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This is a clinician-written, evidence-based guide aligned to the MCC Examination Objectives. It is structured by clinical presentation — the way the MCCQE tests and the way patients actually present. Management reflects current Canadian guidelines (CMA, CFPC, CPS). Always cross-reference with institutional protocols and clinical judgment.
Key points
- Oliguria is low urine output; anuria is near-absent urine output — both require immediate assessment of perfusion, obstruction, and intrinsic renal disease
- Think prerenal, intrinsic renal, postrenal — then look for immediate threats: hyperkalaemia, pulmonary oedema, severe acidosis, uraemic complications, toxins
- The most important bedside steps are vitals, volume status, medication review, bladder scan, catheter if appropriate, urinalysis, creatinine/electrolytes, and renal ultrasound when obstruction is possible
- Postrenal obstruction is reversible and time-sensitive; anuria with hydronephrosis, urinary retention, solitary kidney, or sepsis requires urgent decompression
- Avoid further nephrotoxins and adjust medication doses early — NSAIDs, ACEi/ARB during hypoperfusion, diuretics, contrast, aminoglycosides, lithium, and metformin are common exam traps
Approach to the Presentation
Oliguria/anuria is the clinical front door to acute kidney injury. The MCC AKI objective tests whether the candidate can diagnose cause, severity, complications, and situations requiring urgent intervention. Start with ABCs and haemodynamics, then immediately classify the problem as prerenal hypoperfusion, intrinsic renal injury, or postrenal obstruction. The patient may need fluid resuscitation, vasopressors, treatment of sepsis, relief of obstruction, cessation of nephrotoxins, or urgent dialysis. Urine output is also a vital sign in critical illness; falling urine output may precede creatinine rise.
Differential Diagnosis
| diagnosis | likelihood | key features | distinguishing test |
|---|---|---|---|
| Shock / severe hypoperfusion | must-not-miss | Hypotension, tachycardia, cool peripheries, sepsis, haemorrhage, dehydration, heart failure, cirrhosis; low urine sodium often prerenal if not on diuretics | Clinical volume assessment, lactate, creatinine trend, urinalysis; response to haemodynamic optimization |
| Postrenal obstruction | must-not-miss | Anuria, suprapubic pain, LUTS/BPH, pelvic malignancy, stones, solitary kidney, bilateral obstruction, catheter blockage | Bladder scan and catheter; renal ultrasound for hydronephrosis; CT if stone/malignancy suspected |
| Acute tubular injury/necrosis | must-not-miss | Ischaemia after shock/sepsis/surgery or nephrotoxins; muddy brown granular casts; persistent AKI despite fluids | Urine microscopy; creatinine trend; FeNa may support but is context-dependent |
| Rapidly progressive glomerulonephritis | must-not-miss | Oliguria with hematuria, proteinuria, red cell casts, hypertension, oedema, systemic vasculitis/lupus, pulmonary haemorrhage | Urine microscopy, ACR/PCR, complements, ANA, ANCA, anti-GBM; urgent nephrology ± biopsy |
| Acute interstitial nephritis | common | Recent beta-lactam, PPI, NSAID, diuretic or infection; fever, rash, eosinophilia may be absent; sterile pyuria/WBC casts | Medication history + urinalysis; nephrology if severe or persistent |
| Cardiorenal syndrome | common | Heart failure with congestion, elevated JVP, oedema, pulmonary crackles, low effective arterial volume | Clinical exam, BNP if helpful, CXR, echo, urine sodium; response to decongestion |
| Hepatorenal physiology | less common | Advanced cirrhosis/ascites, low urine sodium, bland sediment, no shock or nephrotoxin after evaluation | Clinical criteria after excluding other AKI causes; hepatology/nephrology input |
| Rhabdomyolysis | less common | Muscle pain/weakness, dark urine, trauma, seizures, statins, cocaine, prolonged immobilization; dipstick blood with few RBCs | Creatine kinase markedly elevated; potassium, phosphate, calcium abnormalities |
| Thrombotic microangiopathy / HUS-TTP | rare | AKI with thrombocytopenia, haemolysis, neurologic symptoms, diarrhoeal prodrome or pregnancy/drugs | CBC smear schistocytes, LDH, haptoglobin, platelets, creatinine; urgent haematology/nephrology |
Red Flags & Key History
Symptoms
Anuria or rapidly falling urine output — obstruction, severe AKI, shock, or catheter problem
Dyspnoea, orthopnoea, frothy sputum — pulmonary oedema from fluid overload
Weakness, palpitations, syncope — possible severe hyperkalaemia
Confusion, pericarditic chest pain, bleeding, seizures — uraemic complications
Hematuria, rash, arthralgia, haemoptysis — glomerulonephritis/vasculitis
Recent vomiting/diarrhoea, poor intake, diuretics, ACEi/ARB, NSAIDs — prerenal/nephrotoxic AKI
Lower urinary tract symptoms, pelvic cancer, stone history — obstruction
