Synopsis
Detect acute kidney injury despite low muscle mass and non-specific decline, distinguish hypovolaemia from congestion and obstruction, and restore perfusion safely while adjusting medicines, nutrition and community monitoring.
- Diagnose AKI by creatinine change or urine output using current NICE criteria; a value inside the laboratory range can still represent AKI.
- First-line assessment reviews previous renal results, urine output, losses, sepsis, bleeding, obstruction, heart failure, medicines and recent contrast or procedures.
- Examine perfusion and congestion together: blood pressure, refill, mucosa, postural symptoms, jugular venous pressure, oedema, lungs, weight and bladder.
- Measure post-void residual and obtain renal ultrasound urgently when obstruction is possible or the cause remains unclear under NICE criteria.
- Urinalysis helps identify blood and protein patterns; send microscopy and renal serology only when intrinsic disease is clinically plausible.
- For hypovolaemic resuscitation, NICE CG174 uses 500 mL isotonic crystalloid over under 15 minutes, with smaller cautious aliquots and immediate reassessment when frailty, heart or kidney disease limits tolerance.
- Do not give fluid for a raised creatinine automatically; congested heart failure often needs decongestion rather than hydration.
- Review NSAIDs, ACE inhibitors, ARBs, diuretics, metformin, SGLT2 inhibitors, anticoagulants, opioids, gabapentinoids and antimicrobials against current physiology and indication.
- Temporary medicine withholding needs a written restart trigger; failure to restart beneficial treatment after recovery creates long-term harm.
- After AKI, document cause, peak and recovery, repeat kidney and electrolyte testing, review albuminuria and provide recurrence and sick-day education.
Key red flags
ECG change, muscle weakness or rapidly rising potassium requires emergency hyperkalaemia treatment and monitoring.
Anuria, painful bladder, hydronephrosis or sepsis with obstruction requires urgent urinary drainage and specialist care.
Hypoxia, crackles, raised venous pressure or pulmonary oedema means further routine fluid may be dangerous.
Hypotension, mottling, raised lactate or ongoing losses requires urgent resuscitation with repeated response assessment.
Haematuria, proteinuria, systemic rash, low platelets or inflammatory features raises intrinsic renal disease needing specialist investigation.
Confusion, reduced intake, falls or medicine accumulation may be the first clinical expression of AKI in frailty.
Retention, anuria, palpable bladder or hydronephrosis directs urgent drainage and imaging.
New sedation, bleeding, hypoglycaemia or neurotoxicity follows renal decline without an intentional dose change.
Refractory potassium, acidosis, pulmonary oedema or uraemic symptoms requires immediate nephrology assessment.
Investigation priorities
Diagnose, stage and follow AKI first line.
Management branches
Creatinine rises, urine falls or frailty presents with possible renal accumulation.
- Compare baseline and current creatinine and urine output and assess potassium, acidosis, overload, uraemia and shock.
- Examine perfusion and congestion, review losses, sepsis, bleeding, medicines and obstruction and obtain targeted urine and imaging tests.
- Treat the cause and complication, adjust exposure and record a fluid, urine, laboratory and escalation plan.