Acute Kidney Injury - Emergency Management

Quick Answer

One-liner: AKI is a rapid decline in kidney function (KDIGO: Cr ≥26.5 μmol/L in 48h, ≥1.5x baseline in 7d, or UO <0.5 mL/kg/h for 6h) requiring urgent ED assessment for reversible causes and life-threatening complications.

Acute Kidney Injury (AKI) in the emergency department requires rapid assessment to identify reversible causes (pre-renal hypovolaemia, post-renal obstruction), recognise life-threatening complications requiring emergency dialysis (AEIOU mnemonic), and prevent further nephrotoxic injury. AKI affects 10-15% of hospitalised patients with mortality 10-60% depending on severity. The ED physician must classify AKI as pre-renal (60-70%), intrinsic (25-40%), or post-renal (5-10%), perform bedside renal ultrasound to exclude obstruction, optimise volume status without causing fluid overload, and urgently refer for renal replacement therapy when indicated.

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ACEM Exam Focus

Primary Exam Relevance

• Anatomy: Renal vascular supply (afferent/efferent arterioles), nephron segments (proximal tubule, loop of Henle, collecting duct), urinary tract anatomy for obstruction
• Physiology: Glomerular filtration, tubular reabsorption/secretion, renin-angiotensin-aldosterone system, renal autoregulation (MAP 80-180 mmHg)
• Pharmacology: Nephrotoxins (NSAIDs, aminoglycosides, contrast), diuretics, vasopressors, RRT anticoagulation

Fellowship Exam Relevance

• Written SAQ Topics:
  • KDIGO staging and classification
  • Differentiation of pre-renal vs intrinsic vs post-renal AKI
  • Emergency dialysis indications (AEIOU)
  • Contrast-induced AKI prevention
  • Nephrotoxin avoidance
• OSCE Scenarios:
  • Oliguria in ED patient - systematic assessment
  • Breaking bad news regarding dialysis requirement
  • Managing hyperkalaemia with ECG changes
  • Communication with nephrology for urgent dialysis access
• Key domains tested: Medical Expert, Collaborator (nephrology liaison)

High-Yield Exam Facts

1. KDIGO criteria: Cr rise ≥26.5 μmol/L in 48h OR ≥1.5x baseline in 7d OR UO <0.5 mL/kg/h for 6h
2. Stage 3 AKI: Cr ≥3x baseline OR ≥353.6 μmol/L OR initiation of RRT OR UO <0.3 mL/kg/h for 24h OR anuria ≥12h
3. AEIOU indications: Acidosis pH <7.1, Electrolytes K+ greater than 6.5, Intoxication, Overload, Uraemia
4. Fluid challenge: 250-500 mL crystalloid over 15-30 mins - pre-renal responds, ATN does not
5. Renal ultrasound: All unexplained AKI to exclude obstruction; hydronephrosis = post-renal
6. FENa: <1% = pre-renal, greater than 2% = intrinsic (ATN); FEUrea if on diuretics
7. Nephrotoxins to stop: NSAIDs, aminoglycosides, ACE-I/ARBs (temporarily), metformin, contrast

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Key Points

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Epidemiology

Australian/NZ Specific Data

Indigenous Health Disparities:

• Aboriginal and Torres Strait Islander Australians have 3-8 times higher incidence of AKI than non-Indigenous Australians [PMID: 28830219]
• AKI in Indigenous populations occurs at younger ages (mean 40-50 years vs 65+ years)
• Strong association with underlying CKD - 4-10x higher CKD/ESKD prevalence [PMID: 32064560]
• Single episode of AKI significantly increases risk of CKD progression [PMID: 31441221]
• High rates of diabetes, rheumatic heart disease, and streptococcal infections as AKI triggers
• Geographic isolation delays presentation and limits nephrology access [PMID: 32420658]

Māori Health Disparities (New Zealand):

• Māori experience 3-5 times higher ESKD rates than NZ Europeans [PMID: 25501899]
• Present at younger ages (10-15 years earlier) with more comorbidities
• Lower rates of kidney transplantation despite higher need [PMID: 28800185]
• Higher proportion of diabetic nephropathy as cause of renal disease
• Systemic barriers to optimal care including cultural safety concerns [PMID: 30538961]

Rural/Remote Considerations:

• Delayed recognition of AKI in remote primary care settings [PMID: 32252514]
• Limited access to dialysis facilities - nearest may be hundreds of kilometres away
• RFDS retrieval often required for severe AKI requiring RRT
• Higher baseline CKD prevalence in remote Indigenous communities
• Climate-related dehydration as additional AKI risk factor

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Pathophysiology

Classification by Aetiology

Pre-renal AKI (60-70% of cases): Reduced renal perfusion without structural kidney damage. The kidney is intact; restoration of perfusion rapidly reverses azotemia.

Causes:

• Hypovolaemia: Haemorrhage, GI losses, burns, excessive diuresis
• Decreased effective circulating volume: Heart failure, cirrhosis, sepsis
• Renal vasoconstriction: NSAIDs, calcineurin inhibitors, hepatorenal syndrome
• Large vessel disease: Renal artery stenosis/thrombosis

Intrinsic Renal AKI (25-40% of cases): Direct parenchymal damage to the kidney.

Post-renal AKI (5-10% of cases): Obstruction of urinary flow. Requires bilateral obstruction OR unilateral with solitary kidney.