Signs
Hypotension, shock, mottling, altered mental status
Pulmonary crackles, elevated JVP, severe oedema
Palpable distended bladder or catheter not draining
Hypertension with oedema and active urine sediment
Dry mucous membranes, poor skin turgor, orthostatic hypotension
Approach to Investigation
First-line
Serum creatinine/eGFR, urea, electrolytes, bicarbonateAssess AKI stage and complications, especially potassium, sodium, calcium, phosphate, and metabolic acidosis
Urinalysis and urine microscopyBland sediment suggests prerenal/postrenal; muddy brown casts suggest tubular injury; RBC casts/dysmorphic RBCs suggest glomerulonephritis; WBC casts suggest interstitial nephritis/pyelonephritis
Bladder scan ± urinary catheterRapidly identifies retention/catheter obstruction and allows accurate urine output measurement
ECGMandatory if hyperkalaemia suspected or potassium elevated; look for peaked T waves, PR prolongation, QRS widening, sine-wave pattern
Second-line
Renal ultrasoundAssess hydronephrosis and kidney size; particularly important in anuria, LUTS, solitary kidney, pelvic malignancy, stone risk, or unclear AKI
Urine sodium/FeNa/FeUreaCan support prerenal vs tubular injury, but unreliable with diuretics, CKD, contrast, sepsis, and mixed states; never use in isolation
CK, uric acid, phosphate, calciumIf rhabdomyolysis, tumour lysis, seizures, trauma, prolonged immobilization, or drug/toxin exposure possible
Serology for intrinsic renal diseaseIf active sediment/systemic features: complements, ANA, ANCA, anti-GBM, hepatitis/HIV testing, serum/urine electrophoresis as appropriate
Specialist
Urgent nephrology consultationFor severe AKI, refractory hyperkalaemia/acidosis, pulmonary oedema, uraemic complications, rapidly progressive GN, transplant kidney, or dialysis consideration
Urgent urology/interventional radiologyFor obstructive AKI requiring catheter, ureteric stent, or nephrostomy, particularly if infection or solitary kidney
Management Principles
KDIGO AKI guideline with Canadian Society of Nephrology commentary and Choosing Wisely Canada nephrology principles1
Immediate stabilization
- Assess ABCs, haemodynamics, oxygenation, sepsis, and fluid status
- Treat shock: appropriate isotonic crystalloid if hypovolaemic, source control/antibiotics for sepsis, vasopressors when needed
- Stop or hold nephrotoxins and dose-adjust renally cleared medications
- Measure strict input/output and daily weights; insert catheter if accurate output monitoring or retention assessment is needed
2
Treat life-threatening complications
- Hyperkalaemia with ECG changes or severe elevation: IV calcium for membrane stabilization, insulin/dextrose, beta-agonist, potassium removal strategy, and dialysis if refractory
- Pulmonary oedema: oxygen/ventilatory support, loop diuretic if responsive, dialysis/ultrafiltration if refractory
- Severe acidosis: treat cause; bicarbonate selected cases; dialysis if severe/refractory
3
Relieve obstruction
- Bladder outlet obstruction: catheterize unless urethral injury suspected
- Upper tract obstruction with infection, solitary kidney, bilateral obstruction, or AKI: urgent urology for stent or nephrostomy
4
Renal replacement therapy indications
- Use AEIOU framing: Acidosis, Electrolytes refractory, Intoxications, Overload, Uraemic complications
- Do not start chronic dialysis solely on an eGFR number; Canadian nephrology Choosing Wisely emphasizes symptoms, complications, and shared decision-making
Complications & Pitfalls
- Creatinine delay: Creatinine may lag behind real-time GFR loss; falling urine output can be the earliest warning.
- Fluid reflex: Not all oliguria needs fluids — congested heart failure/cardiorenal syndrome may need decongestion.
- Missed obstruction: Anuria should trigger immediate bladder scan and obstruction evaluation.
- Medication harm: NSAIDs, ACEi/ARB during hypoperfusion, aminoglycosides, contrast, metformin, lithium, and potassium-sparing drugs are common AKI contributors.
- Delayed nephrology: Active urine sediment with rising creatinine can represent rapidly progressive glomerulonephritis; delay can cost renal recovery.
MCCQE1 Exam Tips
- 1For AKI/anuria, always classify into prerenal, intrinsic, postrenal — then identify immediate dialysis/decompression indications
- 2Anuria + distended bladder = catheter; anuria + hydronephrosis/solitary kidney/infection = urgent decompression
- 3Hyperkalaemia with ECG changes: IV calcium comes first, before insulin/dextrose
- 4RBC casts + proteinuria + rising creatinine = glomerulonephritis; urgent nephrology is the next best step
- 5Muddy brown casts after shock/sepsis/nephrotoxins = acute tubular injury
- 6Do not over-trust FeNa; diuretics, CKD, sepsis, and mixed causes make it unreliable
- 7AEIOU is the exam-friendly dialysis indication framework
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