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Oliguria Workup

  • Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD  more...
Updated: Jun 10, 2014

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.[14, 15] 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 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.

Contributor Information and Disclosures

Prasad Devarajan, MD, FAAP Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of the Nephrology Fellowship Program, Medical Director of the Kidney Stone Center, Co-Director of the Institutional Office of Pediatric Clinical Fellowships, Director of Clinical Nephrology Laboratory, CEO of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine

Prasad Devarajan, MD, FAAP is a member of the following medical societies: American Heart Association, American Society of Nephrology, American Society of Pediatric Nephrology, National Kidney Foundation, Society for Pediatric Research

Disclosure: Received none from Coinventor on patents submitted for the use of NGAL as a biomarker of kidney injury for none.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.


Laurence Finberg, MD Clinical Professor, Department of Pediatrics, University of California, San Francisco, School of Medicine and Stanford University School of Medicine

Laurence Finberg, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Luther Travis, MD Professor Emeritus, Departments of Pediatrics, Nephrology and Diabetes, University of Texas Medical Branch School of Medicine

Luther Travis, MD is a member of the following medical societies: Alpha Omega Alpha, American Federation for Medical Research, International Society of Nephrology, and Texas Pediatric Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Pathogenesis of prerenal failure
Compensatory mechanisms for preventing a fall in glomerular filtration rate (GFR) in the presence of prerenal failure
Mechanisms of intrinsic acute renal failure.
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