• Oliguria is decreased urine output.
  • Infants: < 0.5 mL/kg per hour for 24 hours
  • Older children: < 500 mL/1.73 m² body surface area per day
• Anuria is absence of any urine output.
  • Normal, healthy newborns may have no urine output for 24 hours after birth.
• Oliguria is much more common than anuria but can lead to anuria, resulting in serious renal damage that requires specialized care.

• Incidence of oliguria or anuria is unknown in previously healthy children.
• In hospitalized patients
  • Oliguric acute renal failure (ARF) occurs in:
    • 10% of newborns in the intensive care unit
    • 2–3% of older children requiring intensive care
    • 8% of patients undergoing cardiac surgery
• Prevalence of ARF in newborns
  • Prerenal: 85%
  • Renal: 11%
  • Postrenal: 3%
• Prevalence of ARF in older children
  
  • Prerenal: 66%
  • Renal: 33%
  • Postrenal: < 1%

Causes of oliguria, anuria, and ARF

• Common causes of oliguria, anuria, or ARF are best defined in relation to the patient’s age.
• Prerenal ARF caused by dehydration is the most common cause of oliguria/anuria (70% of community-acquired cases of ARF and up to 60% of hospital-acquired cases).
• Renal ARF caused by intrinsic renal damage can be categorized into 3 types.
  • Acute tubular necrosis (ATN) results from prolonged ischemia or drug- or toxin-mediated renal tubular injury (reversible).
  • Glomerular lesions may occur with postinfectious glomerulonephritis.
  • Vascular lesions may occur with hemolytic-uremic syndrome or Henoch-Schönlein purpura.
• Postrenal ARF
  • Mechanical or functional obstruction to urine flow
    • May be in lower urinary tract, eg, posterior urethral valves
    • May be bilaterally in the upper tract, eg, bilateral ureteropelvic junction obstruction (rare)
  • Unilateral obstruction can cause ARF in patients with only 1 functioning kidney.
  • More common in newborns than in older infants

Most common causes of oliguria and anuria in neonates and children

• Neonates
  • Prerenal
    • Perinatal asphyxia
    • Respiratory distress syndrome
    • Hemorrhage
    • Sepsis or shock
    • Congenital heart disease
    • Dehydration
    • Drugs (indomethacin, maternal use of ACE inhibitors or nonsteroidal antiinflammatory drugs)
  • Renal
    • Acute tubular necrosis
    • Exogenous toxins (aminoglycosides, amphotericin B)
    • Endogenous toxins (hemoglobin, myoglobin, uric acid)
    • Congenital kidney diseases
    • Vascular (renal vein thrombosis, renal artery thrombosis)
  • Postrenal
    • Posterior urethral valves
    • Meatal stenosis
    • Bilateral ureteral obstruction
    • Neurogenic bladder
• Children
  • Prerenal
    • Dehydration
    • Hemorrhage
    • Burns
    • Third-space loss (surgery, trauma, nephrotic syndrome)
    • Renal loss (diabetes mellitus, diabetes insipidus, diuretics)
    • Shock
    • Decreased cardiac output
  • Renal
    • Acute tubular necrosis
    • Glomerulonephritis
    • Exogenous toxins (aminoglycosides, amphotericin B)
    • Endogenous toxins (hemoglobin, myoglobin, uric acid)
    • Vascular (hemolytic-uremic syndrome, vasculitis)
  • Postrenal
    • Posterior urethral valves
    • Meatal stenosis
    • Bilateral ureteral obstruction
    • Neurogenic bladder

