eMedicine Specialties > Pediatrics: General Medicine > Nephrology

Oliguria

Author: Prasad Devarajan, MD, Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of Clinical Nephrology Laboratories, Chief Executive Officer of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine
Contributor Information and Disclosures

Updated: Dec 3, 2008

Introduction

Background

Oliguria is defined as a urine output that is less than 1 mL/kg/h in infants, less than 0.5 mL/kg/h in children, and less than 400 mL/d in adults. It is one of the clinical hallmarks of renal failure and has been used as a criterion for diagnosing and staging acute renal failure. At onset, oliguria is frequently acute. It is often the earliest sign of impaired renal function and poses a diagnostic and management challenge to the clinician. All cases of acute renal failure are not characterized by oliguria. For example, subjects with acute renal failure due to nephrotoxins, interstitial nephritis, or neonatal asphyxia are typically nonoliguric. In addition, the degree of oliguria depends on hydration and concomitant use of diuretics.   

In most clinical situations, acute oliguria is reversible and does not result in intrinsic renal failure. However, identification and timely treatment of reversible causes is crucial because the therapeutic window may be small.

Pathophysiology

Oliguria may result from 3 broad pathophysiologic processes: prerenal, intrinsic renal, and postrenal mechanisms.

Prerenal insufficiency is a functional response of structurally normal kidneys to hypoperfusion. Globally, prerenal insufficiency accounts for approximately 70% of community-acquired cases of acute renal failure and as many as 60% of hospital-acquired cases. A decrease in circulatory volume evokes a systemic response aimed at normalizing intravascular volume at the expense of the glomerular filtration rate (GFR).

Baroreceptor-mediated activation of the sympathetic nervous system and renin-angiotensin axis results in renal vasoconstriction and the resultant reduction in the GFR (see Media file 1). The early phase of renal compensation for reduced perfusion includes autoregulatory maintenance of the GFR via afferent arteriolar dilatation (induced by myogenic responses, tubuloglomerular feedback, and prostaglandins) and via efferent arteriolar constriction (mediated by angiotensin II). These changes are shown in Media file 2.   

The early phase also includes enhanced tubular reabsorption of salt and water (stimulated by the renin-angiotensin-aldosterone system and sympathetic nervous system). Rapid reversibility of oliguria following timely reestablishment of renal perfusion is an important characteristic and is the usual scenario in prerenal insufficiency. For example, oliguria in infants and children is most often secondary to dehydration and reverses without renal injury if the dehydration is corrected. However, prolonged renal hypoperfusion can result in a deleterious shift from compensation to decompensation.

This decompensation phase is characterized by excessive stimulation of the sympathetic and renin-angiotensin systems, with resultant profound renal vasoconstriction and ischemic renal injury. Iatrogenic interference with renal autoregulation by administration of vasoconstrictors (eg, cyclosporine, tacrolimus), inhibitors of prostaglandin synthesis (eg, nonsteroidal anti-inflammatory drugs), or ACE inhibitors can precipitate oliguric acute renal failure in individuals with reduced renal perfusion.

Intrinsic renal failure is associated with structural renal damage. This includes acute tubular necrosis (from prolonged ischemia, drugs, or toxins), primary glomerular diseases, or vascular lesions. Advancements in the care of critically ill neonates, infants with congenital heart disease, and children who undergo bone marrow and solid organ transplantation have lead to a dramatic broadening of the epidemiology of pediatric acute renal failure. Although multicenter epidemiological data on pediatric acute renal failure are not available, single-center data and literature reviews from the 1980s and 1990s reported hemolytic uremic syndrome and other primary renal diseases as the most prevalent causes.

More recent single-center data have detailed the underlying causes of pediatric acute renal failure in large cohorts of children. In a study of 226 children with acute renal failure, Bunchman et al reported that congenital heart disease, acute tubular necrosis, sepsis, and bone marrow transplantation were the most common causes.¹ Another retrospective review of 248 patients with a diagnosis of acute renal failure upon discharge or death revealed acute tubular necrosis and nephrotoxins to be the most common causes of acute renal failure.² Thus, the epidemiology of pediatric acute renal failure has evolved in developed countries from primary kidney diseases or prerenal failure to secondary effects of other systemic illnesses or their treatment.

The pathophysiology of ischemic acute tubular necrosis is well studied. Ischemia leads to altered tubule cell metabolism (eg, depletion of ATP, release of reactive oxygen species) and cell death with resultant cell desquamation, cast formation, intratubular obstruction, backleak of tubular fluid, and oliguria (see Media file 3). In most clinical situations, the oliguria is reversible and associated with repair and regeneration of tubular epithelial cells.

