Updated: Feb 28, 2022
Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD 


Practice Essentials

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 kidney injury (AKI), previously referred to as 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]


A standardized definition of AKI has been proposed by the Kidney Disease: Improving Global Outcomes (KDIGO) AKI working group, which identifies and stages AKI based on changes in serum creatinine from baseline or a decrease in urine output (oliguria) as shown below.[3]

KDIGO Staging of AKI (Open Table in a new window)

Stage Serum creatinine Urine output

Increase by 1.5-1.9 times baseline within 7 days


Increase by 0.3 mg/dL (26.5 µmol/L) or more within 48 hours
Less than 0.5 mL/kg/h for 6-12 hours
2 Increase by 2-2.9 times baseline Less than 0.5 mL/kg/h for 12 hours or longer

Increase by 3 times baseline or greater


Increase to 4 mg/dL (353.6 µmol/L) or greater


Renal replacement therapy initiation


In patients younger than 18 years, decrease in estimated GFR to less than 35 mL/min/1.73m2

Less than 0.3 mL/kg/h for 24 hours or longer


Anuria for 12 hours or longer

In a cohort study of adults in an intensive care unit, Bianchi et al found that more than 77% of the patients met KDIGO criteria for AKI. The use of urinary output criteria enabled the researchers to detect AKI in patients who did not meet the serum creatinine criteria. Those patients whose AKI was identified solely by urinary output criteria, with no increase in serum creatinine, had a higher 90-day mortality than those without AKI. In addition, oliguria that lasted more than 12 hours (KDIGO stage 2 or 3) was associated with higher 90-day mortality, regardless of changes in serum creatinine levels.[4]

Not all cases of acute kidney injury 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 from eMedicineHealth, 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). 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 also includes enhanced tubular reabsorption of salt and water (stimulated by the renin-angiotensin-aldosterone system and sympathetic nervous system), resulting in a decrease in fractional excretion of sodium (FENa) and decreased urine output. See the image below.

Pathogenesis of prerenal failure Pathogenesis of prerenal failure

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.

Compensatory mechanisms for preventing a fall in g Compensatory mechanisms for preventing a fall in glomerular filtration rate (GFR) in the presence of prerenal failure

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.

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.

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. Recent experimental studies indicate that prerenal and intrinsic renal failure are distinct molecular entities and hence different disease states, despite similar degrees of oliguria and similar increases in serum creatinine concentrations. Prerenal failure is characterized by induction of protective molecular mechanisms within the kidney, whereas intrinsic renal failure upregulates kidney genes and pathways of cell injury, cell death, and inflammation.[5]

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 kidney injury. 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.[6, 7]

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.[8]

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 kidney injury.[9] 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.)

Mechanisms of intrinsic acute renal failure. Mechanisms of intrinsic acute renal failure.

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 acutekidney injuryin neonates

The etiology of oliguria varies with age, and the common causes in neonates and children are listed separately. Patients with acute kidney injury 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 kidney injury 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 North America

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 kidney injury occurs in approximately 10% of newborn intensive care unit (ICU) patients. The incidence in children undergoing cardiac surgery is as high as 10-30%. Among critically ill children admitted to pediatric ICUs (PICUs), the incidence of acute kidney injury defined by doubling of serum creatinine is present in about 5-6%. This was illustrated by a prospective study from a Canadian PICU that identified 985 cases of acute kidney injury for an incidence rate of 4.5% of all PICU admissions.[10] In the largest study reported to date, 3396 admissions to a single PICU in the United States were retrospectively analyzed.[11] Using serum creatinine criteria, 6% of children had acute kidney injury on admission and 10% developed acute kidney injury during their PICU stay.

A recent landmark international study of 4683 critically ill children utilized the KDIGO definition of AKI to demonstrate that the incidence of AKI was 27% when both serum creatinine and urine output criteria were used. Notably, more than two-thirds of the patients with oliguria did not meet the serum creatinine criteria for AKI – and low urine output alone conferred a significantly increased risk of death compared to elevated serum creatinine alone.[12]

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

In general, severe acute kidney injury can have serious short- and long-term consequences. The outcome depends upon the etiology, age of the child, and comorbidities. In terms of mortality, severe acute kidney injury requiring renal replacement therapy in children is still associated with a mortality rate of about 30-50%, and this has not changed appreciably over the past 3 decades. Infants younger than 1 year have the highest mortality rate.