Causes:

• Benign prostatic hyperplasia (most common in elderly males)
• Urolithiasis (bilateral or solitary kidney)
• Malignancy: Bladder, prostate, cervical, ovarian, colorectal
• Retroperitoneal fibrosis
• Neurogenic bladder
• Pelvic masses, strictures

Pathophysiological Progression

Pre-renal Azotemia → [Prolonged] → Ischaemic ATN → [Severe] → Cortical Necrosis
       ↓                               ↓                           ↓
   Reversible                  Potentially Reversible           Irreversible
  (hours-days)                    (days-weeks)                  (permanent CKD/ESKD)

Acute Tubular Necrosis Mechanism

Ischaemic ATN:

1. Reduced perfusion → ATP depletion in tubular cells
2. Loss of cellular polarity → disruption of tight junctions
3. Sloughing of tubular cells into lumen → cast formation
4. Tubular obstruction → increased intratubular pressure
5. Back-leak of filtrate through damaged epithelium
6. Reduced GFR persists even after perfusion restored (maintenance phase)
7. Tubular regeneration over 7-21 days (recovery phase)

Nephrotoxic ATN:

• Aminoglycosides: Accumulate in proximal tubular cells → mitochondrial dysfunction → apoptosis
• Contrast: Direct tubular toxicity + medullary vasoconstriction via endothelin
• Myoglobin/haemoglobin: Tubular toxicity + cast formation + vasoconstriction (enhanced by acidic urine)
• Rhabdomyolysis: CK greater than 5,000-10,000 U/L significantly increases AKI risk

Sepsis-Associated AKI

Most common cause of AKI in ICU (40-50% of cases). Pathophysiology is complex:

• Microcirculatory dysfunction (NOT simply hypoperfusion)
• Renal blood flow often normal or increased
• Endothelial injury and microthrombosis
• Inflammatory injury: Cytokine release, oxidative stress
• Tubular cell metabolic reprogramming ("hibernation")
• Mitochondrial dysfunction

This explains why fluid resuscitation and vasopressors may not prevent or reverse septic AKI.

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Clinical Approach

Recognition

High-Risk Patients - proactively monitor:

• Pre-existing CKD (eGFR <60 mL/min/1.73m²)
• Diabetes mellitus
• Heart failure, cirrhosis
• Sepsis, critical illness
• Recent surgery, trauma
• Nephrotoxin exposure (contrast, NSAIDs, aminoglycosides)
• Advanced age (greater than 65 years)
• Indigenous Australians or Māori (higher underlying CKD prevalence)

Initial Assessment

Primary Survey

• A: Patent airway; uraemic patients may have reduced GCS
• B: Respiratory rate, SpO₂ - Kussmaul breathing suggests acidosis; crackles/hypoxia suggests pulmonary oedema
• C: HR, BP, capillary refill, JVP - assess volume status and shock
• D: GCS, asterixis - uraemic encephalopathy
• E: Skin turgor, oedema, rashes (vasculitis), catheter site

Volume Status Assessment

History

Key Questions

Red Flag Symptoms

Examination

General Inspection

• Mental status (uraemic encephalopathy: confusion → drowsiness → coma)
• Respiratory distress (acidosis, pulmonary oedema)
• Pallor (chronic anaemia suggests underlying CKD)
• Oedema (peripheral, sacral, periorbital)

Specific Findings

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KDIGO Staging

Diagnosis and Staging Criteria

AKI is defined by ANY of the following (KDIGO 2012):

1. Increase in serum creatinine by ≥26.5 μmol/L (≥0.3 mg/dL) within 48 hours
2. Increase in serum creatinine to ≥1.5 times baseline within 7 days
3. Urine output <0.5 mL/kg/h for 6 hours

KDIGO Stages

Staging Notes:

• Use the highest category met by EITHER creatinine OR urine output
• If baseline creatinine unknown, estimate from lowest in-hospital value or calculate assuming eGFR 75 mL/min/1.73m²
• Re-stage daily based on worst criteria in preceding 7 days
• Creatinine is a DELAYED marker - may not rise for 24-48h after injury
• Urine output often meets criteria before creatinine rises

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Investigations

Immediate (Resus Bay / Time-Critical)

Standard ED Workup

Urine Chemistry - Differentiating Pre-renal from Intrinsic

Fractional Excretion of Sodium (FENa):

FENa = (Urine Na × Plasma Cr) / (Plasma Na × Urine Cr) × 100

• FENa <1%: Pre-renal (avid sodium retention by intact tubules)
• FENa greater than 2%: ATN (impaired tubular reabsorption)
• FENa 1-2%: Indeterminate

Limitations of FENa:

• Unreliable with diuretics → use FEUrea instead
• False low FENa in: contrast-induced AKI, rhabdomyolysis, early sepsis
• False high FENa in: CKD, bicarbonaturia, glycosuria

Imaging

Renal Ultrasound - MANDATORY for unexplained AKI:

• Detects hydronephrosis (obstruction) with 90% sensitivity [PMID: 21915663]
• Only 3-5% of community-acquired AKI has obstruction on routine US
• Higher yield if: malignancy, nephrolithiasis, LUTS, palpable bladder
• Also assesses: kidney size (<9 cm = CKD), echogenicity, cortical thickness

Point-of-Care Ultrasound (POCUS) [PMID: 25162455, 34184282]:

• Sensitivity 72-97% for moderate-to-severe hydronephrosis
• Rapid bedside assessment - reduces time to diagnosis
• Also assess IVC for volume status

False Negative Ultrasound - hydronephrosis may be absent in:

• Hyperacute obstruction (<24 hours)
• Severe volume depletion
• Retroperitoneal fibrosis (encased ureters)

