Anuria and oliguria

Anuria is the absence of urine production, and oliguria is reduced production of urine. Anuria and oliguria can be physiological (e.g., following physical exertion) or reflect significant underlying renal or systemic pathology. Pathological causes include prerenal acute kidney injury (AKI), intrinsic AKI, postrenal AKI, and chronic kidney disease (CKD). Clinical features vary according to the underlying cause. Initial evaluation includes hemodynamic assessment, laboratory tests (e.g., serum electrolytes and creatinine), urinalysis, and imaging (e.g., renal and bladder ultrasound) to detect obstruction. A focused approach to identify and address the underlying cause is essential to improve outcomes.

Reduced urinary output in adults may be defined by absolute volume or weight-based estimates.

• Anuria: < 50 mL/24 hours ^[1]
• Oliguria
  • < 400 mL/24 hours (in adults) ^[1]
  • < 0.5 mL/kg/hour for ≥ 6 hours ^[2][3]
• Physiological oliguria: a transient reduction in urinary output that does not increase the risk of subsequent renal impairment ^[3][4]

Prerenal ^[1][5]

• ↓ Effective arterial blood volume
  • Dehydration, e.g.:
    • Inadequate fluid intake
    • Vomiting
    • Diarrhea
  • Shock, e.g.:
    • Hypovolemic shock
    • Septic shock
    • Cardiogenic shock
  • Medications (e.g., ACE inhibitors, angiotensin receptor blockers)
• Renal vascular insufficiency (e.g., renal artery stenosis or renal vein occlusion)

Intrinsic renal ^[1][5]

• Intrinsic AKI, e.g.:
  • Acute tubular necrosis (ATN)
  • Acute tubulointerstitial nephritis (ATIN)
  • Glomerulonephritis
• CKD

Postrenal ^[1][5]

• Lower urinary tract obstruction (UTO)
  • Mechanical, e.g.:
    • Enlarged prostate
    • Obstructed indwelling urinary catheter
  • Functional, e.g.:
    • Neurogenic lower urinary tract dysfunction
    • Drug-induced urinary retention
• Bilateral upper UTO (e.g., retroperitoneal fibrosis)

Focused history

• Reduced urinary output
  • Time of onset and duration
  • Volume of urine
• Precipitating factors
  • Inadequate fluid intake or excess losses (e.g., vomiting, diarrhea)
  • Symptoms of sepsis
  • Recent episodes of severe hypotension or shock
  • Recent crush injuries, seizures, or immobilization
  • Symptoms of a new systemic illness (e.g., fever, rash, joint pain)
  • Suprapubic or flank pain
  • Recent medical interventions (e.g., abdominal surgery, bladder catheterization)
• Past medical history
  • CKD, heart failure, hypertension, diabetes, and/or autoimmune disease
  • Renal vascular abnormality
  • Urinary tract anatomic abnormality
  • Prostatic enlargement (e.g., benign prostatic hypertrophy)
  • Pelvic or abdominal malignancy
• Medications
  • Nephrotoxic medications
  • Medications that may cause urinary retention (see “Drug-induced urinary retention”)

AKI does not always manifest with oliguria. Nonoligurgic patterns also occur (e.g., in toxin-mediated or interstitial causes or during early phases of AKI). ^[1]

Focused examination

• Initial assessment
  • Clinical assessment of volume status
  • Review of indwelling urinary catheter for kinks or plugs
• Abdominal examination
  • Suprapubic tenderness
  • Palpable bladder
  • Ballotable kidneys
  • Flank tenderness
  • Bruits
• Cardiac examination: signs of heart failure
• Neurological examination: signs of spinal cord lesions or cauda equina syndrome

General principles ^[1][4]

• Prompt evaluation of reduced urinary output is indicated to determine the underlying cause.
  • Hemodynamic assessment
  • Exclusion of UTO
  • Evaluation for intrinsic AKI
• Strict input/output monitoring
• See also “Noninvasive testing for specific underlying causes of AKI” and “Diagnostics for chronic kidney disease.”

Initial studies ^[1][5]

Laboratory studies

• Urinalysis
  • Urine dipstick: hematuria, proteinuria, and/or leucocytes
  • Urine osmolality
  • Urinary sediment: Urinary casts suggest intrinsic AKI.
• Urinary indices (e.g., fractional excretion of sodium to evaluate for AKI causes)
• Blood tests
  • BMP: serum creatinine, BUN, and electrolytes
  • Blood gases: ABG or VBG
  • Additional blood tests based on suspected diagnosis (e.g., creatine kinase in rhabdomyolysis)

Imaging studies

Imaging studies are used to evaluate for UTO.

• Renal and bladder ultrasound: preferred
• CT abdomen and pelvis: Consider when ultrasound is inconclusive.

Management is based on the underlying cause. ^[3][4][5]

• Discontinue nephrotoxic substances and adjust doses of renally cleared medications.
• Optimize renal perfusion, e.g.:
  • Fluid resuscitation in dehydration and hypovolemia
  • Immediate hemodynamic support in shock
  • Treatment of heart failure
• Management of intrinsic AKI causes
• Immediate relief of UTO
  • Management of lower UTO: bladder catheterization
  • Management of upper UTO: Consult urology.
  • Monitor for and manage postobstructive diuresis after decompression.
• See also “Treatment for the underlying cause of AKI” and “CKD management.”
• Monitor electrolytes, renal function, and acid-base balance.