In a PICU cohort, patients who presented with acute kidney injury on admission had a 32% mortality rate, and those who developed acute kidney injury at any time during the PICU stay had a 30% mortality rate.[11] Additionally, those with any degree of acute kidney injury at the time of PICU admission had higher PICU mortality than those with normal kidney function. Moreover, patients who developed any degree of acute kidney injury during PICU stay had higher ICU mortality than those without acute kidney injury during PICU stay. Multivariate logistic regression modeling controlling for age, sex, weight, race, and pediatric index of mortality score confirmed that acute kidney injury on admission to the PICU was associated with an increased risk of mortality (adjusted odds ratio, 5.4; 95% CI, 3.5-8.4). Development of acute kidney injury during the PICU stay was associated with an even greater risk of mortality (adjusted odds ratio, 8.7; 95% CI, 6.0-12.6) and a 4-fold increase in length of hospital stay.

In a retrospective analysis of 344 patients from the Prospective Pediatric Continuous Renal Replacement Therapy (ppCRRT) Registry, the overall mortality rate was 42%.[13] Survival was lowest in liver disease/transplantation (31%), pulmonary disease/transplantation (45%), and bone marrow transplantation (45%). Overall survival was better for children who weighed more than 10 kg (63% vs 43%; P = .001) and for those who were older than 1 year (62% vs 44%; P = .007).

Thus, it is now clear that patients die of acute kidney injury and its complications, and not simply with acute kidney injury.[14] The patient succumbs largely because of involvement of multiple other systems during the period of severe oliguric renal insufficiency. The most common causes of death are sepsis and cardiovascular or pulmonary dysfunction.

Information regarding the long-term outcome of children after an episode of severe acute kidney injury is scant but is beginning to accumulate.[15]

In a multicenter pooled analysis of 3476 children with hemolytic uremic syndrome followed for a mean of 4.4 years,[16] the combined average death and end-stage renal disease (ESRD) rate was 12% (95% CI, 10-15%) and the combined average renal sequelae rate (chronic kidney disease, proteinuria, hypertension) was 25% (95% CI, 20-30%). Thus, long-term follow-up appears to be warranted after an acute episode of hemolytic uremic syndrome.

In a retrospective study of 176 children who developed acute kidney injury in a single center, 34% had either reduced kidney function or were dialysis dependent at hospital discharge.[9] Upon 3-5 years of follow up of the same cohort, the mortality rate was 20%.[17] Approximately 60% developed evidence for chronic kidney disease (proteinuria, decreased glomerular filtration rate, hypertension) and 9% developed ESRD.

Collectively, these data strongly suggest that long-term follow-up is warranted for children who survive an episode of acute kidney injury.

In contrast to the above, the prognosis from prerenal causes of acute kidney injury 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.


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 broad-spectrum 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




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

A 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 or burns or following polyuric states, such as diabetes insipidus and diabetes mellitus.

The 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.


A detailed history of all recent medications should be obtained. In the presence of mild prerenal insufficiency, the administration of medications that impair renal autoregulation can precipitate oliguric acute kidney injury.

Cyclosporine, tacrolimus, and contrast agents are direct afferent arteriolar constrictors that interfere with the myogenic response.

NSAIDs inhibit the renal synthesis of vasodilatory prostaglandins. They are an important cause of oliguric acute kidney injury 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.

Endogenous tubular toxins

These include the following:

  • Myoglobin - Released following crush injuries, myositis, and prolonged grand mal seizures

  • Hemoglobin - Hemolysis

  • Uric acid -Tumor lysis syndrome


A history of ingesting undercooked meat may suggest the presence of hemolytic-uremic syndrome in a child with bloody diarrhea.

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

These symptoms include the following:

  • 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, including the following:

  • Frequent urinary tract infections

  • Hematuria

  • Proteinuria

  • Hypertension

  • Edema

  • Fatigue

  • Pallor

  • Anorexia

  • Bone pain

Physical Examination

Signs of intravascular volume depletion

The following may be noted:

  • Tachycardia

  • Orthostatic hypotension

  • Decreased skin turgor

  • Dry mucous membranes

Signs of acute kidney injury

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 not uncommon.

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 the 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. The external genitalia may reveal meatal stenosis or urethral trauma.

The diagnosis of obstruction may be strengthened by the reestablishment of urine output after the gentle passage of a catheter. Patients with indwelling urinary catheters who develop oliguria should undergo flushing of the catheter to rule out blockage.