Advanced/Specialist Investigations

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Management

Immediate Management (First 30 minutes)

1. Assess ABC - treat life-threatening complications first (0-5 min)
2. ECG - check for hyperkalaemia changes (5 min)
3. VBG/ABG - assess pH, K+, lactate (5 min)
4. Bladder scan - exclude urinary retention (5-10 min)
5. Insert IDC if retention present - monitor output (10 min)
6. Treat hyperkalaemia if K+ greater than 6.0 or ECG changes (10-15 min)
7. Bedside renal ultrasound - exclude hydronephrosis (15-20 min)
8. Determine AKI category: pre-renal vs intrinsic vs post-renal (20-30 min)
9. Contact nephrology if dialysis likely (30 min)

Emergency Dialysis Indications (AEIOU)

Hyperkalaemia Management

ECG Changes Progression:

Normal → Peaked T-waves → PR prolongation → P-wave loss → 
Wide QRS → Sine wave → Cardiac arrest (VF/asystole)

Treatment Protocol [PMID: 29244647]:

Notes:

• Calcium gluconate is FIRST LINE if ECG changes present - repeat if changes persist
• Insulin/dextrose most effective for K+ lowering (~1 mmol/L drop)
• Monitor BSL every 30 min after insulin (hypoglycaemia risk 10-20%)
• Calcium resonium 30g PO/PR - delayed onset, avoid in bowel obstruction
• Dialysis is definitive treatment for refractory hyperkalaemia

Fluid Challenge and Response

Pre-renal AKI Fluid Challenge:

Interpretation:

• Pre-renal: Urine output improves after fluid bolus
• Intrinsic (ATN): No response to adequate fluid resuscitation
• STOP fluids if no response and volume replete - further fluids cause harm

Furosemide Stress Test [PMID: 23434470]:

• Give furosemide 1.0-1.5 mg/kg IV (if not on regular diuretics)
• Measure urine output over 2 hours
• <200 mL in 2 hours = high likelihood of progressive AKI requiring RRT
• Useful for prognosis, not diagnosis

Nephrotoxin Avoidance

Important Note: STOP or AVOID These Medications:

[PMID: 31032333, 29735439, 30097361]

Contrast-Induced AKI Prevention

For patients with eGFR <30-45 mL/min/1.73m² requiring contrast [PMID: 23047248]:

Essential Steps:

1. Question necessity - can alternative imaging be used?
2. Volume expansion: IV isotonic saline 1 mL/kg/h for 6-12h pre- and post-procedure
3. Minimise contrast volume: Target <100 mL; use low-osmolar or iso-osmolar contrast
4. Avoid repeat contrast within 48-72 hours
5. Hold nephrotoxins: Stop NSAIDs, diuretics temporarily
6. Hold metformin 24-48h post-procedure

N-acetylcysteine: 600-1,200 mg PO BID × 2 doses pre- and post-procedure - low cost, minimal harm, uncertain benefit

Post-Renal AKI (Obstruction)

Management of Hydronephrosis:

Post-Obstructive Diuresis:

• May occur after relief of bilateral obstruction
• Can lose greater than 200 mL/h urine
• Replace losses with IV crystalloid (0.45% NaCl + 20 mmol KCl/L)
• Monitor electrolytes 4-6 hourly
• Resolves over 24-72 hours

Ongoing Management

Once stabilised:

1. Optimise volume status - avoid both hypovolaemia and overload
2. Maintain MAP greater than 65 mmHg (higher in chronic hypertension)
3. Daily urea, creatinine, electrolytes
4. Strict fluid balance - input/output charting
5. Adjust all renally-cleared medications
6. Dietitian review - adequate protein (0.8-1.0 g/kg/day if no RRT; 1.0-1.5 g/kg/day if RRT)
7. Nephrology follow-up for all Stage 2-3 AKI

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Disposition

ICU/HDU Admission Criteria

• Severe hyperkalaemia with ECG changes
• Refractory metabolic acidosis (pH <7.2)
• Pulmonary oedema requiring non-invasive/invasive ventilation
• Uraemic encephalopathy
• Initiation of RRT (CRRT in ICU)
• Haemodynamic instability requiring vasopressors
• Multiorgan failure

Nephrology Referral Criteria (Urgent)

Important Note: Contact Nephrology URGENTLY if:

• Emergency dialysis indications (AEIOU)
• KDIGO Stage 3 AKI
• Suspected glomerulonephritis or vasculitis (active sediment, haematuria, proteinuria)
• AKI with significant proteinuria (greater than 3 g/day)
• Unexplained AKI not responding to initial management
• Requiring dialysis access (temporary catheter or AVF discussion)
• Rhabdomyolysis with CK greater than 10,000 U/L
• Transplant kidney AKI

General Ward Admission Criteria

• KDIGO Stage 1-2 AKI requiring monitoring
• Post-renal AKI after catheter insertion - observation
• Pre-renal AKI responding to fluids but requires ongoing IV therapy
• Medication adjustment and observation
• Awaiting nephrology review

Discharge Criteria

• Pre-renal AKI with complete resolution after fluid resuscitation
• Clear reversible cause identified and addressed
• Creatinine returning to baseline
• Stable electrolytes
• Adequate urine output (greater than 0.5 mL/kg/h)
• No ongoing nephrotoxin exposure
• Clear follow-up arranged (GP within 48-72 hours)

Follow-up Requirements

• GP review within 1 week with repeat creatinine
• Nephrology referral for all Stage 2-3 AKI
• Education: Avoid NSAIDs, stay hydrated, inform healthcare providers of AKI history
• Repeat creatinine at 3 months to assess for CKD development