Postrenal failure is a consequence of mechanical or functional obstruction to the flow of urine. This form of oliguria and renal insufficiency usually responds to release of the obstruction.

Renal failure is not always associated with oliguria. Renal failure that results from nephrotoxic injury, interstitial nephritis, and neonatal asphyxia is frequently of the nonoliguric type, is related to a less severe renal injury, and has a better prognosis.

Frequency

United States

Frequency widely varies depending on clinical setting. In adults, incidence is about 1% at admission, 2-5% during hospitalization, and 4-15% after cardiopulmonary bypass. Oliguric acute renal failure occurs in approximately 10% of newborn ICU patients and 2-3% of pediatric ICU patients. Incidence in children undergoing cardiac surgery is as high as 8%.

Mortality/Morbidity

Mortality rates in oliguric acute renal failure widely vary according to the underlying cause and associated medical condition. It ranges from 5% for patients with community-acquired acute renal failure to 80% among patients with multiorgan failure in the ICU.

The most common causes of death are sepsis, cardiovascular and pulmonary dysfunction, and withdrawal of life support.

Race

No racial predilection is noted.

Sex

Both sexes are equally affected.

Age

Oliguria affects people of all ages. It is more common in neonatal and older age groups because of comorbid conditions and is more common in early childhood because of the high incidence of illnesses that lead to dehydration.

Clinical

History

Careful evaluation of the patient's history and physical examination often reveals the cause of oliguria. This is especially important in prerenal and postrenal processes because early diagnosis and treatment frequently results in complete recovery.

• Fluid losses 
  • Recent history of diarrhea or vomiting should be sought because this is the most common cause in children.
  • Less commonly, fluid loss may result from traumatic hemorrhage, burns, or following polyuric states such as diabetes insipidus and diabetes mellitus.
  • Loss of intravascular fluid volume into the interstitial space accompanies surgery, shock syndromes, and nephrotic syndrome. Children with fluid losses may report thirst, dizziness, palpitations, and fatigue, and a history of weight loss may be present.
• Drugs
  • A detailed history of recent medications should be obtained. In the presence of mild prerenal insufficiency, administration of medications that impair renal autoregulation can precipitate oliguric acute renal failure.
  • Cyclosporine, tacrolimus, and contrast agents are direct afferent arteriolar constrictors that interfere with the myogenic response.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the renal synthesis of vasodilatory prostaglandins. They are an important cause when administered to febrile children with intercurrent dehydration.
  • Drugs that induce direct tubular necrosis include aminoglycosides, amphotericin B, cyclosporine, tacrolimus, antineoplastic agents (eg, methotrexate, cisplatin), and contrast agents.
  • Acyclovir and sulfonamides can precipitate within the tubular lumen and result in obstruction.
  • In addition, a large number of medications, especially penicillins, cephalosporins, sulfonamides, ciprofloxacin, NSAIDs, and diuretics, can cause interstitial nephritis.
  • History of ingesting undercooked meat may suggest hemolytic-uremic syndrome.
• Endogenous tubular toxins
  • Myoglobin (released following crush injuries, myositis, and prolonged grand mal seizures)
  • Hemoglobin (hemolysis)
  • Uric acid (tumor lysis syndrome)
• Symptoms of glomerular disease
  • Many children have a history of gross hematuria and edema. An antecedent streptococcal infection may suggest a postinfectious glomerulonephritis, and a history of bloody diarrhea often precedes the hemolytic-uremic syndrome.
  • Suspect systemic lupus erythematosus or allergic interstitial nephritis in children with fever, joint symptoms, and skin rashes who present with oliguria.
  • A history of recurrent sinusitis or lower respiratory tract infections may suggest Wegener granulomatosis, and hemoptysis may suggest Goodpasture disease.
• Symptoms of urinary tract obstruction
  • Complete absence of urine output
  • Alternating periods of polyuria and oligoanuria
  • Poor urinary stream or dribbling
• Symptoms of chronic renal failure
  • Although oliguria is usually acute at initial presentation, it may also be a presenting symptom of chronic renal failure.
  • Children may have additional symptoms suggestive of previous renal disease such as frequent urinary tract infections, hematuria, proteinuria, hypertension, edema, fatigue, pallor, anorexia, and bone pain.

