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Pediatric Acute Tubular Necrosis Workup

  • Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD  more...
Updated: Jan 19, 2016

Approach Considerations

The following studies are indicated in patients with acute tubular necrosis (ATN):

  • Urinalysis
  • Urinary indexes
  • Blood urea nitrogen (BUN) and serum creatinine
  • Serum electrolytes (sodium, potassium, phosphate, and calcium)
  • Arterial blood gases
  • Complete blood cell count

Although acute renal failure (ARF) is usually secondary to ischemic or nephrotoxic injury, other causes of intrinsic ARF should be kept in mind and excluded by history, physical examination, and laboratory evaluation. Laboratory evaluation should include urine cultures and serologic tests (including C3 and C4 in all patients) and lupus serologies and hepatitis profiles when appropriate.



Careful examination of freshly voided urine is a rapid and inexpensive way of distinguishing prerenal failure from ATN. In prerenal failure, a few hyaline and fine granular casts may be observed with little protein, heme, or red blood cells (RBCs). Broad, brown granular casts are typically found in ischemic or nephrotoxic ATN. Heme-positive urine in the absence of erythrocytes in the sediment suggests ATN due to hemolysis or rhabdomyolysis.


Urinary Indices

Simultaneous measurement of urinary and serum sodium, creatinine, and osmolality can help differentiate between prerenal azotemia (in which the reabsorptive capacity and concentrating ability of the kidney are preserved or enhanced) and ATN (in which these functions are impaired).

In prerenal failure, urine specific gravity and the ratio of urine to plasma creatinine levels are high, and the urinary sodium concentration is low (see Table, below). In contrast, the urine in ATN is isosthenuric with a low urine-to-plasma creatinine ratio and high urine sodium concentration.

The fractional excretion of sodium (FENa) is the percentage of filtered sodium that is excreted. It is easily calculated by the formula FENa (%) = ([U/P]Na)/([U/P]Cr) x 100, where Na and Cr represent concentrations of sodium and creatinine in the urine (U) and plasma (P), respectively. The FENa is typically more than 1% in ATN and less than 1% in prerenal azotemia. Be alert to the fact that FENa may be low in intrinsic renal failure from glomerular diseases.

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

Urinary indexes suggestive of prerenal failure (FENa, < 1%) may be observed in the ATN of contrast nephropathy and rhabdomyolysis (see Table, below).

Table. Urinary Indexes in Acute Tubular Necrosis vs Prerenal Failure (Open Table in a new window)

  ATN Prerenal
Urine specific gravity 1010 >1020
Urine sodium (mEq/L) >40 < 10
Urine/plasma creatinine < 20 >40
FENa (%) >2 < 1

Measurement of Blood Urea Nitrogen and Serum Creatinine Levels

The hallmark of established ARF is a daily increase in serum creatinine (by 0.5-1.5 mg/dL/d) and BUN (by 10-20 mg/dL/d) levels. In ATN, the BUN-to-creatinine ratio is usually around 10, as opposed to a ratio of more than 20 that is commonly observed in prerenal failure (due to enhanced proximal tubular reabsorption of urea). However, the BUN-to-creatinine ratio may be misleading in patients whose conditions are wasting or in infants with physiologically low muscle mass.[30]

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

Serum creatinine is the current criterion standard for the diagnosis of ARF. However, important limitations have been noted, as follows:

  • First, serum creatinine levels can widely vary with age, sex, lean muscle mass, muscle metabolism, and hydration status.
  • Second, serum creatinine levels may not change until about 50% of kidney function has been lost.
  • Third, at lower glomerular filtration rates (GFRs), the amount of tubular secretion of creatinine results in overestimation of renal function.
  • Finally, during acute changes in glomerular filtration, serum creatinine does not accurately depict kidney function until steady-state equilibrium has been reached, which may require several days.

In the future, defining ARF by either a predictive biomarker of kidney damage or a sensitive measure of decrease in kidney function may be appropriate. Fortunately, novel biomarkers are currently undergoing evaluation and validation.[31, 32]

Go to Novel Biomarkers of Renal Function for more complete information on this topic.