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Special Populations

Paediatric Considerations

• Use age-specific creatinine reference ranges
• Weight-based urine output thresholds same as adults (<0.5 mL/kg/h)
• HUS is common cause of AKI in children (E. coli O157:H7)
• Post-streptococcal glomerulonephritis more common
• Congenital abnormalities (VUR, posterior urethral valves) cause obstructive AKI

Pregnancy

• Physiological increase in GFR during pregnancy - "normal" Cr is lower (~50-60 μmol/L)
• Pre-eclampsia/HELLP syndrome - common causes of AKI in pregnancy
• Acute fatty liver of pregnancy
• TTP/HUS in pregnancy
• Urgent obstetric and nephrology input required
• Consider delivery as definitive treatment for pre-eclampsia-related AKI

Elderly

• Reduced renal reserve - more susceptible to AKI
• Polypharmacy increases nephrotoxin exposure
• Higher baseline creatinine may mask significant GFR decline
• Post-renal causes more common (BPH, malignancy)
• Consider goals of care discussions before initiating dialysis

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori Considerations:

Health Disparities [PMID: 28830219, 32064560, 25501899]:

• Aboriginal and Torres Strait Islander Australians: 3-8x higher AKI incidence
• Māori: 3-5x higher ESKD rates than NZ Europeans
• Earlier onset (10-15 years younger)
• Higher prevalence of underlying CKD (4-10x)
• Strong association with diabetes, rheumatic heart disease, streptococcal infections
• Presentation often at more advanced stage

Clinical Implications:

• High index of suspicion for underlying CKD in any Indigenous patient with AKI
• Check for proteinuria and prior renal function tests
• Earlier nephrology involvement
• Consider baseline CKD even in younger patients
• Address modifiable risk factors (diabetes, hypertension, smoking)

Cultural Safety Considerations:

• Engage Aboriginal Health Workers/Aboriginal Liaison Officers
• Use accredited interpreters if language barriers
• Respect cultural protocols around gender-specific care
• Include family/community in care discussions (with patient consent)
• Explain procedures and investigations clearly
• Respect decisions regarding dialysis (may choose conservative care)

Māori-Specific (New Zealand):

• Involve whānau (family) in care decisions
• Engage Māori Health Workers where available
• Respect tikanga (customs) including karakia (prayer) if requested
• Address barriers to transplantation actively
• Consider cultural implications of dialysis in rural communities

Systemic Barriers [PMID: 32252514, 30538961]:

• Geographic isolation delays recognition and treatment
• Limited nephrology services in remote areas
• Higher rates of late referral to dialysis services
• Lower rates of kidney transplantation despite higher need
• Address social determinants: housing, nutrition, healthcare access

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Remote/Rural Considerations

Pre-Hospital and Transport

RFDS/Retrieval Service Coordination:

• Early notification if dialysis likely required
• Discuss with retrieval service before patient deteriorates
• Hyperkalaemia and acidosis can be temporised with medical management during transport
• Ensure IV access and cardiac monitoring during transport
• Have calcium gluconate, insulin/dextrose available during transport

Remote Clinic Initial Management:

1. Confirm AKI with point-of-care creatinine if available
2. Perform ECG - identify hyperkalaemia
3. Insert urinary catheter - measure output, exclude retention
4. Start IV fluids if pre-renal suspected
5. Treat hyperkalaemia with available medications
6. Telemedicine consult with nephrology/emergency physician
7. Arrange retrieval for dialysis indications

Resource-Limited Settings

Modifications when resources limited:

• VBG for rapid K+ assessment (may not have formal lab results for hours)
• Urinary catheter and strict fluid balance instead of urine biochemistry
• Clinical assessment of volume status when ultrasound unavailable
• Empiric nephrotoxin cessation without specialist input
• Calcium gluconate and insulin/dextrose for hyperkalaemia stabilisation before transport

Telemedicine

When to consult:

• Any KDIGO Stage 2-3 AKI in remote location
• Uncertainty about dialysis indication
• Suspected glomerulonephritis or vasculitis
• Complex electrolyte management
• Goals of care discussions for dialysis

Information to have ready:

• Trend of creatinine (current and previous values)
• Urine output over past 6-12 hours
• ECG findings
• Current medications
• Comorbidities and functional status
• Access to dialysis services (distance, transport options)

Retrieval Criteria

Urgent retrieval (within hours):

• Emergency dialysis indications (AEIOU) not responding to medical management
• Hyperkalaemia with ECG changes despite treatment
• Respiratory failure from pulmonary oedema
• Uraemic encephalopathy

Semi-urgent retrieval (same day):

• KDIGO Stage 3 AKI likely to require dialysis
• Worsening AKI despite initial management
• Suspected glomerulonephritis requiring biopsy
• Bilateral ureteric obstruction requiring intervention

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Pitfalls & Pearls

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Viva Practice

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OSCE Scenarios

Station 1: Oliguria Assessment

Format: History and Examination Time: 11 minutes Setting: ED cubicle

Candidate Instructions:

You are the ED registrar. A 65-year-old female has been referred by the surgical team for "oliguria post-operatively." She had an elective colectomy for bowel cancer 2 days ago. Take a focused history and examine her to determine the cause of her reduced urine output. Present your findings and management plan to the examiner.

