📋 Key Information Summary
- Definition: Acute kidney injury (AKI) is an abrupt decline in kidney function occurring within hours to days, defined by a rise in serum creatinine (≥26.5 µmol/L within 48 h or ≥1.5× baseline within 7 days) or a fall in urine output (<0.5 mL/kg/h for ≥6 h).
- KDIGO staging (Stage 1–3) guides severity assessment and determines thresholds for renal replacement therapy (RRT).
- Aetiological classification: Pre-renal (55–60 %), intrinsic renal (35–40 %), and post-renal (<5 %) — systematic exclusion of obstruction is mandatory in all cases.
- Urine indices (fractional excretion of sodium, urea, urine osmolality) help differentiate pre-renal azotaemia from intrinsic tubular injury.
- Fluid resuscitation with isotonic crystalloid (0.9 % NaCl or balanced solutions) is first-line for pre-renal AKI; avoid nephrotoxins (NSAIDs, aminoglycosides, iodinated contrast) where possible.
- RRT indications: Refractory hyperkalaemia, severe metabolic acidosis (pH <7.1), pulmonary oedema unresponsive to diuretics, uraemic complications, or specific toxin removal.
- Drug dosing: Renally adjust all renally cleared medications; consult eTG and pharmacy for GFR-based dosing. Aminoglycosides require therapeutic drug monitoring (TDM).
- AKI is preventable: At least 30 % of hospital-acquired AKI is avoidable through early recognition, nephrotoxin avoidance, and haemodynamic optimisation.
- Transition to CKD: AKI episodes increase the risk of chronic kidney disease (CKD) and end-stage kidney disease; post-AKI follow-up with eGFR at 90 days is recommended.
- Aboriginal and Torres Strait Islander peoples have a 2–3× higher incidence of AKI and are more likely to present with advanced disease — culturally safe, community-based pathways improve outcomes.
- Medicare (MBS) items support serum creatinine (item 66500), renal ultrasound (item 55021), and dialysis services in public and private settings.
- Pregnancy-related AKI (pre-eclampsia, HELLP, thrombotic microangiopathy) requires multidisciplinary obstetric–renal management.
Introduction & Australian Epidemiology
Acute kidney injury (AKI) is a common and potentially life-threatening clinical syndrome characterised by an abrupt decline in renal function occurring over hours to days. It encompasses a spectrum from mild, transient elevations in serum creatinine to severe anuric kidney failure requiring renal replacement therapy (RRT). AKI is not a single disease but the final common pathway of diverse insults to the kidney.
In Australia, AKI complicates approximately 15–20 % of all hospital admissions and up to 50 % of intensive care unit (ICU) stays. The Australian Institute of Health and Welfare (AIHW) reports that AKI-related hospitalisations have risen by over 30 % in the past decade, driven by an ageing population, increasing comorbidity burden (diabetes, hypertension, heart failure), and greater use of nephrotoxic agents. In-hospital mortality for AKI ranges from 10 % for Stage 1 to >40 % for Stage 3 requiring dialysis.
Key Australian data: Aboriginal and Torres Strait Islander Australians experience AKI at 2–3 times the rate of non-Indigenous Australians, with higher rates of community-acquired AKI related to infections, dehydration, and limited access to nephrology services in remote areas. The incidence of dialysis-requiring AKI in the Northern Territory is among the highest in the developed world.
Early recognition and timely intervention remain the cornerstones of AKI management. National Safety and Quality Health Service (NSQHS) Standard 9 (Recognising and Responding to Acute Deterioration) mandates the use of early warning scoring systems that incorporate urine output and creatinine trends. The internationally adopted KDIGO (Kidney Disease: Improving Global Outcomes) criteria provide a standardised definition and staging framework, facilitating consistent recognition, research, and audit across Australian hospitals.