• Common underlying comorbid conditions
  • Neurologic conditions
    • Compromised thirst mechanism
    • Serious disability and total dependence on others for nutrition and hydration, eg, patients with severe cerebral palsy
  • Renal diseases that impair ability to concentrate the urine, eg, salt-losing nephropathy or chronic renal failure
  • Gastrointestinal conditions that cause hypoalbuminemia and decreased intravascular volume, eg, celiac disease or hepatic failure
  • Endocrine disease, such as:
    • Diabetes insipidus, associated with increased hypotonic urine output
    • Diabetes mellitus, associated with osmolar diuresis
  • Hematologic conditions that impair urine concentration mechanism
• Oncologic emergencies, eg tumor lysis syndrome (causes renal failure, particularly if patient is not well hydrated)
• Therapy that may predispose to renal failure because they impair renal autoregulation in the presence of mild renal insufficiency or dehydration
  • Nonsteroidal antiinflammatory drugs
  • Angiotensin-converting enzyme inhibitors
  • Aminoglycosides
  • Radiologic contrast media

• Clinicians need to search for specific signs of underlying renal disease.
  • Severe anemia due to hemolytic-uremic syndrome
  • Butterfly rash on face/musculoskeletal involvement in systemic lupus erythematosus
  • Purpuric rash over buttocks and extensor surface of lower extremity in Henoch-Schönlein purpura.
  • Palpable kidney may be due to:
    • Renal vein thrombosis
    • Polycystic kidney disease
    • Multicystic dysplastic kidney
    • Hydronephrosis

• Palpable bladder with weak urine stream or dribbling suggests obstruction.
• Sacral tuft of hair or myelomeningocele may be seen with neurogenic bladder (can cause obstructive uropathy/postrenal oliguria or anuria).
• Symptoms of prerenal cause
  • Vomiting
  • Diarrhea
  • Hemorrhage
  • Sepsis
  • Decreased oral intake
  • Increased thirst
  • Palpitations
  • Fatigue
  • Clinical signs of dehydration
  • Weight loss
• Symptoms of hypovolemia (ie, prerenal pathology)
  • Tachycardia
  • Dry mucous membranes
  • Sunken eyes
  • Orthostatic blood pressure changes
  • Decreased skin turgor
  • Hypotension
• Symptoms of intrinsic renal disease
  • Gross hematuria
    • Pharyngitis or impetigo a few weeks before the onset of gross hematuria
  • Hypertension
  • Edema
  • Bloody diarrhea
    • Often precedes hemolytic-uremic syndrome
  • Younger children, particularly infants: signs of congestive heart failure
    • Hepatomegaly
    • Gallop rhythm
    • Pulmonary edema
• Symptoms of systemic vasculitis (eg, systemic lupus erythematosus)
  • May see history of fever, joint pains, and skin rash
• Recurrent sinusitis or lower respiratory tract infections may suggest Wegener granulomatosis.
• Hemoptysis may indicate pulmonary-renal syndrome, due to either:
  • Goodpasture syndrome
  • Microscopic polyangiitis

• Thorough history and physical examination are important in identifying the cause of oliguria or anuria.
  • Comprehensive physical examination is key to assessing severity of the disease process and possible cause.
  • In prerenal and postrenal ARF, early diagnosis and prompt treatment often result in quick recovery.
• Detailed history of recent or ongoing long-term medication use is important for excluding possible interstitial nephritis.
• In neonates, history of umbilical artery catheterization implies renal artery thrombosis.
• Family history is helpful in diagnosing such conditions as diabetes insipidus and polycystic kidney disease.

• Risk factors, history, and results of physical examination will help in the selection of appropriate laboratory tests.
• Urinalysis is the most important noninvasive diagnostic test.
  • Thorough examination of a freshly voided or bladder-catheterized urine sample helps distinguish prerenal from renal causes.
    • Normal or near-normal urinalysis, with few cells, few or no casts, or little or no proteinuria, is seen in prerenal disease, obstruction, and some cases of acute tubular necrosis.
    • A sample showing muddy-brown granular casts and epithelial cell casts strongly suggests acute tubular necrosis.
    • Erythrocyte casts are diagnostic of glomerulonephritis.
    • Proteinuria indicates glomerular disease.
• Urinary indices important for diagnosis of oliguria
  • Urinary sodium
    • < 10 mEq/L in oliguria resulting from intravascular volume depletion
    • Neonates: prerenal disease is associated with urine sodium concentration < 20–30 mEq/L.
  • Specific gravity
    • > 1020 in prerenal oliguria
  • Creatinine
    • Urine/plasma creatinine ratio > 40 in prerenal oliguria
    • Urine/plasma creatinine ratio < 20 if renal cause
  • Osmolality
    • Urine/plasma osmolality > 1.5 in prerenal oliguria
    • Urine/plasma osmolality < 1.5 if renal cause
• Fractional excretion of sodium
  