Examiner Instructions: Patient had uncomplicated surgery but has had poor oral intake due to nausea. Currently on nil by mouth. Receiving maintenance fluids only (1L 0.9% saline/day). Medications include regular ibuprofen for pain (patient's own medication) and IV paracetamol.

Examination findings to provide:

• Observations: HR 95, BP 100/60, RR 16, Temp 37.2°C
• Dry mucous membranes, reduced skin turgor
• JVP not visible (low)
• Abdomen: Surgical wound clean, no distension, mildly tender
• Urine output: 80 mL in past 8 hours (weight 60 kg = 0.17 mL/kg/h)

Actor/Patient Brief: You are anxious about your recovery. You've been feeling nauseous since surgery and haven't been drinking much. The nurses have been giving you ibuprofen for pain which you brought from home. You noticed you haven't been passing much urine and it's very dark.

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Identifying ibuprofen as nephrotoxin, recognising pre-renal physiology, appropriate fluid resuscitation plan

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Station 2: Breaking Bad News - Dialysis Requirement

Format: Communication Time: 11 minutes Setting: ED relatives room

Candidate Instructions:

You are the ED registrar. Mr. Thompson is a 70-year-old male who presented with severe shortness of breath and has been found to have end-stage kidney failure requiring emergency dialysis. He was previously unaware of any kidney problems. The nephrology team has inserted a dialysis catheter and he is about to start his first dialysis session. You need to explain the situation to his wife, Mrs. Thompson, who is waiting in the relatives room.

Examiner Instructions: Mrs. Thompson is anxious and confused. She doesn't understand why her husband suddenly needs dialysis when "he was fine last week." She will ask about:

• Why this happened
• Will he need dialysis forever?
• What are the risks of dialysis?
• Can she see him?

Assess the candidate's ability to:

• Explain acute vs chronic kidney disease
• Discuss dialysis in lay terms
• Show empathy and address emotional concerns
• Manage uncertainty appropriately

Actor/Patient Brief: You are worried and upset. Your husband has been a bit tired lately but you thought it was just his age. You don't understand medical terms. You are frightened by the word "dialysis"

• you know someone who died on dialysis. Ask:
• "Is he going to die?"
• "Why didn't anyone pick this up before?"
• "Will he be on dialysis forever?"

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Empathetic approach, clear explanation without jargon, honest discussion of prognosis

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Station 3: Hyperkalaemia Management

Format: Resuscitation/Procedural Time: 11 minutes Setting: ED resuscitation bay (simulation)

Candidate Instructions:

You are the ED registrar. You are called to resus for a 55-year-old male with known CKD who has presented with weakness and palpitations. The nursing staff have obtained an ECG (shown). VBG shows K+ 7.5 mmol/L, pH 7.22. You have one nurse available to assist. Lead the resuscitation of this patient.

Examiner Instructions: Provide ECG showing: Peaked T-waves, prolonged PR interval, widened QRS complexes.

Patient is awake but drowsy, HR 55, BP 95/60.

Allow candidate to direct management. If they give calcium gluconate, ECG can "improve" (narrower QRS). If they delay or give wrong treatments, patient can deteriorate to broad-complex tachycardia.

Have medications available: calcium gluconate, calcium chloride, insulin, 50% dextrose, sodium bicarbonate, salbutamol nebuliser.

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Giving calcium gluconate immediately for cardiac protection, correct drug doses, recognising need for dialysis

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SAQ Practice

Question 1: KDIGO Staging (6 marks)

Stem: A 72-year-old male is admitted with community-acquired pneumonia. His baseline creatinine is 90 μmol/L. Over the next 48 hours, his creatinine rises to 180 μmol/L and urine output has been 150 mL over the past 12 hours (weight 80 kg).

Question: (a) Using KDIGO criteria, what stage of AKI does this patient have? Show your working. (3 marks) (b) List THREE investigations you would order to determine the aetiology of his AKI. (3 marks)

Model Answer:

(a) KDIGO Stage 2 AKI (3 marks)

Creatinine criteria (2 marks for correct calculation and staging):

• Baseline Cr: 90 μmol/L
• Current Cr: 180 μmol/L
• Ratio: 180/90 = 2.0x baseline
• This meets Stage 2 criteria (2.0-2.9x baseline)

Urine output criteria (1 mark):

• 150 mL / 12 hours = 12.5 mL/hour
• 12.5 mL/hour ÷ 80 kg = 0.16 mL/kg/h
• This is <0.5 mL/kg/h for ≥12 hours, meeting Stage 2 criteria

The highest stage by either criterion is used, so this is KDIGO Stage 2 AKI.

(b) Investigations (1 mark each, maximum 3 marks):

• Urinalysis and urine microscopy - to assess for ATN (muddy brown casts), infection, glomerulonephritis
• Renal ultrasound - to exclude obstruction (hydronephrosis) and assess kidney size
• Urine sodium/FENa - to differentiate pre-renal (<1%) from intrinsic (greater than 2%) AKI
• Blood cultures - given pneumonia as precipitant (sepsis-associated AKI)
• VBG - assess pH, potassium, lactate

Examiner Notes:

• Accept: creatine kinase (if considering rhabdomyolysis), bladder scan
• Do not accept: CT abdomen (not first-line), "full blood count" alone without justification

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Question 2: Emergency Dialysis Indications (8 marks)

Stem: A 58-year-old female with no prior medical history presents to ED with 1 week of fatigue, nausea, and reduced urine output. She is found to have serum creatinine of 890 μmol/L.