KDIGO Classification & Staging
The KDIGO 2012 AKI guideline provides the current standard definition used in Australian practice. AKI is defined by any of the following:
- Increase in serum creatinine ≥26.5 µmol/L (≥0.3 mg/dL) within 48 hours; or
- Increase in serum creatinine to ≥1.5 × baseline, which is known or presumed to have occurred within the prior 7 days; or
- Urine volume <0.5 mL/kg/hour for 6 hours.
| Stage | Serum Creatinine Criteria | Urine Output Criteria |
|---|---|---|
| Stage 1 | 1.5–1.9 × baseline or ≥26.5 µmol/L increase within 48 h | <0.5 mL/kg/h for 6–12 h |
| Stage 2 | 2.0–2.9 × baseline | <0.5 mL/kg/h for ≥12 h |
| Stage 3 | ≥3.0 × baseline or ≥353.6 µmol/L increase or initiation of RRT | <0.3 mL/kg/h for ≥24 h or anuria ≥12 h |
Clinical pearl: Both creatinine AND urine output criteria must be assessed. A patient meeting urine output criteria for Stage 3 but creatinine criteria for Stage 1 should be classified as Stage 3. Using the worst applicable stage is mandatory.
Paediatric modification (pRIFLE): In children, the pRIFLE (paediatric Risk, Injury, Failure, Loss, End-stage) criteria incorporate estimated creatinine clearance (eCCl) and urine output thresholds adjusted for body weight. pRIFLE is more sensitive than KDIGO in detecting AKI in paediatric populations and is recommended by the Australian and New Zealand Paediatric Nephrology Association (ANZPNA).
Risk Factors for AKI in Australian Practice
- Age ≥65 years
- Pre-existing CKD (eGFR <60 mL/min/1.73 m²)
- Diabetes mellitus
- Heart failure or chronic liver disease
- Sepsis or critical illness
- Nephrotoxic drug exposure (NSAIDs, aminoglycosides, iodinated contrast, ACE inhibitors/ARBs in volume depletion)
- Major surgery (especially cardiac, vascular, emergency laparotomy)
- Obstructive uropathy (benign prostatic hyperplasia, urolithiasis)
Pre-renal, Intrinsic & Post-renal Causes
Systematic classification of AKI into pre-renal, intrinsic, and post-renal aetiologies is essential for targeted management. Pre-renal azotaemia accounts for 55–60 % of AKI in hospitalised patients, intrinsic renal injury 35–40 %, and post-renal obstruction <5 %.
Pre-renal
Reduced Renal Perfusion
- Volume depletion: Haemorrhage, GI losses (vomiting, diarrhoea), burns, third-spacing
- Reduced effective circulating volume: Sepsis, heart failure, cirrhosis, nephrotic syndrome
- Pharmacological: NSAIDs, ACE inhibitors/ARBs, diuretics, calcineurin inhibitors
- Afferent arteriolar constriction: Hepatorenal syndrome, hypercalcaemia
Kidney structurally intact — reversible if perfusion restored promptly
Intrinsic
Parenchymal Injury
- Acute tubular necrosis (ATN): Ischaemic (prolonged pre-renal), nephrotoxic (aminoglycosides, contrast, cisplatin, myoglobin — rhabdomyolysis)
- Acute interstitial nephritis (AIN): Drug-induced (PPIs, antibiotics — flucloxacillin, NSAIDs), infection-related, autoimmune
- Glomerulonephritis: ANCA-associated vasculitis, anti-GBM disease, lupus nephritis, IgA nephropathy, post-infectious GN
- Vascular: Malignant hypertension, thrombotic microangiopathy (TTP/HUS), renal artery thrombosis/embolism, cholesterol crystal embolisation
- Intratubular obstruction: Uric acid (tumour lysis syndrome), myoglobin, oxalate crystals
Structural damage present — may require immunosuppression or specific therapy
Post-renal
Urinary Tract Obstruction
- Bladder outflow: Benign prostatic hyperplasia, prostate carcinoma, urethral stricture, neurogenic bladder
- Ureteric: Calculi, malignancy (cervical, bladder, colorectal), retroperitoneal fibrosis, external compression
- Intrarenal: Crystal nephropathy, myeloma cast nephropathy (functional obstruction)
- Bilateral involvement (or unilateral in a solitary kidney) is required to cause AKI
Often rapidly reversible with decompression — always exclude obstruction early
Mandatory first step: All patients presenting with AKI should have a renal ultrasound (MBS item 55021) or point-of-care bladder scan within 24 hours to exclude post-renal obstruction — especially in elderly males, patients with known pelvic malignancy, or those with anuria.