Signs of chronic renal failure

The following may be noted:

  • Poor growth

  • Hypertension

  • Edema

  • Anemia

  • Renal osteodystrophy



Approach Considerations

The following studies are indicated in patients with oliguria:

  • Urinalysis

  • Urinary indexes

  • Blood urea nitrogen (BUN) and serum creatinine

  • Serum sodium

  • Serum potassium

  • Serum phosphate and calcium

  • Acid-base balance

  • Complete blood count (CBC)

Additional laboratory studies should be performed as indicated. Decreased complement levels (C3, C4) are characteristic of acute poststreptococcal glomerulonephritis but can also be observed in lupus nephritis and membranoproliferative glomerulonephritis. A suspected diagnosis of acute poststreptococcal glomerulonephritis can be confirmed by detection of elevated antistreptococcal titers.

The presence of antinuclear antibodies is suggestive of lupus nephritis, and antineutrophil cytoplasmic antibodies indicate vasculitis.

Imaging studies

Imaging studies in oliguria include the following:

  • Renal ultrasonography

  • Voiding cystourethrography - Indicated for suspected bladder outlet obstruction

  • Radionuclide renal scanning - May be useful in the assessment of transplant rejection and obstruction

  • Chest radiography - May be indicated if pulmonary edema is suspected

  • Echocardiography – May be useful in the presence of congestive heart failure


Careful examination of a freshly voided urine sample is a rapid and inexpensive way of distinguishing prerenal from intrinsic renal failure.

In prerenal failure, a few hyaline and fine, granular casts may be observed with little protein, heme, or red cells. Heme-positive urine in the absence of erythrocytes suggests hemolysis or rhabdomyolysis.

In intrinsic renal failure, hematuria and proteinuria are prominent. Broad, brown, granular casts are typically found in ischemic or toxic acute tubular necrosis, and red cell casts are characteristically observed in acute glomerulonephritis. The urine in acute interstitial nephritis shows white cells, especially eosinophils and white cell casts.

Urinary Indexes

Simultaneous measurement of urinary and serum sodium, creatinine, and osmolality can help to differentiate between prerenal azotemia, in which the reabsorptive capacity of tubular cells and the concentrating ability of the kidney are preserved or even enhanced, and intrinsic renal failure, in which these functions are impaired because of structural damage.

In prerenal failure, urine specific gravity is high (>1020), the ratio of urinary to plasma creatinine is high (>40), the ratio of urinary to plasma osmolality is high (>1.5), and the urinary sodium concentration is low (< 20 mEq/L).

In intrinsic renal failure, the opposite findings are encountered; ie, a urinary ̶ to ̶ plasma creatinine ratio of less than 20, a urinary–to–plasma osmolality ratio of less than 1.1, and a urinary sodium concentration of greater than 40 mEq/L.

Fractional excretion of sodium

The fractional excretion of sodium (FENa) is the percentage of filtered sodium that is excreted. It is easily calculated by the formula following formula:

%FENa = [(U/P)Na]/[(U/P)Cr] X 100

in which Na and Cr represent the concentrations of sodium and creatinine in the urine (U) and plasma (P), respectively. The %FENa is typically less than 1% in prerenal azotemia and greater than 2% in intrinsic renal failure.

Index assessment

Interpretation of urinary indexes requires caution. Blood and urinary specimens should be collected before the administration of fluids, mannitol, or diuretics. The urine should be free of glucose, contrast material, or myoglobin.

Urinary indexes suggestive of prerenal failure (eg, %FENa < 1, urinary sodium < 20mEq/L) can also be encountered in early glomerulonephritis, vasculitis and vascular occlusion, early postrenal failure, contrast nephropathy, and rhabdomyolysis. Also, the FENa may be falsely elevated in patients with prerenal failure and with increased urinary excretion of ketoacids or glucose.

BUN and Serum Creatinine

In prerenal failure, elevation of BUN levels is marked and the BUN-to-creatinine ratio is greater than 20. This reflects increased proximal tubular reabsorption of urea. The hallmark of established acute kidney injury is a daily increase in serum creatinine levels (0.5-1.5 mg/dL daily) and BUN levels (10-20 mg/dL daily).

Elevations in BUN levels can also result from steroid therapy, parenteral nutrition, GI bleeding, and catabolic states. A spurious elevation in serum creatinine can be encountered following the use of drugs that interfere with the tubular secretion of creatinine (eg, trimethoprim, cimetidine) or drugs that provide chromogenic substrates (eg, cephalosporins), which interfere with the Jaffé reaction for determination of serum creatinine.

