Synopsis
Quantify abnormal urine output, distinguish filtration failure, obstruction, water diuresis, solute diuresis and nocturnal bladder symptoms, and prevent sodium or volume emergencies.
- Measure output before labelling it. In adults, NICE AKI recognition uses oliguria below 0.5 mL/kg/hour; catheter patency, collection errors and actual body weight must be checked.
- Anuria is particularly concerning for complete obstruction, catheter blockage, severe shock, vascular catastrophe or advanced intrinsic failure and warrants immediate reassessment.
- Oliguria is a functional signal that can precede creatinine rise. It does not prove hypovolaemia, and a fluid bolus can worsen heart failure or renal venous congestion.
- Adult polyuria usually means more than about 3 litres in 24 hours, not urinary frequency. A bladder diary separates large total volume from frequent small voids.
- Solute diuresis follows glucose, urea, sodium or certain medicines and produces relatively concentrated urine; water diuresis from primary polydipsia or vasopressin deficiency/resistance produces dilute urine.
- Check plasma sodium and paired serum/urine osmolality before water-deprivation or desmopressin testing. Formal dynamic testing belongs in an endocrine unit because unsafe dehydration and hyponatraemia can occur.
- Known arginine vasopressin deficiency is treated with life-sustaining desmopressin. Omission or restricted access to water can rapidly cause severe hypernatraemic dehydration.
- Nocturia is waking from sleep to void. Causes include nocturnal polyuria, global polyuria, reduced bladder capacity, sleep apnoea, heart failure, oedema redistribution and poorly timed fluids or diuretics.
- A three-day frequency-volume chart records time and volume of drinks and voids, bedtime and waking, urgency and leakage, allowing nocturnal urine fraction and bladder capacity to be assessed.
- After urinary retention is relieved, monitor for post-obstructive diuresis rather than replacing every millilitre automatically; fluid and electrolytes are individualised to avoid perpetuating salt loss.
Key red flags
Output below the weight-adjusted threshold with acute illness, creatinine rise, hypotension, congestion or nephrotoxin exposure requires rapid cause and complication assessment. Oliguria can exist without a catheter if measurement is reliable.
Sudden absent urine, suprapubic pain, palpable bladder, catheter blockage, bilateral stones or pelvic malignancy suggests obstruction. A non-distended bladder does not exclude bilateral ureteric obstruction.
Intense thirst, very dilute high-volume urine and high or rising sodium suggests vasopressin deficiency or resistance; low sodium suggests primary polydipsia or excessive desmopressin more strongly.
High urine output after catheterisation, stent or nephrostomy may be physiological clearance or pathological salt and water loss. Postural hypotension, rising sodium or potassium/magnesium depletion indicates danger.
Investigation priorities
Confirm oliguria, anuria or true polyuria and establish severity.
Management branches
Output below 0.5 mL/kg/hour, no urine or an unexpected sharp decline.
- Confirm measurement and catheter patency, perform ABCDE, assess depletion versus congestion and obtain urgent potassium, creatinine, bicarbonate and ECG where indicated.
- Use bladder scanning and urgent ultrasound when obstruction is possible; involve urology immediately for infected obstruction, solitary-kidney blockage or unrelieved retention.
- Treat the cause and life threats, monitor response and seek nephrology advice for intrinsic AKI, severe complications or persistent oliguria rather than repeating unassessed fluid boluses.