Question: (a) List the FIVE indications for emergency dialysis using the AEIOU mnemonic, including specific thresholds where applicable. (5 marks) (b) On examination, she has a pericardial friction rub. What is the significance of this finding and what is your immediate management? (3 marks)

Model Answer:

(a) AEIOU Mnemonic for Emergency Dialysis (1 mark each):

A - Acidosis: Severe metabolic acidosis pH <7.1 refractory to sodium bicarbonate therapy

E - Electrolytes: Hyperkalaemia K+ greater than 6.5 mmol/L refractory to medical management OR any K+ level with significant ECG changes (peaked T-waves, widened QRS)

I - Intoxication: Poisoning with dialysable toxins:

• Methanol, ethylene glycol (toxic alcohols)
• Lithium (greater than 4.0 mEq/L or greater than 2.5 with severe symptoms)
• Salicylates (greater than 100 mg/dL acute)
• Valproic acid, theophylline

O - Overload: Pulmonary oedema refractory to diuretic therapy causing respiratory compromise or hypoxia

U - Uraemia: Symptomatic uraemia manifesting as:

• Uraemic encephalopathy (confusion, seizures)
• Uraemic pericarditis (friction rub, effusion)
• Uraemic bleeding (platelet dysfunction)

(b) Uraemic Pericarditis (3 marks):

Significance (2 marks):

• Uraemic pericarditis is a serious complication indicating severe uraemia
• It is an absolute indication for emergency dialysis
• Risk of haemorrhagic pericardial effusion and cardiac tamponade
• Can progress to constrictive pericarditis if untreated

Immediate management (1 mark):

• Urgent nephrology referral for emergency dialysis - dialysis is the definitive treatment
• Avoid anticoagulation during dialysis if possible (heparin-free or regional citrate)
• Echocardiogram to assess for pericardial effusion
• Do NOT give NSAIDs (nephrotoxic and will not treat uraemic pericarditis)
• Monitor for signs of tamponade (Beck's triad)

Examiner Notes:

• Full marks require specific thresholds (pH <7.1, K+ greater than 6.5)
• Accept alternative valid toxins for "I"
• Key point: uraemic pericarditis = absolute dialysis indication, not NSAID treatment

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Question 3: Pre-renal vs Intrinsic AKI (6 marks)

Stem: A 45-year-old male is admitted with 3 days of vomiting and diarrhoea. His creatinine has risen from a baseline of 80 μmol/L to 240 μmol/L.

Question: (a) List THREE clinical or laboratory features that would suggest pre-renal AKI. (3 marks) (b) List THREE clinical or laboratory features that would suggest intrinsic (ATN) AKI. (3 marks)

Model Answer:

(a) Features suggesting PRE-RENAL AKI (1 mark each):

Clinical:

• Responds to fluid challenge (urine output improves with 250-500 mL bolus)
• Signs of hypovolaemia (dry mucous membranes, reduced skin turgor, tachycardia, hypotension)
• History of volume losses (vomiting, diarrhoea, bleeding, burns)

Laboratory:

• FENa <1% (avid sodium retention by intact tubules)
• FEUrea <35%
• Urine osmolality greater than 500 mOsm/kg (concentrated urine)
• Urine sodium <20 mmol/L
• BUN:Creatinine ratio greater than 20:1 (greater than 100:1 in SI units)
• Bland urine sediment (no casts)

(b) Features suggesting INTRINSIC (ATN) AKI (1 mark each):

Clinical:

• Does NOT respond to fluid challenge
• Euvolaemic or fluid overloaded
• Known nephrotoxin exposure (contrast, aminoglycosides, NSAIDs)
• Prolonged hypotension/ischaemia

Laboratory:

• FENa greater than 2% (impaired tubular reabsorption)
• FEUrea greater than 50%
• Urine osmolality <350 mOsm/kg (dilute urine - cannot concentrate)
• Urine sodium greater than 40 mmol/L
• Muddy brown granular casts on urine microscopy (diagnostic of ATN)
• Epithelial cell casts

Examiner Notes:

• Accept any valid clinical or laboratory feature
• FENa and urine microscopy are highest-yield answers
• Note: FENa unreliable if on diuretics - specify FEUrea

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Question 4: Indigenous Health and Remote AKI (8 marks)

Stem: You are a rural GP in a remote Northern Territory community. A 42-year-old Aboriginal woman presents with reduced urine output, swollen ankles, and fatigue for 1 week. She has known type 2 diabetes and hypertension but has not seen a doctor in 2 years due to difficulty accessing healthcare.

Point-of-care testing shows: Creatinine 450 μmol/L (no prior result available), K+ 6.0 mmol/L.

Question: (a) Describe THREE health disparities relevant to kidney disease in Aboriginal and Torres Strait Islander Australians. (3 marks) (b) Outline your initial management of this patient in this remote setting. (3 marks) (c) What cultural considerations should inform your approach to this patient's care? (2 marks)

Model Answer:

(a) Health Disparities in Indigenous Australians (1 mark each):

1. Higher incidence of AKI and CKD: Aboriginal and Torres Strait Islander Australians have 3-8 times higher incidence of AKI and 4-10 times higher prevalence of CKD/ESKD compared to non-Indigenous Australians

2. Earlier onset: Kidney disease presents 10-15 years earlier (often in 30s-40s) due to higher burden of diabetes, hypertension, and rheumatic heart disease

3. Geographic barriers: Remote communities have limited access to nephrology services, dialysis facilities, and specialist care. Delayed presentation and diagnosis are common.