  • < 1% suggests reabsorption of almost all filtered sodium in response to decreased renal perfusion (prerenal).
  • In acute tubular necrosis: > 2%
• Blood urea nitrogen (BUN) and serum creatinine
  • In prerenal oliguria, increased BUN level is marked and the BUN/serum creatinine ratio is > 20.
  • BUN/creatinine ration of 10–15 suggests intrinsic renal damage.

• Renal ultrasonography
  • Generally not indicated in children with prerenal failure from dehydration who respond promptly to fluid resuscitation
  • Provides important information regarding
    • Kidney size and echogenicity
    • Renal blood flow
    • Collecting system
    • Urinary bladder
  • Children with intrinsic causes
    • Echogenic and slightly enlarged kidneys
  • Bilateral hydronephrosis or hydroureteronephrosis and bladder wall thickening indicate obstruction of bladder outlet causing postrenal oliguria/anuria.
  • Ultrasonography can detect congenital disorders, such as polycystic kidney disease and multicystic dysplastic kidney.
• Doppler examination of renal blood flow is helpful in diagnosing renal vascular thrombosis.

• Prerenal: dehydration is the most common cause of oliguria/anuria in children.
• Renal: intrinsic renal disorders, such as acute tubular necrosis and glomerulonephropathies
• Postrenal: obstruction to urinary flow in posterior urethral valves in boys

• Major goal of treatment of prerenal oliguria/anuria is to restore intravascular volume.
• Oliguria/anuria due to intrinsic renal conditions needs to be managed by a pediatric nephrologist.
• Urology needs to be consulted in patients with postrenal obstructive lesions.

• A dehydrated child with oliguria/anuria should receive a fluid bolus of normal saline or lactated Ringer’s solution at 20 mL/kg to restore fluid volume.
  • Depending on response, another bolus may be needed.
• Estimation of volume status is needed to begin and continue fluid therapy.
• Amount is assessed by history and physical exam that includes assessment of:
  • Body weight
  • Anterior fontanelle in infants
  • Heart rate
  • Mucous membranes
  • Skin turgor
  • Capillary refill
  • Peripheral edema
  • Blood pressure
• Children with oliguria and volume overload may:
  
  • Benefit from furosemide
  • Require fluid restriction
  • Need blood pressure and acid-base monitoring
• Children with oliguria due to obstruction may require urinary catheterization.
  • Relief of obstruction may be followed by postobstructive diuresis and may need fluid/electrolyte replacement.

• See When to Refer.

• Refer to a nephrologist or admit (or both) if child has any of the following:
  • Persistent oliguria or anuria despite adequate fluid challenge in a dehydrated child
  • Persistent oliguria or anuria that continues after removal of the offending nephrotoxins
  • Oliguria or anuria associated with:
    • Swelling
    • Hypertension
    • Gross hematuria
    • Abnormal blood chemistry
    • Severe systemic signs or symptoms
  • Urology referral for oliguria or anuria caused by obstructive uropathy

• The key to preventing oliguria or anuria is adequate hydration in at-risk patients.
  • Patients who have just undergone surgery
  • Patients receiving nephrotoxic medications
    • Amphotericin B
    • Acyclovir
    • Radiocontrast agent
  • Patients at risk of tumor lysis syndrome
  • Patients at risk of pigment nephropathy caused by hemoglobinuria or myoglobinuria

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• Andreoli SP. Clinical evaluation and management of acute renal failure. In: Avner ED, Harmon WE, Niaudet P, eds. Pediatric Nephrology. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004.
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• Moghal NE, Brocklebank JT, Meadow SR. A review of acute renal failure in children: incidence, etiology and outcome. Clin Nephrol. 1998;49:91-95.  [PMID:9524778]