Determination of Serum Electrolyte Concentrations

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

Hyperkalemia is a common and often serious complication of ATN. Contributing factors include reduced GFR, reduced tubular secretion, metabolic acidosis (each 0.1 unit reduction in arterial pH raises serum potassium by 0.3-0.4 mEq/L), and associated catabolic state. Hyperkalemia is most pronounced in individuals with excessive endogenous potassium production, such as in rhabdomyolysis, hemolysis, and tumor lysis syndrome. Symptoms are nonspecific and may include malaise, nausea, and muscle weakness.

Hyperkalemia represents a life-threatening emergency that must be promptly and aggressively treated, primarily because of its depolarizing effect on cardiac conduction pathways.

Hyperphosphatemia and hypocalcemia frequently complicate ATN. The phosphate excess is secondary to reduced renal excretion and can lead to hypocalcemia and calcium phosphate deposition in various tissues.

Hypocalcemia results predominantly from hyperphosphatemia and impaired absorption of calcium from the GI tract because of inadequate 1,25-hydroxyvitamin D3 production by the diseased kidneys. Severe hypocalcemia results in tetany, seizures, and cardiac arrhythmias.

Determining ionized calcium concentration may be important because this unbound form of serum calcium determines physiologic activity. Acidosis increases the fraction of serum calcium that is in the ionized form, while correction of acidosis may decrease it; thus, overzealous bicarbonate therapy can acutely decrease ionized calcium.

Hypomagnesemia is a prominent finding in nephrotoxic ATN, particularly associated with gentamicin, amphotericin B, cisplatinum, or pentamidine administration.


Evaluation of Acid-Base Balance

The high anion gap metabolic acidosis of ATN is a consequence of impaired renal excretion of nonvolatile acids. Decreased tubular reabsorption of bicarbonate further contributes to the metabolic acidosis.

Severe acidosis can develop in children who are hypercatabolic (shock, sepsis) or who have inadequate respiratory compensation.[24]


Complete Blood Cell Count

A mild-to-moderate anemia is commonly observed as a result of dilution and decreased erythropoiesis. Severe anemia should prompt a search for hemolysis from a variety of causes, because it can result in hemoglobinuric ATN. These patients usually display elevated serum lactate dehydrogenase levels.

Microangiopathic hemolytic anemia with schistocytes and thrombocytopenia are indicative of possible hemolytic-uremic syndrome (HUS), which is an important cause of intrinsic ARF in children.

Prolonged ATN also can result in bleeding due to dysfunctional platelets.


Tests for Rhabdomyolysis and Tumor Lysis Syndrome

A suspicion of rhabdomyolysis may be confirmed by direct determination of urinary myoglobin and elevation of serum creatine kinase (specifically the CK3 isoenzyme). Children with rhabdomyolysis also usually display marked increases in serum potassium and phosphate.

In the tumor lysis syndrome following cancer chemotherapy, a marked elevation in serum uric acid occurs along with hyperkalemia and hyperphosphatemia.


Determination of Serum Nephrotoxin levels

Serum levels of nephrotoxins should be determined and serially followed, particularly when using gentamicin, vancomycin, cyclosporine, or tacrolimus.


Renal Ultrasonography

Ultrasonography of the kidneys and bladder with Doppler flow is essential in the workup of ARF. Exceptions to this rule may include children with unmistakable prerenal failure from well-documented dehydration who respond promptly to fluid therapy or children with renal insufficiency secondary to obvious glomerular disease, hypoxia-ischemia, or exposure to nephrotoxins.[33]

Ultrasonography provides important information regarding kidney size, contour, echogenicity, corticomedullary differentiation, and blood flow. In ischemic or nephrotoxic ATN, the kidneys are of normal size or slightly enlarged, with increased echogenicity. With prolonged ATN, renal cortical necrosis may result in decreased kidney size. Bilateral small scarred kidneys are indicative of chronic renal disease.