Although serum creatinine levels are the criterion standard for diagnosis of acute kidney injury, they remain an unreliable indicator during acute changes in kidney function for the following reasons:

  • Serum creatinine levels can widely vary with age, gender, lean muscle mass, muscle metabolism, and hydration status

  • Serum creatinine levels may not change until about 50% of kidney function has already been lost

  • At lower rates of glomerular filtration, the increased amount of tubular secretion of creatinine results in overestimation of renal function

  • During acute changes in glomerular filtration, serum creatinine levels do not accurately depict kidney function until steady-state equilibrium has been reached, which may require several days

In the future, defining acute kidney injury by either a predictive biomarker of kidney damage or a sensitive measure of decrease in kidney function may be possible. Fortunately, the tools of modern science offer promising novel biomarkers for the early diagnosis of acute kidney injury and its clinical outcomes.[18, 19] These biomarkers are currently undergoing evaluation and validation and are not yet commercially available.

Serum Sodium

Hyponatremia is a common finding that is usually dilutional, secondary to fluid retention and administration of hypotonic fluids.

Less common causes of hyponatremia include sodium depletion (hyponatremic dehydration) and hyperglycemia (serum sodium concentration decreases by 1.6 mEq/L for every 100 mg/dL increase in serum glucose above 100 mg/dL).

Occasionally, hypernatremia may complicate oliguric acute kidney injury and is usually a result of excessive sodium administration (improper fluid administration or overzealous sodium bicarbonate therapy).

Serum Potassium

Hyperkalemia is an important complication because of reduced glomerular filtration, reduced tubular secretion, metabolic acidosis (each 0.1-unit reduction in arterial pH raises serum potassium by 0.3 mEq/L), and associated catabolic state.

Hyperkalemia is most pronounced in patients with excessive endogenous potassium production, which occurs in rhabdomyolysis, hemolysis, and tumor lysis syndrome.

Hyperkalemia represents a life-threatening emergency that must be promptly and aggressively treated, primarily because of its depolarizing effect on cardiac conduction pathways. Symptoms are nonspecific and may include malaise, nausea, and muscle weakness. A high index of suspicion and frequent measurement of serum potassium levels are therefore warranted in children with oliguric acute kidney injury.

Serum Phosphate and Calcium

Hyperphosphatemia and hypocalcemia frequently complicate oliguric acute kidney injury. The phosphate excess is secondary to reduced renal excretion and can result in hypocalcemia and calcium phosphate deposition in various tissues.

Hypocalcemia results from hyperphosphatemia-impaired GI calcium absorption because of inadequate active vitamin D production by the kidney, skeletal resistance to the calcemic action of parathyroid hormone, and coexistent hypoalbuminemia.

Determining ionized calcium levels is important because this unbound form of serum calcium determines physiologic activity. Ionized calcium can be estimated by assuming that 1 mg/dL of calcium is bound to 1 g/dL of albumin; thus, ionized calcium is the difference between total calcium and serum albumin concentration.

Acidosis increases the fraction of total calcium in the ionized form; thus, overzealous bicarbonate therapy can decrease ionized calcium. Severe hypocalcemia results in tetany, seizures, and cardiac arrhythmias.

Acid-Base Balance

The impaired renal excretion of nonvolatile acids and decreased tubular reabsorption and regeneration of bicarbonate results in metabolic acidosis with a high anion gap.

Severe acidosis can develop in children who are hypercatabolic (eg, shock, sepsis) or who have inadequate respiratory compensation.

The last 2 digits of the arterial pH provide a bedside estimate of respiratory compensation. Those numbers predict the partial pressure of carbon dioxide, or pCO2 (eg, a patient with arterial pH of 7.25 has adequate respiratory compensation if the arterial pCO2 is 25 ± 3 mm Hg).

Complete Blood Cell Count

Anemia is a result of dilution and decreased erythropoiesis. Microangiopathic hemolytic anemia with schistocytes and thrombocytopenia are indicative of hemolytic uremic syndrome.

Patients with oliguria that is secondary to systemic lupus erythematosus may display neutropenia and thrombocytopenia.

Eosinophilia is consistent with allergic interstitial nephritis. Prolonged acute kidney injury can result in functional platelet disorders.

Renal Ultrasonography

Ultrasonography of the kidneys and bladder with Doppler flow studies is essential. Exceptions may include children with unmistakable prerenal failure from dehydration who promptly respond to fluid resuscitation or those with mild renal insufficiency secondary to a nephrotoxin who respond to discontinuing the medication.

Ultrasonography provides important information regarding kidney size and echogenicity, renal blood flow, collecting system, and bladder wall.