Physical

• Signs of intravascular volume depletion
  • Tachycardia
  • Orthostatic hypotension
  • Decreased skin turgor
  • Dry mucous membranes
• Signs of acute renal failure
  • Children may present with edema, anemia, and signs of congestive heart failure such as hepatomegaly, gallop rhythm, and pulmonary edema.
  • Hypertension is common, especially in acute glomerulonephritis, and may be secondary to volume overload and alterations in vascular tone.
  • Although many children with hypertension are asymptomatic, encountering patients with signs of congestive heart failure, visual disturbances, or encephalopathy is common.
• Signs specific to the underlying renal disease
  • A butterfly rash on the face and joint swelling are highly suggestive of systemic lupus erythematosus.
  • Patients with Henoch-Schönlein purpura present with a characteristic purpuric rash over the buttocks and extensor surface of the lower extremity.
  • Acute interstitial nephritis may be accompanied by fever, arthralgias, and fleeting maculopapular or urticarial rashes.
  • Various skin rashes may be detected in vasculitides.
  • Oliguria with palpable kidneys during infancy suggests renal vein thrombosis, polycystic kidneys, multicystic dysplasia, or hydronephrosis. In older children, enlarged kidneys should also raise the suspicion of tumors. A transplanted kidney that is tender to palpation is indicative of rejection.
• Signs of postrenal failure
  • Poor urinary stream, urinary dribbling, and a palpably enlarged urinary bladder are indicative of obstruction. Diagnosis may be strengthened by reestablishment of urine output after gentle passage of a catheter.
  • The external genitalia may reveal meatal stenosis or urethral trauma. Patients with indwelling urinary catheters who develop oliguria should undergo flushing of the catheter to rule out blockage.
• Signs of chronic renal failure
  • Poor growth
  • Hypertension
  • Edema
  • Anemia
  • Renal osteodystrophy

Causes

Etiology varies with age, and the common causes in neonates and children are listed separately. Subjects with acute renal failure secondary to nephrotoxins, interstitial nephritis, and perinatal asphyxia frequently do not have oliguria. 

• Principal causes of oliguric acute renal failure in neonates
  • Prerenal
    • Perinatal asphyxia
    • Respiratory distress syndrome
    • Hemorrhage (eg, maternal antepartum, twin-twin transfusion, intraventricular)
    • Hemolysis
    • Polycythemia
    • Sepsis or shock
    • Congenital heart disease
    • Dehydration
    • Drugs (eg, indomethacin, maternal NSAIDs, maternal ACE inhibitors)
  • Intrinsic renal
    • Acute tubular necrosis
    • Exogenous toxins (eg, aminoglycosides, amphotericin B, contrast agents)
    • Endogenous toxins (eg, hemoglobin, myoglobin, uric acid)
    • Congenital kidney disease (eg, agenesis, polycystic kidney, hypoplasia, dysplasia)
    • Vascular (eg, renal vein thrombosis, renal artery thrombosis)
    • Transient renal dysfunction of the newborn
  • Postrenal
    • Bladder outlet obstruction (eg, posterior urethral valves, meatal stenosis)
    • Neurogenic bladder
    • Ureteral obstruction, bilateral
• Principal causes of oliguric acute renal failure in children
  • Prerenal
    • GI losses (eg, vomiting, diarrhea)
    • Blood losses (eg, hemorrhage)
    • Renal losses (eg, diabetes insipidus, diabetes mellitus, diuretics, salt-wasting nephropathy)
    • Cutaneous losses (eg, burns)
    • Third space losses (eg, surgery, trauma, nephrotic syndrome, capillary leak)
    • Shock (eg, septic, toxic, anaphylactic)
    • Impaired autoregulation (eg, cyclosporine, tacrolimus, ACE inhibitors, NSAIDs)
    • Impaired cardiac output (eg, congenital and acquired heart disease)
  • Intrinsic renal
    • Acute tubular necrosis (eg, prolonged prerenal failure)
    • Glomerulonephritis
    • Interstitial nephritis, vascular (eg, hemolytic-uremic syndrome, vasculitis)
    • Exogenous toxins (eg, aminoglycosides, amphotericin B, cyclosporine, chemotherapy, heavy metals, contrast agents)
    • Endogenous toxins (eg, hemoglobin, myoglobin, uric acid)
    • Transplant rejection
  • Postrenal
    • Bladder outlet obstruction (eg, posterior urethral valves, blocked catheter, urethral trauma)
    • Neurogenic bladder
    • Ureteral obstruction, bilateral

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