Oliguria 

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 daily 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. (See Presentation and Workup.)^{[1, 2]}

Not all cases of acute renal failure are characterized by oliguria. Renal failure that results from nephrotoxic injury, interstitial nephritis, or neonatal asphyxia is frequently of the nonoliguric type, is related to a less severe renal injury, and has a better prognosis. In addition, the degree of oliguria depends on hydration and the 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. (See Prognosis, Presentation, Workup, Treatment, and Medication.)

Patient education

For patient education information, see the Diabetes Center, as well as Acute Kidney Failure and Chronic Kidney Disease.

Oliguria may result from prerenal, intrinsic renal, or postrenal processes.

Prerenal failure

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). (See the image below.)

Baroreceptor-mediated activation of the sympathetic nervous system and renin-angiotensin axis results in renal vasoconstriction and the resultant reduction in the GFR.

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 the image below.

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 angiotensin-converting enzyme (ACE) inhibitors can precipitate oliguric acute renal failure in individuals with reduced renal perfusion.

Intrinsic renal failure

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 led to a dramatic broadening of the etiology of pediatric acute renal failure. Although multicenter etiologic 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.^{[3, 4]}

Subsequent 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.^[5]

A 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.^[6]

Thus, the etiology of pediatric acute renal failure has evolved in industrialized 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 adenosine triphosphate [ATP], release of reactive oxygen species) and cell death, with resultant cell desquamation, cast formation, intratubular obstruction, backleak of tubular fluid, and oliguria. (See the image below.)

In most clinical situations, the oliguria is reversible and associated with repair and regeneration of tubular epithelial cells.

Postrenal failure

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

Principal causes of oliguric acute renal failure in neonates

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

Prerenal causes include the following:

• Perinatal asphyxia
• Respiratory distress syndrome
• Hemorrhage - Eg, maternal antepartum, twin-twin transfusion, and intraventricular
• Hemolysis
• Polycythemia
• Sepsis or shock
• Congenital heart disease
• Dehydration
• Drugs - Eg, indomethacin, maternal nonsteroidal anti-inflammatory drugs (NSAIDs), and maternal ACE inhibitors

Intrinsic renal causes include the following:

• Acute tubular necrosis
• Exogenous toxins - Eg, aminoglycosides, amphotericin B, and contrast agents
• Endogenous toxins - Eg, hemoglobin, myoglobin, and uric acid
• Congenital kidney disease - Eg, agenesis, polycystic kidney, hypoplasia, and dysplasia
• Vascular - Eg, renal vein thrombosis and renal artery thrombosis
• Transient renal dysfunction of the newborn

Postrenal causes include the following:

• Bladder outlet obstruction - Eg, posterior urethral valves and meatal stenosis
• Neurogenic bladder
• Ureteral obstruction, bilateral

Principal causes of oliguric acute renal failure in children

Prerenal causes include the following:

• Gastrointestinal (GI) losses - Eg, vomiting and diarrhea
• Blood losses - Eg, hemorrhage
• Renal losses - Eg, diabetes insipidus, diabetes mellitus, diuretics, and salt-wasting nephropathy
• Cutaneous losses - Eg, burns
• Third space losses - Eg, surgery, trauma, nephrotic syndrome, and capillary leak
• Shock - Eg, septic, toxic, and anaphylactic
• Impaired autoregulation - Eg, cyclosporine, tacrolimus, ACE inhibitors, and NSAIDs
• Impaired cardiac output - Eg, congenital and acquired heart disease

Intrinsic renal causes include the following:

• Acute tubular necrosis - Eg, prolonged prerenal failure
• Glomerulonephritis
• Interstitial nephritis, vascular - Eg, hemolytic-uremic syndrome and vasculitis
• Exogenous toxins - Eg, aminoglycosides, amphotericin B, cyclosporine, chemotherapy, heavy metals, and contrast agents
• Endogenous toxins - Eg, hemoglobin, myoglobin, and uric acid
• Transplant rejection

Postrenal causes include the following:

• Bladder outlet obstruction - Eg, posterior urethral valves, blocked catheter, and urethral trauma
• Neurogenic bladder
• Ureteral obstruction, bilateral

Occurrence in the United States

The frequency of oliguria widely varies depending on the clinical setting. In adults, the 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 intensive care unit (ICU) patients and in 2-3% of pediatric ICU patients. The incidence in children undergoing cardiac surgery is as high as 8%.

Age-related demographics

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.

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.

Although patients die with renal failure, however, they do not die not because of renal failure. The patient succumbs because of involvement of other systems during the period of renal insufficiency.^[7] The most common causes of death are sepsis, cardiovascular and pulmonary dysfunction, and withdrawal of life support. Oliguric acute renal failure is an independent risk factor for mortality, as well as for nonrenal complications.

The prognosis from prerenal causes of acute renal failure or from acute tubular necrosis in the absence of significant comorbid conditions is usually quite good if appropriate therapy is instituted in a timely fashion.

Complications

Infections develop in 30-70% of patients and affect the respiratory system, urinary tract, and indwelling catheters. Impaired defenses due to uremia and the inappropriate use of antibiotics may contribute to the high rate of infectious complications.

Cardiovascular complications are a result of fluid and sodium retention. They include hypertension, congestive heart failure, and pulmonary edema. Hyperkalemia results in electrocardiographic abnormalities and arrhythmias.

Other complications include the following:

• GI - Anorexia, nausea, vomiting, ileus, and bleeding
• Hematologic - Anemia and platelet dysfunction
• Neurologic - Confusion, asterixis, somnolence, and seizures
• Other electrolyte/acid-base disorders - Metabolic acidosis, hyponatremia, hypocalcemia, and hyperphosphatemia