AKI/haemolysis), WCC (infection/vasculitis), platelets (TTP/HUS)
Venous blood gas — pH <7.2 = metabolic acidosis → emergency

Additional bloods

LFTs, albumin — hepatorenal syndrome, nutritional status
CRP, ESR, CK — infection, inflammation, rhabdomyolysis
Glucose, HbA1c — diabetic nephropathy background
LDH, blood film — TTP/HUS if microangiopathic picture

Urine

Dipstick — blood + protein = glomerulonephritis; nitrites/leucocytes = UTI/pyelonephritis
MSU MC&S — if infection suspected
ACR (albumin:creatinine ratio) — quantify proteinuria once stable
Urine Na+ — <20 mmol/L = pre-renal (sodium conserved); >40 = intrinsic (tubular damage)

ECG

Mandatory if K⁺ ≥6.0 mmol/L. Peaked T waves → widen QRS → sine wave → VF. Treat before blood results return if ECG is abnormal

Imaging

Renal USS — first-line if obstruction suspected (bilateral hydronephrosis), asymmetric kidneys (renovascular), or cause unclear. NOT needed in obvious pre-renal AKI. Arrange same-day if obstruction likely
CXR — if fluid overload or pulmonary cause suspected

Specialist tests

If intrinsic renal disease suspected (nephrology input): ANCA, ANA, anti-GBM, complement, immunoglobulins, protein electrophoresis, hepatitis B/C serology, HIV, ASOT

Do NOT order

Routine renal biopsy in primary care. Renal biopsy if cause is obvious pre-renal or post-renal. Repeat creatinine in stable CKD without acute change

Potassium and ECG are the most time-critical results — hyperkalaemia kills before renal failure does. Urine sodium helps differentiate pre-renal (kidneys conserving Na, UNa <20) from intrinsic renal damage (tubules fail to reabsorb Na, UNa >40). USS is essential if obstruction is in the differential — bilateral hydronephrosis confirms the diagnosis and mandates same-day urology referral. Autoimmune screen (ANCA, ANA, anti-GBM) is only relevant if there are features of glomerulonephritis — initiating this in primary care can save 24–48 hours before nephrology initiates immunosuppression.

6

Refer

Referral Criteria — Who needs hospital and how urgently

Done

Most AKI detected in primary care requires same-day assessment at minimum. Very few patients can be safely managed in the community.

999 Emergency

Same-day hospital

Same-day urology

Bilateral hydronephrosis on USS | Acute urinary retention (catheterise first) | Ureteric stone causing obstruction + AKI | Suspected malignant obstruction

Nephrology 2WW/urgent

Haematuria + proteinuria + AKI (possible GN) | Suspected vasculitis or AIN | Rapidly declining eGFR without clear pre-renal cause | AKI superimposed on CKD stage 4–5 | Nephrotic syndrome

Primary care manageable

Medication on admission

Advise A&E/ward to flag: ACEi, ARBs, diuretics, NSAIDs, metformin, lithium, aminoglycosides — all require dose adjustment or suspension in AKI

NICE NG148 explicitly states that AKI Stage 2–3 warrants hospital admission for IV fluid resuscitation, ECG monitoring, and specialist input. Only mild stage 1 AKI with a clear reversible cause and a well patient can be monitored in primary care — and even then, 48-hour review is mandatory. Nephrology input improves outcomes in immune-mediated AKI (early immunosuppression for GN reduces irreversible fibrosis). Post-renal obstruction: each hour of obstruction causes nephron loss — urology must be contacted same-day. A common GP error is watchful waiting with AKI when the threshold for referral has been crossed — this generates complaint and medicolegal risk.

7

Treat

Treatment — Pharmacological management in primary care

Done

Primary care treatment is targeted at: (1) removing precipitants, (2) optimising fluid balance, (3) managing hyperkalaemia if mild, (4) adjusting nephrotoxic medications. IMMEDIATE ACTIONS — Apply to all AKI in primary care

Stop nephrotoxins

HOLD immediately: NSAIDs, ACEi, ARBs, diuretics, metformin (lactic acidosis risk if AKI), lithium (toxic accumulation), gentamicin, vancomycin, trimethoprim. Document clearly in notes

Fluid challenge

Oral rehydration if tolerated — encourage 2–3L/day water. If unable to drink → IV fluids in hospital. Do NOT give fluids if fluid overloaded (crackles, elevated JVP)

Treat underlying cause

UTI/pyelonephritis: co-amoxiclav 500/125 mg TDS (adjust dose for severity) or cefalexin 500 mg QDS. Sepsis → 999. Vomiting → antiemetics (cyclizine 50 mg TDS)