Investigations & Urine Indices
A structured investigation approach should identify the cause, assess severity, and detect complications of AKI.
Baseline Investigations
Essential
Serum creatinine, urea, electrolytes
MBS item 66500. Establish baseline if not known; calculate eGFR using CKD-EPI equation. Serial measurements (at least daily) to track trajectory.
Essential
Full blood count (FBC)
MBS item 65070. Anaemia, thrombocytopaenia (consider TMA), eosinophilia (suggestive of AIN or cholesterol emboli).
Essential
Urinalysis with microscopy
MBS item 69310. Red cell casts (glomerulonephritis), muddy brown granular casts (ATN), white cell casts (AIN), crystals (uric acid, oxalate).
Essential
Urine electrolytes & osmolality (spot sample)
Collect BEFORE fluid resuscitation or diuretics. Enables calculation of urine indices (see below).
Available
Renal ultrasound ± Doppler
MBS item 55021. Hydronephrosis indicates obstruction. Small echogenic kidneys suggest pre-existing CKD. Renal artery Doppler to assess for thrombosis.
Available
Chest X-ray
Pulmonary oedema, infection, underlying malignancy.
Available
Blood gas (venous or arterial)
Metabolic acidosis (pH, bicarbonate, lactate). High anion-gap acidosis suggests lactic acidosis, ketoacidosis, or uraemia.
Urine Indices for Differentiating Pre-renal from Intrinsic AKI
| Index | Pre-renal | Intrinsic (ATN) | Notes |
|---|---|---|---|
| Urine Na⁺ (mmol/L) | <20 | >40 | Unreliable after diuretics |
| FENa (%) | <1 % | >2 % | Invalid if on diuretics; use FEUrea instead |
| FEUrea (%) | <35 % | >50 % | Preferred if patient on diuretics |
| Urine osmolality (mOsm/kg) | >500 | <350 | Kidney's concentrating ability preserved in pre-renal |
| BUN : Creatinine ratio | >100:1 | <40:1 | Reabsorption of urea in pre-renal state |
Fractional excretion of sodium (FENa) formula:
FENa = (Urine Na × Serum Cr) / (Serum Na × Urine Cr) × 100 %
Fractional excretion of urea (FEUrea) formula:
FEUrea = (Urine Urea × Serum Cr) / (Serum Urea × Urine Cr) × 100 %
Collect a spot urine sample at the same time as bloods. FEUrea is the preferred index in patients already receiving diuretics.
FENa = (Urine Na × Serum Cr) / (Serum Na × Urine Cr) × 100 %
Fractional excretion of urea (FEUrea) formula:
FEUrea = (Urine Urea × Serum Cr) / (Serum Urea × Urine Cr) × 100 %
Collect a spot urine sample at the same time as bloods. FEUrea is the preferred index in patients already receiving diuretics.
Further Investigations (as Clinically Indicated)
Specialist
Autoimmune screen
ANCA (MPO, PR3), anti-GBM antibodies, ANA, dsDNA, complement (C3, C4). Indicated if glomerulonephritis suspected (active urine sediment, haemoptysis, rash, joint pain).
Specialist
Serum & urine protein electrophoresis, free light chains
Suspected myeloma cast nephropathy. Serum free light chain assay (κ/λ ratio) is more sensitive than urine Bence Jones protein.
