NephrologyTier 1Approach to a presentation

Acute oligo-anuria

Red flags

  • Anuria (<50 mL/24h) - think complete obstruction, bilateral renal artery/vein occlusion, or cortical necrosis, not just "severe AKI"
  • Hyperkalaemia with ECG changes - treat before anything else
  • Signs of pulmonary oedema from fluid overload
  • Uraemic encephalopathy or pericarditis (pericardial rub, chest pain worse lying flat)
  • Palpable bladder / painless anuria in an elderly man - acute urinary retention until proven otherwise
  • Single functioning kidney or known bilateral disease + new oliguria - obstruction of that kidney is a nephrology emergency
  • Recent contrast, nephrotoxic drugs, or hypotensive episode - clue to the mechanism

Differential by mechanism

Pre-renal (commonest, ~60-70%)
  • Hypovolaemia - haemorrhage, GI/renal losses, poor intake
  • Hypotension/shock - sepsis, cardiogenic, anaphylaxis
  • Reduced effective circulating volume - heart failure, cirrhosis, nephrotic syndrome
  • Renal hypoperfusion from drugs - NSAIDs, ACEi/ARB (esp. combined with diuretic + volume depletion - "triple whammy")
Renal (intrinsic)
  • Acute tubular necrosis - prolonged pre-renal insult, nephrotoxins (aminoglycosides, contrast, myoglobin), sepsis
  • Glomerulonephritis - rapidly progressive forms cause oligoanuria (ANCA vasculitis, anti-GBM, lupus nephritis)
  • Acute interstitial nephritis - drugs (beta-lactams, PPIs, NSAIDs), infection
  • Vascular - renal artery/vein thrombosis (bilateral or solitary kidney), thrombotic microangiopathy (HUS/TTP), cholesterol emboli
Post-renal (obstructive)
  • Bladder outlet - BPH, prostate cancer, blocked catheter, neurogenic bladder
  • Bilateral ureteric obstruction (or unilateral in a solitary kidney) - stones, pelvic malignancy, retroperitoneal fibrosis, clot

Focused history

Onset and pattern
  • Abrupt anuria -> obstruction, vascular catastrophe, severe ATN
  • Gradual oliguria -> pre-renal, evolving intrinsic renal disease
  • Preceding vomiting/diarrhoea, poor intake, fever, bleeding
Drug and exposure history
  • NSAIDs, ACEi/ARB, diuretics, aminoglycosides, contrast within days
  • New drug (esp. antibiotics, PPI) -> interstitial nephritis (rash, fever, eosinophilia triad present in only a minority)
  • Recent illness with diarrhoea (+/- bloody) -> HUS in a child
Urinary symptoms
  • Poor stream, hesitancy, nocturia -> outlet obstruction
  • Colicky flank pain radiating to groin -> stone
  • Haematuria, oedema, hypertension -> glomerular disease
Background
  • Known CKD, single kidney, diabetes, myeloma, recent surgery (retroperitoneal), pelvic malignancy

Focused examination

  • Volume status - JVP, postural BP, skin turgor, mucous membranes, chest for crackles/effusion, peripheral oedema
  • Palpable bladder / suprapubic dullness - outlet obstruction
  • PR exam - enlarged prostate
  • Abdominal/flank masses, bruits (renal artery)
  • Rash, arthralgia -> vasculitis/interstitial nephritis
  • Signs of chronic liver disease (hepatorenal physiology) or heart failure
  • Livedo reticularis, digital ischaemia -> cholesterol emboli (post-angiography)

