Acute Kidney Injury (AKI)
NICE guideline [NG148] Acute kidney injury: prevention, detection and management. Last updated: Oct 2024.
Background Information
Aetiology
Causes of AKI can be grossly categorised into the following 3 groups:
| Group | Mechanism | Common causes |
|---|---|---|
| Pre-renal | ↓ Kidney perfusion |
|
| Renal | Intrinsic (direct) kidney damage |
Acute tubular necrosis causesDrugs that cause direct tubular toxicity Endogenous toxins Ischaemia (prolonged / severe pre-renal causes can lead to intrinsic damage)
Acute interstitial nephritis causesAcute interstitial nephritis is a type IV hypersensitivity. Drugs (most common cause) Systemic diseases (e.g. SLE, sarcoidosis) Infection (e.g. Hanta virus, staphylococci) |
| Post-renal | Obstruction of urinary flow to the urethra |
|
Nephrotoxic Drugs
“Nephrotoxic drug” is a broad and often misused term. In practice, such drugs can be classified into two main groups: those associated with CKD, and those associated with AKI.
1) CKD-associated drugs are those that can cause intrinsic renal damage with prolonged use / repeated exposure:
- NSAIDs
- Analgesic nephropathy
- Lithium
- Calcineurin inhibitors (ciclosporin, tacrolimus)
- Cisplatin
- Tenofovir disoproxil
Note that although ACE inhibitors / ARBs need to be temporarily stopped in AKI, they are renoprotective in the context of CKD (in fact, used as 1st line management for proteinuria in CKD).
2) AKI-associated drugs. This is often a source of confusion. In practice, AKI-associated drugs can be grouped into 3 distinct categories based on their mechanism.
| Drugs that cause pre-renal AKI |
|
| Drugs that cause intrinsic AKI | Drugs that cause acute tubular necrosis (direct tubular toxicity):
Drugs that cause acute interstitial nephritis:
|
| Drugs that should be withheld in AKI due to accumulation or toxicity risk, rather than direct nephrotoxicity |
|
The most exam-relevant “nephrotoxic drugs” to temporarily withhold in the acute setting of AKI:
- NSAIDs (apart from cardio-protective dose aspirin), ACE inhibitors, ARBs, diuretics (the ones that reduce renal perfusion)
- Aminoglycosides, vancomycin (the ones that cause direct tubular toxicity)
- LMWH (use UFH instead), metformin, lithium
Drugs associated with acute tubular necrosis can directly cause intrinsic AKI.
In contrast, drugs that cause pre-renal AKI typically impair renal haemodynamics and precipitate AKI in the presence of an additional insult, such as dehydration, sepsis, or hypotension.
Diagnosis
Diagnostic Criteria
AKI can be diagnosed if ANY of the following is present:
- ↑ Creatinine ≥26 mmol/L within 48 hours
- ↑ Creatinine ≥50% within 7 days
- ↓ Urine output to <0.5 mL/kg/hour for >6 hours in adults, >8 hours in children and young people
- ↓ eGFR ≥25% within 7 days in children and young people
Note that a simple raised serum creatinine does NOT diagnose AKI. AKI is a time-based definition, where there is a sudden reduction in kidney function, thus needing multiple tests showing a trend.
A single raised serum creatinine result might just be due to CKD. AKI can occur on top of CKD.
Investigating the Underlying Cause
Key tests:
- Urine dipstick – initial test of choice, perform in all patients
- Bladder scan – if urinary retention is suspected
- Urinary tract ultrasound – if obstruction is suspected / no identifiable cause
Note that NICE recommends NOT to offer an ultrasound routinely if an underlying cause of AKI has already been identified
The following are not mentioned in NICE guidelines and are not widely used in practice. However, it is important in exams to help identify the underlying cause.
Post-renal AKI can usually be easily distinguished based on clinical presentation and/or imaging findings. Pre-renal and renal AKI causes are more challenging to distinguish, often relying on the following information to answer a question.
| AKI category | Urea:creatinine ratio | Urinalysis | Urine microscopy |
|---|---|---|---|
| Pre-renal AKI | >100 (the kidney is still able to retain urea) | The kidney is still able to retain sodium (thus water) and concentrate urine to compensate:
|
Usually normal
Possible findings:
|
| Renal AKI | <40 (the kidney is unable to retain urea) | The kidney can no longer retain sodium (thus water) and cannot concentrate urine due to intrinsic damage:
|
Various findings depending on underlying cause:
|
| Post-renal AKI | 40-100 (normal)
Note that bilateral obstruction is needed for serum creatinine to be deranged |
Imaging of the renal tract has greater diagnostic value | |
Management
Management Approach
Management is mainly supportive and treating underlying cause
- Optimise volume status – to optimise kidney perfusion
- If hypovolaemic → IV isotonic fluid (e.g. 0.9% NaCl) to rehydrate
- If fluid overload → consider loop diuretic
- Stop nephrotoxic medications (see above)
- Treat underlying cause (e.g. fluid resuscitation in rhabdomyolysis, steroids for rapidly progressive glomerulonephritis, relieving any urological obstruction)
Monitoring:
- Volume status assessment
- Weight
- U&E
- Urine input and output (insert urinary catheter)
Do not routinely offer the following to manage AKI
- Loop diuretics (only consider if there is fluid overload or oedema)
- Low-dose dopamine
Renal Replacement Therapy (RRT)
Indications
If patients have ANY of the following NOT responding to medical therapy → refer immediately for RRT
- Acidosis (metabolic)
- Electrolyte – hyperkalaemia
- Ingested toxin (BLAST – barbiturates, lithium, alcohol, salicylate, theophylline)
- Oedema (fluid overload)
- Uraemia (pericarditis / encephalopathy)
Choice of RRT
- Stable patients → intermittent haemodialysis
- Haemodynamically unstable → continuous renal replacement therapy (CRRT)
- Modalities include: haemofiltration, haemodialysis, hemodiafiltration