Specialist
Renal biopsy
Indicated when intrinsic AKI of uncertain aetiology persists beyond 3–5 days, or when glomerulonephritis, AIN, or TMA is suspected. Consult nephrology. Risk of bleeding must be assessed (platelet count, INR, blood pressure).
Available
CT KUB (non-contrast)
Renal tract calculi. Avoid iodinated contrast in AKI unless essential (risk of contrast-induced nephropathy).
Available
Troponin, BNP/NT-proBNP
Type 1 or type 2 myocardial infarction as precipitant or complication of AKI. NT-proBNP (not BNP) preferred in AKI as it is not renally cleared.
Management & Renal Replacement Therapy
Management of AKI is aetiology-specific but follows universal principles: haemodynamic optimisation, nephrotoxin removal, volume management, metabolic complication control, and timely RRT initiation.
General Supportive Measures
1
Identify & Treat the Cause
Treat sepsis (source control, early antibiotics), relieve obstruction (catheterisation, nephrostomy), cease nephrotoxins, correct hypovolaemia.
2
Optimise Volume Status
Isotonic crystalloid (0.9 % NaCl or balanced solutions e.g. Plasma-Lyte®) for hypovolaemia. Avoid fluid overload — target euvolaemia. Assess fluid responsiveness (passive leg raise, dynamic indices).
3
Avoid Nephrotoxins
Stop NSAIDs, review ACEi/ARB (hold if haemodynamically unstable), avoid aminoglycosides, minimise contrast exposure, dose-adjust all renally cleared drugs.
4
Monitor & Manage Complications
Hourly urine output via indwelling catheter, twice-daily (or more) U&E, daily weight, fluid balance chart. Treat hyperkalaemia, metabolic acidosis, pulmonary oedema, uraemia.
Pharmacological Management
0.9 % Sodium Chloride (Normal Saline)
Isotonic crystalloid · Volume resuscitation
Adult dose
250–500 mL IV bolus over 15–30 min for hypovolaemia; reassess after each bolus. Maintenance typically 1–1.5 L/24 h.
Paediatric dose
10–20 mL/kg IV bolus over 20–30 min; repeat as needed. Use balanced solutions preferentially.
Renal adjustment
Caution in oliguric AKI — risk of fluid overload. Monitor serum chloride (hyperchloraemic acidosis).
PBS status
✔ PBS General Benefit
Furosemide (Frusemide)
Lasix® · Loop diuretic · Volume overload
Adult dose
20–80 mg IV slow bolus (max 160 mg single dose). For diuretic challenge: 40–80 mg IV; if no response at 1 h, consider doubling. Infusion: 10–40 mg/h if bolus responsive but relapsing.
Paediatric dose
0.5–1 mg/kg/dose IV (max 4 mg/kg). May repeat every 6–8 h.
Renal adjustment
Higher doses may be needed in established ATN. Ototoxicity risk with doses >240 mg/h IV infusion.
PBS status
✔ PBS General Benefit
Calcium Resonium (Calcium Polystyrene Sulfonate)
Calcium Resonium® · Cation exchange resin · Hyperkalaemia
Adult dose
15–30 g PO/rectal. Onset 2–6 h (oral), 1–2 h (rectal). Repeat every 4–6 h as needed. Max 60 g/24 h.
Paediatric dose
1 g/kg PO/rectal. Neonates: 0.5–1 g/kg per dose via NG or rectum.
PBS status
✔ PBS General Benefit
Insulin–Dextrose (Hyperkalaemia Protocol)
Actrapid® + 50 % dextrose · Intracellular K⁺ shift
Adult dose
10 units Actrapid® IV + 50 mL of 50 % dextrose IV over 15–30 min. Onset 15–30 min. Monitor BGL hourly for 6 h (hypoglycaemia risk).
Paediatric dose
0.1 units/kg insulin + 0.5 g/kg dextrose IV. Monitor BGL every 15–30 min.
