Acute Kidney Injury (AKI)
Summary
Acute Kidney Injury (AKI) is defined as an abrupt decline in renal function, manifested by a rise in serum creatinine and/or decrease in urine output. It is common in hospitalised patients and associated with significant morbidity and mortality. AKI is classified into prerenal (hypovolaemia/hypoperfusion), intrinsic renal (parenchymal damage), and postrenal (obstruction). Early recognition, cessation of nephrotoxic drugs, and treating the underlying cause are the cornerstones of management. Severe AKI may require renal replacement therapy (RRT/dialysis).
Key Facts
- Incidence: 5-20% of hospital admissions
- Mortality: Up to 50% in ICU patients with AKI
- Classification: Prerenal (60%), Renal (30%), Postrenal (10%)
- KDIGO Criteria: ↑Creatinine >26.5 µmol/L in 48h OR ↑ >1.5× baseline in 7d OR UO <0.5 mL/kg/h for 6h
- Key Intervention: Stop nephrotoxic drugs (DA MNN)
- RRT Indications: AEIOU - Acidosis, Electrolytes (K+), Intoxication, Overload, Uraemia
Clinical Pearls
High-Yield Points:
- Always check baseline creatinine - important for staging
- STOP nephrotoxics early: Diuretics, ACE-I/ARBs, Metformin, NSAIDs, Nephrotoxic antibiotics
- Prerenal AKI should respond to fluids; if not, suspect ATN
- Postrenal obstruction requires urgent decompression (catheter or nephrostomy)
- Urine dipstick: Blood and protein suggest intrinsic renal disease
- AKI in context of rash and eosinophilia → acute interstitial nephritis
Why This Matters Clinically
AKI is one of the most common acute medical problems, seen across all specialties. It is frequently iatrogenic (drugs, contrast, surgery). Early recognition and intervention can prevent progression to chronic kidney disease or the need for dialysis. Understanding the approach to oliguria and rising creatinine is essential for any acute medical assessment.
Incidence
| Setting | Incidence |
|---|---|
| Community-acquired | 5% of hospital admissions |
| Hospital-acquired | 5-10% of ward patients |
| ICU | 30-50% of admissions |
Risk Factors
Patient Factors:
- Age >65
- Pre-existing CKD
- Diabetes
- Heart failure
- Liver disease
- Sepsis
Iatrogenic:
- Nephrotoxic drugs (NSAIDs, aminoglycosides, contrast)
- Major surgery
- Volume depletion
Classification
| Type | Cause | Mechanism |
|---|---|---|
| Prerenal (60%) | Hypovolaemia, cardiogenic shock, sepsis | Reduced renal perfusion |
| Intrinsic Renal (30%) | ATN, AIN, glomerulonephritis | Parenchymal damage |
| Postrenal (10%) | Stones, BPH, malignancy | Obstruction |
Prerenal AKI
- Decreased renal blood flow
- GFR falls to preserve tubular integrity
- Reversible if corrected early
- If prolonged → ATN
Intrinsic Renal AKI
Acute Tubular Necrosis (ATN):
- Most common intrinsic cause
- Ischaemic (prolonged prerenal) or toxic (drugs/contrast)
- Characterised by "muddy brown casts" on urinalysis
Acute Interstitial Nephritis (AIN):
- Drug-induced (NSAIDs, PPIs, antibiotics)
- Allergic: Rash, eosinophilia, eosinophiluria
- May require steroids
Glomerulonephritis:
- Rapidly progressive (RPGN) is emergency
- Active sediment: RBC casts, dysmorphic cells
Postrenal AKI
- Bilateral obstruction (or unilateral in solitary kidney)
- Causes: BPH, stones, pelvic malignancy
- Urgent imaging and decompression required
Symptoms
Signs
Clinical Context
| Context | Likely Cause |
|---|---|
| Sepsis + hypotension | Prerenal/ATN |
| Post-contrast | Contrast-induced nephropathy |
| New medication + rash | AIN |
| Elderly male + urinary symptoms | Postrenal (BPH) |
| Young + haematuria + hypertension | Glomerulonephritis |
Assessment
Volume Status (Critical):
- JVP, mucous membranes, skin turgor
- Postural BP, peripheral oedema
- Lung bases (crackles)
Abdomen:
- Palpable bladder (obstruction)
- Renal angle tenderness (pyelonephritis)
General:
- Signs of sepsis
- Rash (vasculitis, AIN)
- Asterixis
KDIGO Staging
| Stage | Creatinine Criteria | Urine Output |
|---|---|---|
| 1 | ↑ ≥26.5 µmol/L or 1.5-1.9× baseline | <0.5 mL/kg/h for 6-12h |
| 2 | 2.0-2.9× baseline | <0.5 mL/kg/h for ≥12h |
| 3 | ≥3× baseline OR ≥353.6 µmol/L OR RRT | <0.3 mL/kg/h for ≥24h or anuria for ≥12h |
Initial Workup
| Investigation | Purpose |
|---|---|
| U&Es, Creatinine | Diagnosis and staging |
| Baseline Creatinine | Needed for staging |
| VBG | Acidosis, potassium |
| Urinalysis | Dipstick, microscopy |
| FBC | Anaemia, infection |
| Ultrasound KUB | Exclude obstruction |
Urinalysis Interpretation
| Finding | Suggests |
|---|---|
| Bland sediment | Prerenal or early ATN |
| Muddy brown casts | ATN |
