acute kidney injury
Contents
Classify by mechanism: prerenal (decreased perfusion), intrinsic (parenchymal damage), or postrenal (obstruction). Urine indices and sediment narrow the differential rapidly. Most hospital AKI is prerenal or ATN — the clinical question is which one, because the management diverges completely.
- hyperkalaemia — ECG immediately if K⁺ >5.5 mmol/L; treat before investigating
- pulmonary oedema with oliguria → urgent dialysis if not responding to diuretics
- urinary obstruction — bladder scan or point-of-care US; relief is the treatment
- rapidly progressive glomerulonephritis — active sediment + rapidly rising creatinine → nephrology same day; delay costs nephrons
- bilateral renal artery occlusion or renal vein thrombosis — consider in flank pain with anuria
KDIGO staging
| stage | creatinine criteria | urine output |
|---|---|---|
| 1 | rise ≥26.5 µmol/L in 48 h OR 1.5–1.9× baseline in 7 d | <0.5 mL/kg/h for 6–12 h |
| 2 | 2.0–2.9× baseline | <0.5 mL/kg/h for ≥12 h |
| 3 | ≥3× baseline OR creatinine ≥353.6 µmol/L OR initiation of RRT | <0.3 mL/kg/h for ≥24 h OR anuria ≥12 h |
Baseline = lowest stable creatinine in preceding 3 months. If unavailable, use the admission value or back-calculate from eGFR 75 mL/min/1.73 m².
A “normal” creatinine does not exclude significant AKI. Urine output is often the earlier signal. In low-muscle-mass patients (elderly, cirrhotic, cachectic), creatinine underestimates the severity.
classification
prerenal (~60% of hospital AKI)
Reduced renal perfusion with intact tubules. Reversible if perfusion restored promptly; prolonged prerenal AKI becomes ATN.
Causes: hypovolaemia (haemorrhage, GI losses, burns), heart failure (cardiorenal), cirrhosis (hepatorenal syndrome), drugs reducing effective perfusion (ACEi/ARBs, NSAIDs, calcineurin inhibitors).
intrinsic
| compartment | examples |
|---|---|
| tubular (ATN, ~85% of intrinsic) | ischaemia (prolonged prerenal), nephrotoxins (aminoglycosides, contrast, myoglobin, tumour lysis syndrome) |
| interstitial (AIN) | drugs (PPIs, antibiotics, NSAIDs), infection, autoimmune |
| glomerular | RPGN (anti-GBM, ANCA vasculitis, lupus nephritis, IgA) |
| vascular | TMA (TTP/HUS, malignant HTN), renal artery thrombosis/dissection, cholesterol emboli |
Drug exposure 7–14 days before AKI onset. Eosinophilia and sterile pyuria suggest it but are absent in >50% of cases. WBC casts on sediment. Urine eosinophils have poor sensitivity — don’t rely on them. Kidney biopsy is definitive.
postrenal (~5–10%)
Obstruction at any level. Bilateral ureteral obstruction (or unilateral in a single kidney) → anuria. Causes: BPH (most common in older men), malignancy (pelvic, retroperitoneal), stones, neurogenic bladder, catheter obstruction.
Bladder scan or US is mandatory in any unexplained AKI — obstruction is the most treatable cause.
workup
urine studies — the first branch point
| test | prerenal | ATN |
|---|---|---|
| urine Na | <20 mmol/L | >40 mmol/L |
| FeNa | <1% | >2% |
| urine osmolality | >500 mOsm/kg | <350 mOsm/kg |
| sediment | bland or hyaline casts | muddy brown granular casts |
FeNa = (urine Na × plasma Cr) / (plasma Na × urine Cr) × 100.
Use FeUrea instead (<35% = prerenal physiology). Also unreliable in CKD, contrast exposure, myoglobinuria, and early obstruction.
sediment — free diagnostic information
- Muddy brown granular casts → ATN
- WBC casts → AIN or pyelonephritis
- RBC casts → glomerulonephritis (urgent nephrology referral)
- Bland → prerenal, obstruction, or HRS
imaging
- Renal US — hydronephrosis (obstruction), kidney size (small = CKD, large = infiltration/amyloid/diabetes), echogenicity
- Bladder scan — post-void residual >200 mL suggests obstruction
further investigations by clinical context
- Suspected glomerulonephritis → ANA, ANCA, anti-GBM, C3/C4, SPEP/UPEP, hepatitis serologies
- Suspected TMA → blood film (schistocytes), LDH, haptoglobin, ADAMTS13
- Suspected rhabdomyolysis → CK, urine myoglobin
- Drug-induced AIN → stop offender; biopsy if no recovery by 5–7 days
management principles
prerenal
Volume resuscitation — balanced crystalloids (Ringer’s lactate preferred over normal saline). Target euvolaemia, not hypervolaemia. In cardiorenal syndrome → diuresis, not volume. In HRS → vasoconstrictors (see hepatorenal syndrome).
intrinsic
- ATN — supportive. Remove the cause, maintain euvolaemia, avoid further nephrotoxins. No pharmacological therapy accelerates recovery.
- AIN — stop the offending drug. Consider corticosteroids (prednisone 1 mg/kg) if no recovery by 5–7 days after withdrawal; evidence is observational.
- RPGN — immunosuppression urgently (pulse methylprednisolone ± cyclophosphamide or rituximab depending on cause). Plasma exchange for anti-GBM with pulmonary haemorrhage.
postrenal
Relieve the obstruction. Foley catheter for bladder outlet obstruction. Nephrostomy or ureteral stent for ureteral obstruction. Monitor for post-obstructive diuresis — can lose litres of fluid; replace appropriately.
renal replacement therapy
Indications (mnemonic AEIOU): Acidosis (refractory), Electrolytes (refractory hyperkalaemia), Ingestion (dialysable toxin), Overload (refractory pulmonary oedema), Uraemia (encephalopathy, pericarditis).
STARRT-AKI (NEJM 2020) — accelerated RRT initiation (within 12 h of KDIGO 3) vs standard strategy (wait for conventional indications): no mortality benefit from early initiation. Start RRT for clinical indications, not for a creatinine number.
traps
- Creatinine alone misses early AKI — a patient can lose 50% of GFR before creatinine exceeds the upper limit of normal. Trend matters more than absolute value.
- “Contrast nephropathy” is overdiagnosed — withholding a necessary contrast-enhanced CT for AKI risk delays diagnosis and rarely helps the kidneys. Volume optimisation before contrast is reasonable; NAC has no benefit. Do not deny a sick patient imaging.
- Assuming AKI in CKD is “just progression” — always check for a reversible superimposed cause (obstruction, drugs, volume depletion).
- NSAIDs in a patient on ACEi + diuretic — the “triple whammy” that causes predictable prerenal AKI. NSAIDs block the afferent arteriole prostaglandin rescue; ACEi blocks the efferent compensation; diuretics reduce volume. Any two are risky; all three nearly guarantee trouble.
- Failing to check post-void residual — especially in older men and patients on anticholinergics. Obstruction is the most fixable cause and the most embarrassing to miss.
related: nephrotic syndrome · hepatorenal syndrome · diuretic therapy · tumour lysis syndrome · spontaneous bacterial peritonitis