PBS status
✔ PBS General Benefit
Sodium Bicarbonate
8.4 % (1 mmol/mL) · Metabolic acidosis
Adult dose
50–100 mL (50–100 mmol) IV over 15–30 min for severe acidosis (pH <7.1). Titrate to target pH 7.2. Maintenance: 1.26 % NaHCO₃ as continuous infusion.
Caution
May worsen hypocalcaemia, paradoxical CSF acidosis, hypernatraemia. Use only when pH <7.1 or bicarbonate <15 mmol/L.
PBS status
✔ PBS General Benefit
Hyperkalaemia Management — Stepwise Approach
Life-threatening hyperkalaemia (K⁺ >6.5 mmol/L or ECG changes) is a medical emergency. Initiate cardiac monitoring immediately. Use the K⁺ Emergency Protocol: stabilise myocardium (calcium), shift K⁺ intracellularly (insulin-dextrose, salbutamol), remove K⁺ from body (resonium, dialysis).
1
Stabilise Myocardium
Calcium gluconate 10 % — 10–20 mL IV over 2–5 min. Repeat if ECG changes persist. Onset 1–3 min. Does not lower K⁺ — protects heart while other measures act. Use calcium chloride via central line if haemodynamically unstable.
2
Shift K⁺ Intracellularly
Insulin-dextrose (10 U Actrapid + 50 mL 50 % dextrose IV). Salbutamol 10–20 mg nebulised (caution in cardiac disease). Sodium bicarbonate if concurrent acidosis.
3
Remove K⁺ from Body
Calcium resonium 30 g PO or sodium zirconium cyclosilicate (Lokelma®) 10 g PO TDS × 48 h. Loop diuretics if urine output adequate. RRT if refractory.
Renal Replacement Therapy (RRT)
RRT should be initiated urgently when life-threatening complications are present, irrespective of a specific creatinine or urea threshold.
Indications for urgent RRT — "AEIOU":
Acidosis — refractory metabolic acidosis (pH <7.1 despite bicarbonate)
Electrolytes — refractory hyperkalaemia (K⁺ >6.5 despite medical management)
Intoxication — methanol, ethylene glycol, lithium, salicylates
Overload — fluid overload causing pulmonary oedema unresponsive to diuretics
Uraemia — encephalopathy, pericarditis, bleeding (uraemic platelet dysfunction)
Acidosis — refractory metabolic acidosis (pH <7.1 despite bicarbonate)
Electrolytes — refractory hyperkalaemia (K⁺ >6.5 despite medical management)
Intoxication — methanol, ethylene glycol, lithium, salicylates
Overload — fluid overload causing pulmonary oedema unresponsive to diuretics
Uraemia — encephalopathy, pericarditis, bleeding (uraemic platelet dysfunction)
| Modality | Indications | Setting |
|---|---|---|
| Intermittent haemodialysis (IHD) | Haemodynamically stable, rapid clearance needed (hyperkalaemia, intoxication) | Dialysis unit, ward |
| Continuous renal replacement therapy (CRRT) | Haemodynamically unstable (sepsis, vasopressor-dependent), cerebral oedema, acute liver failure | ICU |
| Sustained low-efficiency dialysis (SLED) | Hybrid of IHD and CRRT. Suitable for haemodynamically borderline patients. | ICU, HDU |
| Peritoneal dialysis (PD) | When haemodialysis access unavailable, paediatric AKI, resource-limited settings | Ward, remote/tertiary |
Early vs late RRT initiation: The STARRT-AKI (2020) and IDEAL-ICU (2018) trials demonstrated that a strategy of early RRT initiation (based on elevated urea alone) does not improve outcomes compared with a standard-care strategy of waiting for absolute indications. RRT should be initiated based on clinical urgency, not arbitrary urea/creatinine thresholds.
Recovery & Follow-up
- Assess recovery of renal function by serial creatinine measurements. Patients recovering from AKI may undergo a polyuric phase — maintain adequate hydration.