Investigation strategy

First-line
  • Bladder scan / catheterise - immediately excludes/treats outlet obstruction and quantifies output
  • UEC, FBE, VBG (K+, acidosis), CK (rhabdomyolysis), calcium/phosphate/uric acid (tumour lysis)
  • Urinalysis + microscopy - blood + protein + casts (dysmorphic RBC, red cell casts) -> glomerular; muddy brown granular casts -> ATN; eosinophils -> AIN (insensitive)
  • Renal tract ultrasound - hydronephrosis (obstruction), kidney size/echogenicity, post-void residual
Directed by suspected cause
  • Urine microscopy + FENa/FEUrea if diagnosis unclear and not on diuretics (low FENa <1% suggests pre-renal)
  • Autoimmune screen (ANCA, anti-GBM, complement, ANA) if glomerulonephritis suspected - do not wait for results before urgent nephrology referral
  • CT KUB (non-contrast) if stone suspected and ultrasound equivocal
  • Blood film + haptoglobin/LDH if TMA suspected
  • Myeloma screen (serum free light chains, protein electrophoresis) in older patients with unexplained AKI

Management

1. Treat immediate threats to life
  • Hyperkalaemia - calcium gluconate, insulin/dextrose, salbutamol; dialysis if refractory
  • Pulmonary oedema - sit up, oxygen, IV nitrates/diuretic if some residual function, ultrafiltration/dialysis if anuric and unresponsive
  • Severe acidosis - treat cause; bicarbonate/dialysis if severe
2. Relieve obstruction if post-renal
  • Catheterise for outlet obstruction - expect a post-obstructive diuresis, monitor for hypovolaemia/electrolyte loss afterward
  • Nephrostomy/ureteric stent for upper tract obstruction
3. Optimise perfusion if pre-renal
  • Judicious IV fluid to euvolaemia (avoid over-resuscitation - no benefit and worsens oedema/mortality)
  • Stop nephrotoxins - NSAIDs, consider withholding ACEi/ARB/diuretic temporarily
  • Treat sepsis/shock per usual pathway
4. Intrinsic renal disease
  • Suspected rapidly progressive GN or severe AIN/vasculitis -> urgent nephrology referral +/- biopsy - immunosuppression may be time-critical
  • Supportive care for ATN - it resolves with time once the insult is removed; no specific pharmacological therapy accelerates recovery
Indications for urgent dialysis (AEIOU)
  • Refractory acidosis, refractory hyperkalaemia, intoxication with a dialysable toxin, refractory fluid overload, symptomatic uraemia

Traps

  • Anuria is never "just AKI" until obstruction and vascular catastrophe are excluded - bladder scan/catheter and renal tract ultrasound before assuming ATN
  • Post-obstructive diuresis can cause profound volume/electrolyte loss - monitor closely after relieving obstruction, do not just walk away once the catheter is in
  • Normal-sized, non-obstructed kidneys on ultrasound do not exclude glomerulonephritis - urine microscopy is the key test people skip
  • "Triple whammy" (NSAID + ACEi/ARB + diuretic) is a common, preventable precipitant - always check the medication list
  • Over-aggressive fluid resuscitation in oliguric AKI causes harm (pulmonary oedema, worse outcomes) - target euvolaemia, not maximal urine output
  • Eosinophilia/rash/fever triad for interstitial nephritis is present in a minority - absence does not exclude it
  • A single low creatinine reading does not exclude AKI in a patient with reduced muscle mass - trend matters more than one number

Talk track

1. Exclude the emergency-fixable causes first

  • "Bladder scan and catheterise immediately - outlet obstruction is common, easily missed, and easily fixed."

2. Localise: pre-renal, renal, or post-renal

  • "Volume status, medication review, urine microscopy, and a renal tract ultrasound get me most of the way there."

3. Treat life-threats regardless of cause

  • "Hyperkalaemia and pulmonary oedema get treated before I've finished working out the mechanism."

4. Know when this needs nephrology today, not this week

  • "Red cell casts or a vasculitis picture goes to nephrology urgently - immunosuppression can be time-critical."

5. Don't over-resuscitate

  • "I target euvolaemia, not a urine output number - excess fluid in oliguric AKI causes harm."

8 of 8 sections written · drafted 2026-09-13