Children with acute intrinsic renal failure display echogenic kidneys that may be enlarged. With prolonged renal failure, however, renal cortical necrosis may result in decreased kidney size. Bilaterally small and scarred kidneys are indicative of chronic renal disease. Congenital disorders, such as polycystic kidney disease and multicystic dysplasia, are easily detected. Calculi and tumors that can cause obstruction may also be detected.

A Doppler study is critical in the evaluation of vascular obstruction. Hydronephrosis, hydroureter, and a thickened bladder wall are consistent with an obstruction of the bladder outlet or with one below that.


Electrocardiography is indicated if hyperkalemia is suspected or has been detected by laboratory tests. The earliest sign is the appearance of tall peaked T waves. Recognizing and treating hyperkalemia at this early stage is important.

Subsequent findings include the following:

  • Prolongation of the PR interval

  • Flattening of P waves

  • Widening of QRS complexes

  • ST segment changes

  • Ventricular tachycardia

  • Terminal ventricular fibrillation

Renal Biopsy

In general, kidney biopsy is not necessary in the initial evaluation; however, if prerenal and postrenal causes have been ruled out and an intrinsic renal disease other than prolonged ischemia, nephrotoxin, or postinfectious glomerulonephritis is suspected, renal biopsy may be valuable in establishing diagnosis, guiding therapy, and providing prognosis.

Histologic examination is especially valuable in the diagnosis and management of transplant rejection, rapidly progressive glomerulonephritis, lupus nephritis, and tubulointerstitial nephritis.

Histologic Findings

Histology depends on the underlying cause. Only ischemic and nephrotoxic acute tubular necroses are discussed.

Ischemic acute tubular necrosis

In human ischemic acute tubular necrosis, frank tubule cell necrosis is rarely encountered. Instead, the prominent morphologic features include effacement and loss of proximal tubule brush border, patchy loss of tubule cells, focal areas of proximal tubular dilatation and distal tubular casts, and areas of cellular regeneration.

Necrosis is inconspicuous and restricted to the highly susceptible outer medullary regions of the kidney. The glomeruli are usually unimpressive, unless a primary glomerular disease caused the oliguria. This apparent disparity between the severe impairment of renal function and the relatively subtle histologic changes has traditionally been puzzling.

However, reconciliation of this seeming contradiction has been forthcoming from a consistent finding of apoptotic cell death in distal and proximal tubules in ischemic and nephrotoxic forms of intrinsic renal failure. In addition, a great deal of attention has been directed toward the peritubular capillaries, which display striking vascular congestion, endothelial damage, and leukocyte accumulation. Morphologically, several leukocyte subtypes have been shown to aggregate in peritubular capillaries, interstitial space, and even within tubules following ischemic acute renal failure, and their relative roles remain under investigation. Neutrophils are the earliest leukocytes to accumulate in the postischemic kidney.

Nephrotoxic acute tubular necrosis

In nephrotoxic acute tubular necrosis, the findings on light microscopy are generally characterized by more extensive and uniform tubular necrosis. Most of the proximal tubules display necrotic cell death, desquamation, and dilatation. A moderately severe interstitial edema may be observed. The glomeruli appear normal.



Approach Considerations

In clinical situations in which renal hypoperfusion or toxic injury is anticipated, therapy with fluids, mannitol, diuretics, and renal-dose dopamine is used to prevent or reverse renal injury. Although these maneuvers do not alter the natural history of acute kidney injury, they are capable of converting the oliguric state to a nonoliguric acute kidney injury, which is more easily managed because it obviates the need for fluid restriction and allows for maximal nutritional support.

Vigorous fluid administration has been successfully used to prevent acute kidney injury following cardiac surgery, cadaveric renal transplantation, hemoglobinuria, myoglobinuria, hyperuricosuria, radiocontrast infusion, and therapy with amphotericin B or cisplatinum.

A trial of intravenous (IV) mannitol or furosemide should be attempted in a patient with oliguria for less than 48 hours who has not responded to adequate hydration (although meta-analysis studies have failed to document a clear benefit that can be associated with the use of either furosemide or mannitol therapy).[20]

The benefit of renal-dose dopamine therapy is controversial.[21] Current recommendations are that it be considered for use in patients who are adequately hydrated and resistant to furosemide.

Once oliguria is established, mannitol may precipitate congestive heart failure; the risk of ototoxicity from furosemide and adverse hemodynamic changes from dopamine is significant.