| RBC casts | Glomerulonephritis |
| WBC casts, eosinophils | Interstitial nephritis |
| Proteinuria | Glomerular or tubular injury |
Additional Investigations (If Indicated)
- Immunology (ANA, ANCA, anti-GBM, C3/C4)
- Renal biopsy (if intrinsic cause unclear)
- Urine Bence Jones proteins (myeloma)
Principles
- Identify and treat underlying cause
- Stop nephrotoxic drugs
- Optimise volume status
- Manage life-threatening complications
- Consider RRT if indicated
STOP DAMNNN (Nephrotoxic Drugs)
- Diuretics (hold if volume deplete)
- ACE-I/ARBs
- Metformin (risk of lactic acidosis)
- NSAIDs
- Nephrotoxic antibiotics (aminoglycosides, vancomycin)
- New drugs / Contrast
Fluid Management
| Volume Status | Approach |
|---|---|
| Hypovolaemic | IV crystalloid boluses (250-500 mL), reassess |
| Euvolaemic | Maintenance only, avoid overload |
| Fluid overloaded | Diuretics (if not anuric) or RRT |
Hyperkalaemia Management
| Severity | Management |
|---|---|
| K+ >6.5 OR ECG changes | Calcium gluconate 10 mL IV, insulin/dextrose, salbutamol nebs |
| Moderate (5.5-6.5) | Stop K+ supplements, loop diuretics, calcium resonium |
| Refractory | Dialysis |
Indications for RRT (AEIOU)
- Acidosis: Severe metabolic acidosis (pH <7.1)
- Electrolytes: Refractory hyperkalaemia
- Intoxication: Dialysable toxins
- Overload: Refractory pulmonary oedema
- Uraemia: Encephalopathy, pericarditis
Source Control
- Prerenal: Treat underlying cause (sepsis, heart failure)
- Postrenal: Urgent catheter/nephrostomy
- AIN: Remove offending drug ± steroids
- GN: Specialist input, immunosuppression
Acute
| Complication | Management |
|---|---|
| Hyperkalaemia | Cardioprotection, insulin/dextrose, dialysis |
| Pulmonary oedema | Diuretics, dialysis |
| Metabolic acidosis | IV bicarbonate (limited role), dialysis |
| Uraemic encephalopathy | Dialysis |
| Uraemic bleeding | DDAVP, dialysis |
Long-Term
- Progression to CKD (20-50% don't fully recover)
- Increased cardiovascular mortality
- Need for long-term dialysis (5-10% of severe cases)
Outcomes
| Severity | In-Hospital Mortality |
|---|---|
| Stage 1 | 5-10% |
| Stage 2 | 10-20% |
| Stage 3 | 20-50% |
| RRT-requiring | 40-60% |
Recovery
- Most prerenal AKI recovers with fluid resuscitation
- ATN: Recovery usually within 1-3 weeks
- 20-50% of hospital-acquired AKI leads to CKD
Follow-Up
- Repeat creatinine 3 months post-AKI
- Refer to nephrology if persistent renal impairment
Key Guidelines
| Guideline | Organisation | Year |
|---|---|---|
| AKI Prevention, Detection and Management | NICE NG148 | 2019 |
| KDIGO Clinical Practice Guideline for AKI | KDIGO | 2012 |
| Surviving Sepsis Campaign | SCCM | 2021 |
Key Evidence
- Early goal-directed fluid resuscitation improves outcomes
- Nephrotoxic drug cessation is critical
- No benefit from prophylactic RRT (timing trials)
What is AKI?
Acute kidney injury means your kidneys have suddenly stopped working properly. They can't filter waste products and excess fluid from your blood as well as they should.
What causes it?
- Dehydration or low blood pressure: Not enough blood reaching kidneys
- Medications: Some drugs can damage kidneys (ibuprofen, certain antibiotics)
- Infections: Severe infections can affect kidneys
- Blockage: Something blocking urine flow (enlarged prostate, kidney stones)
What are the symptoms?
- Passing less urine than normal
- Swelling in legs or ankles
- Feeling sick, tired, or confused
- Sometimes no symptoms at all
How is it treated?
- Fluids through a drip if dehydrated
- Stopping medications that might be causing it
- Treating the underlying cause (infection, blockage)
- Dialysis (kidney machine) if very severe
What can I do?
- Stay well hydrated
- Avoid ibuprofen and similar painkillers (NSAIDs) unless advised
- Tell your doctor about all medications you take
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NICE. Acute kidney injury: prevention, detection and management (NG148). 2019. nice.org.uk
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KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2(1):1-138.
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Kellum JA, et al. Acute kidney injury. Nat Rev Dis Primers. 2021;7:52. PMID: 34258452
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Chawla LS, et al. Acute kidney disease and renal recovery: consensus report of the ADQI 16 Workgroup. Nat Rev Nephrol. 2017;13(4):241-257. PMID: 28239173
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. It does not replace professional medical judgement.