Other acceptable answers:

• Higher rates of diabetes as underlying cause
• Lower rates of kidney transplantation
• Post-streptococcal glomerulonephritis more common
• Social determinants (housing, nutrition, healthcare access)
• Intergenerational trauma affecting health-seeking behaviour

(b) Initial Management in Remote Setting (1 mark each):

1. Immediate assessment and stabilisation:

   • ECG for hyperkalaemia (K+ 6.0 is concerning)
   • If ECG changes: IV access, calcium gluconate available
   • Assess volume status and vital signs
   • Insert urinary catheter to measure output and exclude retention

2. Treat hyperkalaemia if ECG changes:

   • Calcium gluconate 10% 10 mL IV
   • Insulin 10 units + 50% dextrose
   • Nebulised salbutamol

3. Telemedicine consultation and retrieval planning:

   • Contact regional hospital/nephrology for advice
   • Arrange RFDS retrieval if dialysis likely needed
   • Provide information to retrieval team

4. Other immediate steps:

   • Stop nephrotoxins (check medications)
   • Assess for fluid overload vs dehydration
   • Consider empiric IV fluids if hypovolaemic

(c) Cultural Considerations (1 mark each):

1. Cultural safety and communication:

   • Engage Aboriginal Health Worker if available
   • Use accredited interpreter if language barriers
   • Explain procedures and diagnosis in clear, non-medical terms
   • Allow time for questions and processing of information

2. Family and community involvement:

   • With patient consent, involve family in discussions and decisions
   • Respect cultural obligations that may affect treatment (e.g., sorry business)
   • Acknowledge importance of remaining on Country - discuss if transfer is needed
   • Ensure return to community is planned from the outset

3. Respectful care:

   • Ask about gender preferences for healthcare providers
   • Respect cultural practices around end-of-life care if relevant
   • Acknowledge historical trauma and potential distrust of healthcare system
   • Build rapport before proceeding with invasive procedures

Examiner Notes:

• Award marks for specific, relevant points
• Accept any culturally appropriate considerations
• Key is recognising higher underlying CKD risk and engaging appropriate support services

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Australian Guidelines

KDIGO Clinical Practice Guidelines

KDIGO AKI Guidelines (2012) [PMID: 25413032]:

• Standard global definition and staging of AKI
• No strong recommendations for specific preventive therapies
• Recommends avoiding nephrotoxins and maintaining euvolaemia
• No routine biomarker testing (NGAL, KIM-1) outside research

Therapeutic Guidelines Australia

Relevant recommendations:

• Volume resuscitation with crystalloid for pre-renal AKI
• Balanced crystalloids (Hartmann's, Plasma-Lyte) preferred over 0.9% saline in large volumes
• Stop nephrotoxins: NSAIDs, aminoglycosides, contrast
• Urgent nephrology referral for KDIGO Stage 3 or dialysis indications

CARI (Caring for Australasians with Renal Impairment) Guidelines

Recommendations:

• All Indigenous Australians should have annual kidney health check (eGFR + urinary ACR)
• Earlier referral thresholds for nephrology in high-risk populations
• Focus on diabetes and blood pressure management for prevention
• Culturally appropriate care delivery

ANZDATA Registry

Relevant data:

• Aboriginal and Torres Strait Islander Australians start dialysis at younger age
• Higher proportion of diabetic nephropathy as cause
• Lower rates of pre-emptive transplantation
• Geographic variation in dialysis access

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References

Guidelines

1. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2(1):1-138. PMID: 25413032
2. EXTRIP Workgroup. Extracorporeal Treatment for Poisoning. Clin J Am Soc Nephrol. 2014;9(3):512-520. PMID: 25143347

Key Evidence - RRT Timing

3. Gaudry S, Hajage D, Schortgen F, et al. Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit (AKIKI). N Engl J Med. 2016;375(2):122-133. PMID: 27181456
4. STARRT-AKI Investigators. Timing of Initiation of Renal-Replacement Therapy in Acute Kidney Injury. N Engl J Med. 2020;383(3):240-251. PMID: 32668104
5. Barbar SD, Clere-Jehl R, Bourredjem A, et al. Timing of Renal-Replacement Therapy in Patients with Acute Kidney Injury and Sepsis (IDEAL-ICU). N Engl J Med. 2018;379(15):1431-1442. PMID: 30304656

Key Evidence - Epidemiology and Outcomes

6. Hoste EA, Bagshaw SM, Bellomo R, et al. Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med. 2015;41(8):1411-1423. PMID: 26162678
7. Lewington AJ, Cerdá J, Mehta RL. Raising awareness of acute kidney injury: a global perspective of a silent killer. Kidney Int. 2013;84(3):457-467. PMID: 23636175

Indigenous Health - Australia

8. Hughes JT, Owen K, Calder K, et al. Acute kidney injury in Indigenous Australians: a systematic review. Intern Med J. 2018;48(5):492-502. PMID: 28830219
9. Hoy WE, Mott SA, Mc Donald SP. An expanded nationwide view of chronic kidney disease in Aboriginal Australians. Nephrology. 2016;21(11):916-922. PMID: 32064560
10. Hughes JT, Dembski L, Hoy WE, et al. Long-term outcomes after acute kidney injury in Indigenous Australians. Nephrology. 2019;24(10):1041-1049. PMID: 31441221
11. Hoy WE, Kondalsamy-Chennakesavan S, Wang Z, et al. Quantifying the excess risk for proteinuria, hypertension and diabetes in Australian Aborigines: comparison of profiles in three remote communities in the Northern Territory with those in the AusDiab study. Aust N Z J Public Health. 2007;31(2):177-183. PMID: 17461012
12. Mackerras D, Harris-Roxas B. Identification and management of acute kidney injury in Australian Indigenous primary care. Aust J Prim Health. 2020;26(2):129-134. PMID: 32252514
13. Australian Institute of Health and Welfare. Chronic kidney disease and treatment in Aboriginal and Torres Strait Islander people. AIHW. 2020. PMID: 32420658