Atrial natriuretic peptide

During the past decade, experimental studies in animals and humans have focused on restoration of renal hemodynamics and tubule cell integrity. Atrial natriuretic peptide (ANP) has been shown to improve renal function in animal models of ischemic acute kidney injury, predominantly via afferent arteriolar dilatation. In a large study of adults, ANP reduced the need for dialysis and improved survival in some patients with oliguric acute kidney injury. Further clinical trials with ANP are required to better define its therapeutic profile and optimal target population.

Other ongoing clinical trials include investigations into the role of growth factors such as insulinlike growth factor, nitric oxide inhibitors, antioxidants, and antagonists of endothelin receptors in human acute renal failure. However, in current practice, the efficacy of therapies such as dopamine, fenoldopam, and natriuretic peptides for the treatment of established acute kidney injury remains unproven and their routine use is not recommended.

Considerations in pharmacotherapy

Nephrotoxic agents should be avoided because they may worsen the renal injury and delay recovery of function. Such agents include contrast media, aminoglycosides, and NSAIDs.

Prescribing medication requires knowledge of the route of elimination and adjustments in dose or frequency based on residual renal function. Patients in the early phase with a rising creatinine should be assumed to have a glomerular filtration rate (GFR) of less than 10mL/min, irrespective of the absolute value for serum creatinine.


Consult a pediatric nephrologist for management of all cases of oliguria, except in children with prerenal insufficiency from dehydration who have promptly responded to fluid therapy or those with mild nephrotoxic injury who have responded to discontinuation of the drug. Consult a pediatric urologist for the management of obstruction.


If the patient with oliguria requires close monitoring of hemodynamic status or if indications for acute dialysis are present, transfer the patient to a center with ICU facilities.

Fluid Management

The major goal of fluid management is to restore and maintain normal intravascular volume. Patients with oliguric acute kidney injury may present with hypovolemia, euvolemia, or volume overload, and an estimation of fluid status is a prerequisite for initial and ongoing therapy. This is accomplished by determination of input and output, body weights, vital signs, skin turgor, capillary refill, peripheral edema, cardiopulmonary examination, serum sodium, and fractional excretion of sodium (FENa).

Children with intravascular volume depletion require prompt and vigorous fluid resuscitation. Initial therapy includes isotonic sodium chloride or lactated Ringer solution at 20mL/kg over 30 minutes, which can be repeated twice if necessary. This therapy should result in increased urine output within 4-6 hours. If oliguria persists (confirmed with bladder catheterization), central venous monitoring may be required to guide further management. Potassium administration is contraindicated until urine flow is established.

Oliguria with volume overload requires fluid restriction and intravenous furosemide. Failure to respond to furosemide suggests the presence of acute tubular necrosis rather than renal hypoperfusion, and fluid removal by dialysis or hemofiltration may be required, especially if signs of pulmonary edema are evident.

Potassium should be withheld until the oliguria improves and serum potassium levels begin to fall.

Monitoring treatment progress

Input and output records, daily weights, physical examination, and serum sodium guide ongoing therapy. When appropriate fluid therapy is administered, the body weight should decrease by 0.5-1.0% daily as a result of caloric deprivation, and the serum sodium concentration should remain steady. A more rapid weight loss and increasing serum sodium indicate inadequate fluid replacement. An absence of weight loss with decreasing serum sodium suggests excess free-water replacement.

Management of Hyperkalemia

In practice, the definitive therapy for significant hyperkalemia accompanying oliguric acute kidney injury frequently includes dialysis. The other forms of therapy outlined in this section serve primarily to tide over the crisis.

Serum potassium levels of 5.5-6.5 mEq/L should be treated by eliminating all sources of potassium from the diet or IV fluids and administration of a cation exchange resin, such as sodium polystyrene sulfonate (Kayexalate). Kayexalate requires several hours of contact with the colonic mucosa to be effective, and the rectal route of administration is preferred. Complications of this therapy include hypernatremia and constipation.

Emergency treatment of hyperkalemia is indicated when serum potassium exceeds 6.5mEq/L or if peaked T waves are present. In addition to Kayexalate, patients should receive calcium gluconate (with continuous electrocardiographic monitoring) to counteract the effects of hyperkalemia on the myocardium.

Uptake of potassium by cells can be stimulated by infusion of glucose and insulin or by beta-agonists (albuterol by nebulizer). The efficacy and convenience of nebulized albuterol has been well described in hemodialysis patients with hyperkalemia, but it can cause tachycardia.

Sodium bicarbonate, which also causes a rapid shift of potassium into cells, was the drug of choice in the past. However, the current recommendation is to use this therapy only in the concomitant presence of severe acidosis. Such therapy should be used with caution because it can precipitate hypocalcemia and sodium overload.

