Renal & urology
AKT · Renal & urology/AKI & rhabdomyolysis

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

Chronic kidney diseaselong-standing, small kidneys on USS, normochromic anaemia, prior baseline creatinine — but AKI-on-CKD is common
Acute interstitial nephritisdrug trigger (NSAIDs, PPIs, antibiotics) + rash/eosinophilia/eosinophiluria
Rapidly progressive glomerulonephritisactive urinary sediment (red-cell casts), systemic features, positive ANCA/anti-GBM
Myeloma (cast nephropathy)older patient + AKI/CKD + hypercalcaemia + anaemia + Bence-Jones protein — send serum/urine electrophoresis; cross-ref haematology

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)

  1. 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.
  2. 2Correct hyperkalaemia/acidosis/overload, monitor recovery, and avoid further nephrotoxic/contrast insults. Intrinsic GN/vasculitis → immunology + nephrology/biopsy and immunosuppression.
Treat the cause + 'STOP-AKI': Sepsis treat, Toxins/nephrotoxins stop (NSAIDs, ACEi/ARB, gentamicin, contrast), Optimise volume/BP, Prevent harmthe core bundle; IV fluids for pre-renal/hypovolaemia (cautious if overloaded)
Relieve obstruction (catheter / nephrostomy)post-renal AKI — decompress urgently; watch for post-obstructive diuresis
Treat hyperkalaemia / acidosis / overloadcalcium gluconate + insulin-dextrose for hyperK; loop diuretic only for fluid overload (not to treat AKI itself)
Renal replacement therapy (dialysis)for refractory hyperkalaemia/acidosis/overload or uraemic complications (AEIOU)

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