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Acute Kidney Injury — Management

Registrar quick reference · KDIGO aligned
Compiled Jun 2026
Verify doses locally
Exclude obstruction · review every drug
Decision support only — not a substitute for KDIGO, eTG, or your renal team. AKI = SCr rise ≥26.5 µmol/L in 48h, or ≥1.5× baseline in 7 days, or urine output <0.5 mL/kg/h for ≥6h. Management is largely supportive — no drug cures ATN. Treat the emergency, find the cause, stop the nephrotoxins, and don't drown the patient. Verify all doses.
1 Emergency first, then triage the cause
Emergency nowtreat before the workup
Hyperkalaemia, refractory acidosis, fluid overload, uraemic encephalopathy/pericarditis.
Treat immediately (see §4) ± urgent RRT. Don't let the cause hunt delay a life-threatening complication.
Pre-renalmost common
Hypoperfusion: hypovolaemia, sepsis, cardiorenal, hepatorenal; NSAIDs / ACEi-ARB / diuretics.
Restore perfusion, stop nephrotoxins. Reversible early — but sustained hypoperfusion becomes ATN.
Intrinsic (renal)urinalysis is key
ATN (ischaemic/septic/toxic), AIN (drugs), glomerulonephritis, vascular/TMA, rhabdomyolysis, tumour lysis, myeloma.
Urinalysis + microscopy. Blood + protein → think GN/AIN → immunology, urgent nephrology, ?biopsy.
Post-renalalways exclude
Obstruction: bladder outlet, stones, prostate, retroperitoneal/pelvic.
Bladder scan + renal ultrasound. Catheter / nephrostomy. Cheap to check, fully reversible if caught.
Most ward AKI is pre-renal or ATN from a hit (sepsis, hypotension, nephrotoxins) on a susceptible kidney — but never assume before you've dipped the urine and excluded obstruction. AKI <3 months that hasn't recovered is "acute kidney disease" (AKD); persistent ≥3 months is CKD — the same patient on a continuum.
2 Work it up

The bedside & bloods

  • Urine dipThe key test. Blood + protein → glomerular/interstitial disease until proven otherwise.
  • MicroscopyCasts: muddy-brown (ATN), red-cell (GN), white-cell (AIN/pyelonephritis).
  • BloodsFBC, CK (rhabdo), Ca/PO₄/urate/LDH (tumour lysis), serum free light chains/SPEP (myeloma).

Imaging & immunology

  • USExclude obstruction; small kidneys suggest chronicity (CKD, not pure AKI).
  • ImmunologyIf GN suspected: ANCA, anti-GBM, complement (C3/C4), ANA/dsDNA, immunoglobulins.
  • DrugsReview every medication — culprit (nephrotoxin/AIN) and those needing dose adjustment.
3 Manage — supportive, cause-directed

The mainstays

  • VolumeResuscitate if hypovolaemic with isotonic/balanced crystalloid SMART · PLUS — but assess status; fluid overload harms. Not every AKI is dry.
  • NephrotoxinsStop NSAIDs, aminoglycosides; sick-day hold of ACEi/ARB, SGLT2i, diuretics during acute illness.
  • PerfusionAvoid hypotension; vasopressors for shock to a reasonable MAP.
  • ObstructionRelieve promptly — catheter / nephrostomy.

Things that don't work

  • Dopamine"Renal-dose" dopamine has no role — abandoned.
  • DiureticsDon't treat or prevent AKI — use only to manage fluid overload, not to "flush the kidneys."
  • MannitolNo role in AKI prevention.
4 Dialysis & the potassium emergency

When to start RRT

  • AEIOUAcidosis (refractory), Electrolytes (refractory K⁺), Intoxication (dialysable toxin), Overload (refractory), Uraemia (encephalopathy/pericarditis).
  • TimingNo benefit to early/accelerated start STARRT-AKI · AKIKI · IDEAL-ICU — start for an emergent indication, not for a number. (ELAIN was single-centre/positive.)

Hyperkalaemia — in order

  • 1 ProtectCalcium gluconate 10% 10 mL IV if ECG changes — stabilises myocardium (doesn't lower K⁺).
  • 2 ShiftInsulin 10 U + 25 g dextrose; salbutamol 10–20 mg neb.
  • 3 RemoveBinder (resonium/patiromer), treat the cause; dialysis if refractory.
5 Recovery, drugs & traps

After the acute phase

  • AKI→CKDAKI raises long-term CKD/ESKD risk — arrange follow-up renal function; track the AKD window.
  • RestartRestart ACEi/ARB & SGLT2i after recovery — they're renoprotective long-term; sick-day holds aren't permanent stops.
  • ReferNephrology for suspected GN/vasculitis, unexplained or non-recovering AKI, or need for biopsy/RRT.

Traps

  • ContrastContrast-AKI risk is overstated — NAC/bicarbonate don't help PRESERVE. Don't withhold needed imaging over modest CKD; hydrate higher-risk patients.
  • Miss GNDon't anchor on "pre-renal" — an active urinary sediment is treatable glomerular disease and needs urgent action.
  • DrugsDose-adjust/hold metformin, DOACs, many antibiotics; avoid morphine (active metabolites accumulate).
Sources. KDIGO Clinical Practice Guideline for AKI (2012; AKI/AKD 2026 update in public review — definition/staging, volume, nephrotoxin avoidance, sick-day guidance, RRT). ADQI consensus statements. eTG (drug dosing in renal impairment) for Australian practice.   Key trials: STARRT-AKI, AKIKI, IDEAL-ICU (no benefit to early/accelerated RRT) vs ELAIN (single-centre, positive); SMART & PLUS (balanced crystalloid vs saline); PRESERVE (NAC/bicarbonate don't prevent contrast-AKI).   Caveats: AKI on CKD is common — interpret creatinine against baseline. Drug dosing in fluctuating renal function is dynamic; verify against eTG/product information. RRT timing/indications and contrast-hydration strategies are evolving — confirm against local protocol. Companion to the acute/chronic reference set.