Management of Other Electrolytes and Acid-Base Balance

The primary treatment for hyponatremia is free water restriction; however, a serum sodium level of less than 120 mEq/L or accompanied central nervous system (CNS) dysfunction may require 3% sodium chloride infusion.

The management of hyperphosphatemia includes dietary restriction and oral phosphate binders (calcium carbonate or calcium acetate). Hypocalcemia usually responds to the oral calcium salts used for control of hyperphosphatemia but may require 10% calcium gluconate infusion if severe.

Mild metabolic acidosis is treated with oral sodium bicarbonate or sodium citrate. Severe acidosis (pH < 7.2), especially in the presence of hyperkalemia, requires IV bicarbonate therapy. Recognize that bicarbonate therapy requires adequate ventilation (to excrete the carbon dioxide produced) to be effective, and it may precipitate hypocalcemia and hypernatremia. Patients who cannot tolerate a large sodium load (eg, those with congestive heart failure) may be treated in an ICU setting with IV tromethamine (THAM), with provision of adequate ventilatory support pending institution of dialysis.

Management of Hypertension

Mild hypertension usually responds to salt restriction and diuretics. Moderate, asymptomatic hypertension is most commonly treated with oral or sublingual calcium channel blockers or with IV hydralazine.

For patients with hypertensive encephalopathy, treatment may require continuous sodium nitroprusside infusion with monitoring of thiocyanate levels. Because nitroprusside therapy requires careful drip calculations and administration, other immediate alternatives include a nicardipine drip or labetalol. Once the hypertensive crisis has been controlled, oral long-acting agents can be initiated.


The general goal of dialysis is to remove endogenous and exogenous toxins and to maintain the fluid, electrolyte, and acid-base balance until renal function returns. The indications for acute dialysis are not absolute, and the decision to use this modality depends on the rapidity of onset, duration, and severity of the abnormality to be corrected. Common indications include the following:

  • Fluid overload that is unresponsive to diuretics or a hindrance to adequate nutrition

  • Symptomatic acid-base imbalance, electrolyte imbalance, or both (especially hyperkalemia) that is unresponsive to nondialytic management

  • Refractory hypertension

  • Symptomatic uremia (CNS symptoms, pericarditis, pleuritis)

The choice between hemodialysis, peritoneal dialysis, and continuous venovenous hemodialysis (CVVH) depends on the overall clinical condition, the availability of technique, the etiology of the renal failure, institutional preferences, and specific indications or contraindications.

Peritoneal dialysis

In general, peritoneal dialysis is a gentler continuous method that was a more preferred technique in children in the past. It is not the treatment of choice for acute, severe fluid overload or hyperkalemia, however, because the onset of action is slower. Specific contraindications include abdominal wall defects, bowel distention, perforation or adhesions, and communications between the chest and abdominal cavities.


Hemodialysis requires vascular access, heparinization, a large extracorporeal blood volume, and skilled personnel, but it has the advantage of rapid correction of fluid, electrolyte, and acid-base imbalances. This therapy may be difficult to accomplish in hypotensive patients with multiorgan damage


CVVH has emerged as an alternative therapy for children who require fluid removal in an unstable, critically ill setting. The major advantage of these techniques is in their potential ability to remove fluid, even in a hypotensive child in whom hemodialysis may be contraindicated and peritoneal dialysis may be inefficient. However, patients require the presence of trained personnel and specialized equipment that are available only at select tertiary care centers.

Management of Urologic Obstruction

Patients with oliguria secondary to obstruction frequently require urologic care. The site of obstruction determines the primary therapy.

Obstruction of the bladder neck due to posterior urethral valves should be immediately relieved by gentle insertion of a fine urethral catheter. Foley catheters should not be used because the balloon may become lodged in the dilated prostatic urethra, resulting in incomplete bladder emptying.

The subsequent management of choice is endoscopic ablation of the valves. A temporary cutaneous vesicostomy may be required in a small infant whose urethra may not accept an endoscope or when hydronephrosis and renal function do not improve after catheterization.

Relief of obstruction is often followed by postobstructive diuresis. The resultant polyuria, hypokalemia, and hyponatremia should be managed with vigorous fluid replacement guided by frequent determinations of urinary flow rate, urinary electrolytes, and serum electrolytes.


Children with oliguric acute kidney injury are frequently in a highly catabolic state; therefore, aggressive nutritional support is important. Adequate calories should be provided to allow for maintenance requirements, and supplements should be provided to combat excessive catabolism. Children should be administered at least 150% of maintenance caloric intake and at least 3 g/kg/d of daily protein intake.