HYPERKALAEMIA — Primary care ladder (K⁺ 5.5–6.4 mmol/L, no ECG changes)

Step 1 ECG immediately — if peaked T waves or QRS widening: 999 now

Step 2 Dietary advice — low potassium diet: avoid bananas, oranges, potatoes, tomatoes, nuts, chocolate, salt substitutes (LoSalt). Achieves 0.3–0.5 mmol/L reduction

Step 3 Patiromer (Veltassa) 8.4 g OD (potassium binder) — for persistent K⁺ 5.1–6.4 in ambulatory patients. Specialist initiation usually required. OR sodium zirconium cyclosilicate (Lokelma) 10 g TDS for 48h then 5 g OD Both may need shared care

Step 4 Arrange same-day repeat U&Es after 24–48h. K⁺ ≥6.0 or failing to respond → Same-day hospital

MEDICATION REVIEW — AKI-related dose adjustments for primary care management

Metformin

STOP if eGFR <30

Risk of lactic acidosis. Hold during AKI even if eGFR usually >30. Restart only when creatinine stable and eGFR ≥30 for ≥3 months

ACEi / ARB

HOLD during acute illness

Restart once creatinine stable. Acceptable rise ≤30% baseline — document pre-/post-AKI creatinine to guide restart

Diuretics

HOLD during AKI

Furosemide, spironolactone, thiazides — all worsen pre-renal AKI. Restart with caution post-AKI if still indicated

NSAIDs

STOP — use paracetamol instead

NSAIDs constrict afferent arterioles, reducing GFR. Avoid indefinitely in CKD. Paracetamol 1g QDS is safe in AKI

Lithium

HOLD + urgent level

Lithium toxicity rapidly accumulates in AKI. Hold, check level, and review with psychiatry. Therapeutic range 0.6–1.0 — toxicity >1.5

SGLT2i (gliflozins)

HOLD during AKI

Dapagliflozin, empagliflozin etc. — hold if eGFR <45 or acute illness. Restart once stable and eGFR recovered

📋 Sick Day Rules card: Give every patient with CKD or at-risk medications a written sick day rules card — hold ACEi/ARB/diuretics/NSAIDs/metformin if vomiting, diarrhoea, or any illness reducing fluid intake. NHS England prescribing guidance supports this.

Nephrotoxin removal is the most powerful intervention available in primary care — studies show 40–60% of community AKI resolves when precipitants are removed and fluid balance is restored. Metformin accumulates in AKI causing potentially fatal lactic acidosis — hold even in mild AKI. ACEi/ARB hold is supported by NICE NG148 with explicit restart criteria. Patiromer/sodium zirconium cyclosilicate are now preferred over calcium resonium for outpatient hyperkalaemia management (better tolerability, faster action). The sick day rules campaign has been estimated to prevent 40,000 AKI admissions per year in the UK if consistently applied.

8

Lifestyle

Non-Pharmacological — Prevention and recovery optimisation

Done

Lifestyle interventions are primary prevention AND recovery tools. AKI survivors have 3× higher risk of CKD progression — these measures are protective.

Hydration Minimum 1.5–2L fluid daily (water preferred). Increase during hot weather, exercise, illness. Urine should be pale yellow. Dehydration is the most common precipitant of community AKI

Sick Day Rules — Education Written card and verbal explanation: hold ACEi/ARB/diuretics/NSAIDs/metformin during any vomiting, diarrhoea, or illness reducing fluid intake. Restart when eating/drinking normally for 24–48h

NSAID avoidance Use paracetamol instead. NSAIDs are responsible for ~10% of community AKI. Educate patient: avoid ibuprofen even OTC. Especially important with ACEi/ARB ("triple whammy" = NSAID + ACEi + diuretic)

Alcohol reduction Alcohol causes dehydration and direct nephrotoxicity. Target <14 units/week with alcohol-free days. Excessive alcohol is a significant AKI risk factor, particularly in hot weather

Smoking cessation Smoking independently causes renal vasoconstriction and accelerates CKD progression. Post-AKI, smoking cessation reduces GFR decline by up to 50%. Refer to stop smoking service

Blood pressure control Hypertension accelerates CKD progression post-AKI. Target BP <130/80 mmHg in CKD with proteinuria (NICE CKD guideline). ACEi/ARB preferred once creatinine stable (reduce proteinuria 30–40%)