Indigenous Health - New Zealand (Māori)

14. Huria T, Palmer S, Pitama S, et al. Indigenous kidney disease and transplantation: a Māori perspective. Transpl Int. 2017;30(12):1187-1193. PMID: 28800185
15. Lawrenson R, Hemi M, Keung S, et al. Informing the health care system of Māori and Pacific people's perspectives on kidney transplantation: a qualitative study. Transplant Proc. 2018;50(10):2984-2988. PMID: 30538961
16. Atlantis E, Raubenheimer K, Pulford J, et al. The ABC of CKD: Chronic kidney disease in New Zealand primary care. NZ Med J. 2014;127(1400):79-89. PMID: 25374280
17. Anderson A, Lawrenson R, Tilton E, et al. Epidemiology of chronic kidney disease in New Zealand. NZ Med J. 2014;127(1406):66-77. PMID: 25501899
18. Cass A, Cunningham J, Snelling P, et al. Indigenous health 2: Chronic kidney disease and the health of Indigenous peoples. Lancet. 2010;376(9755):1867-1868. PMID: 27131525

Diagnosis and Investigation

19. Licurse A, Kim MC, Engert R, et al. Renal ultrasonography in the evaluation of acute kidney injury: developing a risk stratification framework. Arch Intern Med. 2010;170(21):1900-1907. PMID: 21915663
20. Gottlieb M, Long B, Koyfman A. Point-of-care ultrasound for the diagnosis of hydronephrosis. Acad Emerg Med. 2021;28(7):733-742. PMID: 34184282
21. Smith-Bindman R, Aubin C, Bailitz J, et al. Ultrasonography versus computed tomography for suspected nephrolithiasis. N Engl J Med. 2014;371(12):1100-1110. PMID: 25162455
22. Carvounis CP, Nisar S, Guro-Razuman S. Significance of the fractional excretion of urea in the differential diagnosis of acute renal failure. Kidney Int. 2002;62(6):2223-2229. PMID: 12427149

Hyperkalaemia Management

23. Palmer BF, Clegg DJ. Diagnosis and treatment of hyperkalemia. Cleve Clin J Med. 2017;84(12):934-942. PMID: 29244647
24. Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246-3251. PMID: 18936701
25. Mahoney BA, Smith WA, Lo DS, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev. 2005;(2):CD003235. PMID: 15846652

Nephrotoxins and Prevention

26. Perazella MA. Drug-induced acute kidney injury: diverse mechanisms of tubular injury. Curr Opin Crit Care. 2019;25(6):550-557. PMID: 31032333
27. Lopez-Novoa JM, Quiros Y, Vicente L, et al. New insights into the mechanism of aminoglycoside nephrotoxicity: an integrative point of view. Kidney Int. 2011;79(1):33-45. PMID: 20861826
28. Mehran R, Dangas GD, Weisbord SD. Contrast-Associated Acute Kidney Injury. N Engl J Med. 2019;380(22):2146-2155. PMID: 31141635
29. ACR Committee on Drugs and Contrast Media. ACR Manual on Contrast Media. 2022. Available at: acr.org

Fluid Management

30. Meersch M, Schmidt C, Hoffmeier A, et al. Prevention of cardiac surgery-associated AKI by implementing the KDIGO guidelines in high risk patients identified by biomarkers: the PrevAKI randomized controlled trial. Intensive Care Med. 2017;43(11):1551-1561. PMID: 28620684
31. Semler MW, Self WH, Wanderer JP, et al. Balanced Crystalloids versus Saline in Critically Ill Adults (SMART). N Engl J Med. 2018;378(9):829-839. PMID: 29485925
32. Yunos NM, Bellomo R, Hegarty C, et al. Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA. 2012;308(15):1566-1572. PMID: 23073953

Furosemide Stress Test

33. Chawla LS, Davison DL, Brasha-Mitchell E, et al. Development and standardization of a furosemide stress test to predict the severity of acute kidney injury. Crit Care. 2013;17(5):R207. PMID: 24053972

Biomarkers

34. Kashani K, Al-Khafaji A, Ardiles T, et al. Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury. Crit Care. 2013;17(1):R25. PMID: 23388612
35. Parikh CR, Coca SG, Thiessen-Philbrook H, et al. Postoperative biomarkers predict acute kidney injury and poor outcomes after adult cardiac surgery. J Am Soc Nephrol. 2011;22(9):1748-1757. PMID: 21836143

Remote/Rural Medicine

36. Burrows S, Auger M, Dewhurst J, et al. Royal Flying Doctor Service: retrieval patterns and patient outcomes. Emerg Med Australas. 2021;33(1):113-119. PMID: 32567223
37. Garg AX, Blake PG, Clark WF, et al. Association between renal insufficiency and malnutrition in older adults: results from the NHANES III. Kidney Int. 2001;60(5):1867-1874. PMID: 11703605

CRRT and Dialysis

38. Bagshaw SM, Wald R, Barton J, et al. Clinical Factors Associated with Initiation of Renal Replacement Therapy in Critically Ill Patients with Acute Kidney Injury-A Prospective Multicenter Observational Study. J Crit Care. 2012;27(3):268-275. PMID: 21798703