- At 90 days post-AKI, reassess eGFR. Persistent reduction (eGFR <60 mL/min/1.73 m²) defines transition to CKD.
- Refer to nephrology if: eGFR <30, persistent proteinuria, recurrent AKI, or suspected glomerulonephritis.
- Provide patient education: avoid NSAIDs, maintain hydration, monitor weight, attend GP follow-up within 1–2 weeks of discharge.
Special Populations
Pregnancy
Pre-eclampsia / HELLP syndrome
Most common cause of AKI in pregnancy. Delivery of placenta is definitive treatment. Magnesium sulphate for seizure prophylaxis. Monitor LFTs, platelets, LDH closely.
Thrombotic microangiopathy (TMA)
TTP/HUS may present similarly to HELLP. ADAMTS13 activity <10 % suggests TTP — urgent plasma exchange indicated.
RRT in pregnancy
Haemodialysis or CRRT preferred. Adjust dialysis prescription for pregnancy (smaller molecule clearance, avoid hypotension). Peritoneal dialysis is an alternative if HD unavailable.
Paediatrics
Use pRIFLE criteria
More sensitive than KDIGO in children. Stages: Risk, Injury, Failure, Loss, End-stage. Uses eCCl and UO thresholds.
Common causes
Haemolytic uraemic syndrome (HUS) — most common cause of AKI requiring dialysis in Australian children. Shiga-toxin-producing E. coli (STEC) is the usual trigger; avoid antibiotics in STEC-HUS.
Fluid management
Children are more vulnerable to fluid overload and hyponatraemia. Use weight-based fluid calculations. Balanced crystalloid (Plasma-Lyte®) preferred.
Elderly (≥65 years)
Increased susceptibility
Age-related decline in GFR, reduced renal reserve, polypharmacy, and dehydration risk. Lower threshold for AKI surveillance.
Drug dosing
Always calculate eGFR for drug adjustments. Avoid nephrotoxic combinations (e.g., ACEi + diuretic + NSAID = "triple whammy").
Goals of care
Discuss ceiling of care, advance care planning, and appropriateness of RRT with patient/family early. AKI in frail elderly has high mortality even with RRT.
Pre-existing CKD
Acute-on-chronic AKI
Baseline creatinine must be established (use lowest value in prior 3 months). Acute rise on chronic kidney disease is common and may be more clinically significant.
RRT threshold
Lower threshold for RRT initiation if already on dialysis or near end-stage. Nephrology co-management essential.
Hepatic Impairment
Hepatorenal syndrome (HRS)
Type 1 HRS: rapidly progressive AKI in cirrhosis. Treat with terlipressin (if available) + albumin. Liver transplant is definitive therapy. CRRT preferred over IHD.
Drug metabolism
Combined hepatic and renal impairment significantly alters drug clearance. Specialist pharmacy review essential.
Immunocompromised
Broader differential
Consider drug-induced (calcineurin inhibitors, antivirals — aciclovir, tenofovir), infection-related (CMV nephritis, BK virus nephropathy), tumour lysis syndrome, or TMA (post-transplant).
Transplant patients
AKI in renal transplant recipients requires urgent evaluation for acute rejection, calcineurin inhibitor toxicity, or surgical complications. Maintain immunosuppression unless contraindicated. Nephrology transplant team review.
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
📚 References
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- 2. STARRT-AKI Investigators; Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of Initiation of Renal-Replacement Therapy in Acute Kidney Injury. N Engl J Med. 2020;383(3):240–251.
- 3. Barbar SD, Clere-Jehl R, Bourredjem A, et al. Timing of Renal-Replacement Therapy in Patients with Acute Kidney Injury and Sepsis. N Engl J Med. 2018;379(15):1431–1442 (IDEAL-ICU).
- 4. Australian Institute of Health and Welfare (AIHW). Chronic kidney disease: Australian facts. Cat. no. PHE 229. Canberra: AIHW; 2023.
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