Blood sugar optimisation In diabetic patients, poor glycaemic control drives hyperfiltration and nephron loss. Target HbA1c ≤53 mmol/mol (7%) — reduces progression from AKI to CKD

Low potassium diet (if hyperkalaemia) Avoid: bananas, oranges, tomatoes, potatoes, leafy greens, nuts, chocolate, LoSalt/NoSalt. Dietary change alone can reduce K⁺ by 0.3–0.5 mmol/L. Refer to renal dietitian post-AKI if K⁺ remains elevated

Weight management Obesity drives CKD progression and increases AKI risk via hypertension and metabolic syndrome. Every 5 kg weight loss reduces BP by approximately 4 mmHg. Target BMI <30

Contrast media precautions Pre-hydrate with 0.9% saline before any contrast CT/angiography (hospital to arrange). Alert radiology if eGFR <60 — use lowest-osmolarity contrast, consider alternative imaging

AKI is not a single event — it is a risk marker. Patients who survive AKI have a 3× higher rate of CKD development, 2× higher rate of cardiovascular events, and significantly reduced life expectancy compared to matched controls (NICE NG148). Post-AKI GP care is therefore a major prevention opportunity. Sick day rules are the single most cost-effective primary prevention tool available in primary care. The "triple whammy" combination (NSAID + ACEi + diuretic) is responsible for a significant proportion of AKI deaths and is entirely preventable with patient education. Hydration advice is free and effective — RCTs show adequate hydration reduces recurrent AKI by 25%.

9

Safety

Follow-Up, Monitoring & Safety-Netting

Done

Post-AKI monitoring is a NICE-mandated quality standard. Many patients are discharged from hospital without adequate follow-up — this is the GP's safety net.

48–72 hours

Repeat U&Es + FBC (for community-managed AKI Stage 1). Check creatinine trending down. If stable or improving: continue monitoring. If worsening → escalate to same-day hospital

1 week

Recheck U&Es. Confirm creatinine returning toward baseline. Review medication changes — consider restarting ACEi/ARB/diuretics if creatinine within 30% of pre-AKI baseline

3 months

Full AKI review: U&Es, eGFR, ACR, BP, medication reconciliation. Formally assess for CKD — if eGFR <60 or ACR >3 mg/mmol persists, diagnose CKD and add to CKD register

Annual review

If CKD confirmed post-AKI: annual eGFR, ACR, BP, FBC, bone profile, calcium, phosphate, PTH (if eGFR <30). Refer nephrology if eGFR <30 or rapidly declining

Medication restart

ACEi/ARB: restart when creatinine stable ≤7 days. Acceptable if creatinine <30% above pre-AKI level. Metformin: restart when eGFR ≥30 and stable for ≥3 months. NSAIDs: avoid permanently if CKD persists

Hospital discharge

If patient had inpatient AKI: check discharge summary for AKI stage, cause, nephrotoxin changes, and follow-up instructions. Many discharges are incomplete — active GP review within 1 week is best practice (RCGP/NHS England joint guidance)

Monitoring parameters

eGFR trend, serum creatinine, potassium, bicarbonate (acidosis), haemoglobin (anaemia of CKD), BP, proteinuria (ACR)

🔴 Safety-netting — Advise patient to call 999 / attend A&E if:

Passing no urine For 6+ hours despite drinking well → 999

Breathlessness at rest New or worsening, especially at night → 999

Confusion or drowsiness Any new confusion, not acting normally → 999

Severe weakness Cannot stand, severe muscle pain → 999

Palpitations or chest pain Could indicate hyperkalaemic arrhythmia → 999

Not improving or worsening Despite stopping nephrotoxins and drinking well → Same-day GP call

📝 NICE Quality Standard QS76: AKI survivors should have a structured review within 3 months. Add READ code for AKI episode and CKD register if appropriate. Consider referral to renal dietitian, DSME programme (if diabetic), and BP optimisation clinic as applicable.

Post-AKI care is chronically under-resourced in UK primary care. NICE NG148 and the Taskforce on Kidney Health (2020) highlight that up to 30% of AKI survivors have no formal review within 3 months, missing opportunities to diagnose CKD, optimise BP, and prevent recurrence. An AKI episode is a significant event — 1-year mortality after hospitalised AKI is approximately 25–30%. The 3-month review detects persistent renal impairment, allows safe medication restart, and reduces the risk of a second AKI. Structured follow-up also has medico-legal importance: failing to review post-AKI and missing progression to CKD3–4 is a known complaint trigger. The 48-hour creatinine recheck in community AKI is the safety net that prevents missed deterioration.