Acute kidney injury
Abrupt fall in GFR — pre-renal (hypoperfusion), intrinsic (ATN/GN/AIN), or post-renal (obstruction)
Overview
An abrupt (hours–days) decline in kidney function defined by KDIGO criteria: a rise in creatinine ≥26 µmol/L in 48 h, a ≥1.5× rise from baseline within 7 days, or urine output 6 h. The pivotal first move is the pre-renal / intrinsic / post-renal triage, because it sets the management — fluids, stop nephrotoxins, or relieve obstruction.
Recognise
- Often asymptomatic and found on bloods (rising creatinine/urea, falling output); or symptoms of the cause (sepsis, hypovolaemia, obstruction) and of uraemia/overload
- Pre-renal: volume depletion/hypotension/sepsis/heart failure/NSAIDs+ACEi (the haemodynamic 'triple whammy' with a diuretic)
- Intrinsic: acute tubular necrosis (ischaemia/toxins/contrast/rhabdomyolysis), glomerulonephritis, acute interstitial nephritis (drug-induced — rash/eosinophilia); Post-renal: stones, prostate, pelvic tumour, blocked catheter
Red flags
- Hyperkalaemia with ECG changes, refractory pulmonary oedema, severe acidosis, or uraemic encephalopathy/pericarditis → urgent dialysis (AEIOU)
- Anuria → think obstruction (bladder scan!) or a vascular catastrophe; new AKI + haemoptysis/haematuria → pulmonary-renal/RPGN
Differentials & how to tell them apart
Investigations
U&Es + creatinine (stage by KDIGO), urinalysis (blood+protein → intrinsic/GN; nitrites/leucocytes → infection), bladder scan + renal tract ultrasound (within 24 h if obstruction suspected — hydronephrosis), FBC/CRP, VBG (K, acidosis), CK (rhabdo); immunology (ANCA/anti-GBM/complement) if intrinsic GN suspected; medication review.
Management
Treat the cause + STOP-AKI bundle (stop nephrotoxins, optimise volume, relieve obstruction)
- 1Stage by KDIGO and triage pre-renal vs intrinsic vs post-renal: urinalysis, bladder scan and a renal-tract ultrasound. Apply STOP-AKI — treat sepsis, stop nephrotoxins, optimise volume/BP.Gate: Hyperkalaemia with ECG changes, refractory pulmonary oedema, severe acidosis or uraemic encephalopathy/pericarditis (AEIOU) → urgent dialysis; obstruction → relieve it (catheter/nephrostomy), don't just give fluids.
- 2Correct hyperkalaemia/acidosis/overload, monitor recovery, and avoid further nephrotoxic/contrast insults. Intrinsic GN/vasculitis → immunology + nephrology/biopsy and immunosuppression.
Key points
AKI = rapid creatinine rise / oliguria → triage pre-renal vs intrinsic vs post-renal FIRST (urinalysis + bladder scan + USS). STOP-AKI bundle; relieve obstruction; treat the cause. Dialysis for refractory hyperK/acidosis/overload/uraemia (AEIOU). Blood+protein on dip → think intrinsic GN.
Monitor & prognosis
Daily creatinine/U&Es/K, fluid balance and weight, urine output; recovery or progression; nephrotoxin avoidance.
Often reversible if the cause is treated early; AKI raises later CKD and mortality risk.
Source: NICE NG148 (AKI); KDIGO