Congenital disorders, such as polycystic kidney disease and multicystic dysplasia, are easily detected, and calculi and tumors are also evident. Hydronephrosis is suggestive of urinary tract obstruction, and accompanying hydroureter and a thickened bladder wall are consistent with bladder outlet obstruction. A Doppler study is important in the evaluation of vascular obstruction.


Radionuclide Scanning

Radionuclide scans (functional scans with mercaptotriglycylglycine [MAG-3] or diethylenetriamine penta-acetic acid [DTPA]) are useful in the assessment of obstruction and may provide additional information regarding GFR, renal blood flow, and tubule function. Their major clinical use in children with ATN is in the immediate posttransplant period, when scans can help differentiate between ATN and transplant rejection.[34]



Perform electrocardiography (ECG) if hyperkalemia is suspected or detected by laboratory tests. The following are sequential ECG changes in hyperkalemia:

  • Tall peaked T waves
  • Prolongation of PR interval
  • Widening of QRS complex
  • ST segment changes
  • Ventricular tachycardia
  • Terminal ventricular fibrillation

Renal Biopsy

In general, a kidney biopsy is not necessary in the initial evaluation; however, if prerenal and postrenal causes of ARF have been ruled out and an intrinsic renal disease other than ischemic ATN, nephrotoxic ATN, HUS, or postinfectious glomerulonephritis is a possibility, renal biopsy findings may be valuable in establishing the diagnosis, guiding therapy, and assessing prognosis. Renal biopsy findings may be also useful in the immediate posttransplant period for differentiating between ATN and acute rejection.


Histologic Findings

Typical histologic findings in ATN include the following:

  • Patchy loss of tubular epithelial cells with resultant gaps and exposure of denuded basement membrane
  • Diffuse effacement and loss of proximal tubule cell brush border
  • Patchy necrosis, most typically in the outer medulla where the straight (S3) segment of the proximal tubule and the medullary thick ascending limb (mTAL) of the loop of Henle are located
  • Tubular dilatation and intraluminal casts in the distal nephron segments
  • Evidence of cellular regeneration

Regenerating cells are often detected in biopsies together with freshly damaged cells, suggesting the occurrence of multiple cycles of injury and repair.

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.


Richard Neiberger, MD, PhD Director of Pediatric Renal Stone Disease Clinic, Associate Professor, Department of Pediatrics, Division of Nephrology, University of Florida College of Medicine and Shands Hospital

Richard Neiberger, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Medical Association, American Society of Nephrology, American Society of Pediatric Nephrology, Christian Medical & Dental Society, Florida Medical Association, International Society for Peritoneal Dialysis, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Shock Society, Sigma Xi, Southern Medical Association, Southern Society for Pediatric Research, and Southwest Pediatric Nephrology Study Group

Disclosure: The Osler Institute Honoraria Speaking and teaching

Adrian Spitzer, MD Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director of NIH Training Program, Children's Hospital at Montefiore Medical Center

Adrian Spitzer, MD is a member of the following medical societies: American Academy of Pediatrics, American Federation for Medical Research, American Pediatric Society, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, and Society for Pediatric Research

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.

Robert Woroniecki, MD Assistant Professor, Department of Pediatrics, Section of Pediatric Nephrology, Albert Einstein College of Medicine, Children's Hospital of Montefiore

Disclosure: Nothing to disclose.

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Common causes of oliguric versus nonoliguric acute renal failure in children.
Metabolic alterations in tubule cells following acute tubular necrosis.
Compensatory mechanisms that maintain glomerular filtration rate despite a reduction in renal perfusion pressure.
Pathogenesis of acute tubular necrosis (macrovascular changes).
Alterations in tubule cell morphology in acute tubular necrosis.
Table. Urinary Indexes in Acute Tubular Necrosis vs Prerenal Failure
  ATN Prerenal
Urine specific gravity 1010 >1020
Urine sodium (mEq/L) >40 < 10
Urine/plasma creatinine < 20 >40
FENa (%) >2 < 1
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