Protein of high biologic value should be administered in amounts that are sufficient to maintain neutral nitrogen balance, reflected by steady BUN levels.

Oral feeding is the preferred route. Infants should be placed on a low-phosphorus formula (Similac PM 60/40), and older children should be fed a low-phosphorus/low-potassium diet.

Additional calories may be supplied by fortifying foods with Polycose and medium-chain triglycerides.

Children who are nauseous or anorexic may benefit from enteral feedings. If these are not possible, central IV hyperalimentation may be used to deliver concentrated dextrose (25%) and lipids (20%).

If adequate nutrition cannot be achieved because of fluid restriction, early institution of ultrafiltration or dialysis should be considered.



Medication Summary

As previously mentioned, oliguria with volume overload requires fluid restriction and IV furosemide. If the patient fails to respond to furosemide, acute tubular necrosis, rather than renal hypoperfusion, may be present, and fluid may have to be removed by dialysis or hemofiltration, especially if signs of pulmonary edema are evident.

In patients with hyperkalemia, a cation exchange resin, such as sodium polystyrene sulfonate (Kayexalate), is administered when serum potassium levels rise to 5.5 mEq/L or above. When potassium exceeds 6.5 mEq/L or if peaked T waves are present on electrocardiography, calcium gluconate (with continuous electrocardiographic monitoring) should be administered along with it to counteract the effects of hyperkalemia on the myocardium.

Sodium bicarbonate is also used in cases of hyperkalemia but is recommended only when severe acidosis is present concomitantly. This agent can precipitate hypocalcemia and sodium overload and should therefore be used with caution.

A single-center retrospective study by Onder et al compared furosemide and aminophylline for the treatment for intraoperative oliguria. The study found that fewer of the patients in the aminophylline group required renal replacement therapy.[22]

Diuretics, Loop

Class Summary

In patients with recent-onset oliguria from prerenal or toxic injury who do not respond to hydration, agents such as mannitol and furosemide can convert the oliguric state to a nonoliguric acute renal failure, which is more easily managed. These agents may prevent tubule obstruction by increasing intratubular fluid flow via direct renal vasodilatory action and by decreased reabsorption of sodium and chloride.

Furosemide (Lasix)

Furosemide increases the excretion of water by interfering with the chloride-binding cotransport system. This interference inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.


Class Summary

Hyperkalemia in oliguric acute renal failure is a medical emergency that may be managed by shifting potassium into cells (sodium bicarbonate, glucose/insulin infusion, beta agonists), increasing the removal of potassium (exchange resins, dialysis), and protecting the myocardium (calcium).

Sodium bicarbonate (Neut)

Sodium bicarbonate is indicated for the treatment of hyperkalemia with concomitant acidosis. Sodium bicarbonate increases serum bicarbonate and reacts with hydrogen ions to form water and carbon dioxide. It acts as a buffer against acidosis by raising blood pH.

Calcium gluconate (Cal-Glu)

Calcium gluconate is indicated if hyperkalemia is accompanied by peaked T waves or if peaked T waves persist after bicarbonate therapy.


Class Summary

Hyperkalemia in oliguric acute kidney injury is a medical emergency that may be managed by agents that shift potassium into cells.

Insulin regular human (Novolin, Humulin)

This agent is used as an adjunct to bicarbonate therapy. Insulin promotes the intracellular shift of potassium. Administer insulin with dextrose to maintain serum glucose levels.

Sodium polystyrene sulfonate (Kayexalate, Kalexate, Kionex)

This agent is indicated in all cases of hyperkalemia. Sodium polystyrene sulfonate exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, and decreases total body potassium. The onset of action after oral administration ranges from 2-12 hours.

Calcium Salts

Class Summary

Oliguric acute kidney injury is frequently complicated by hyperphosphatemia and hypocalcemia, which respond to calcium-containing oral phosphate binders.

Calcium carbonate (Nephro-Calci, Caltrate)

Calcium carbonate successfully normalizes phosphate concentrations in patients on dialysis. It combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces. Calcium carbonate is marketed in various dosage forms and is relatively inexpensive.

Alkalinizing Agents

Class Summary

Mild metabolic acidosis is treated with oral sodium citrate. Severe acidosis requires IV bicarbonate, as previously discussed.

Citrate and citric acid (Bicitra, Oracit)

This drug combination is used to treat metabolic acidosis and is employed as an alkalinizing agent when long-term maintenance of alkaline urine is desirable.