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Pediatric Acute Tubular Necrosis

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


Acute tubular necrosis (ATN) is clinically characterized by acute renal failure (ARF), which is defined as a rapid (hours to days) decline in the glomerular filtration rate (GFR) that leads to retention of waste products such as BUN and creatinine.[1, 2, 3, 4, 5, 6, 7, 8, 9, 10]

The various etiologies of ARF can be grouped into 3 broad categories: prerenal, intrinsic renal, and postrenal. Prerenal ARF (55% of ARF cases) is a functional response of structurally normal kidneys to hypoperfusion, whereas postrenal ARF (< 5% of ARF cases) is a consequence of mechanical or functional obstruction to urine flow. Intrinsic ARF (40% of ARF cases) is the result of structural damage to the renal tubules, glomeruli, interstitium, or renal vasculature.

Most intrinsic ARF cases are associated with ATN from prolonged ischemia or toxic injury, and the terms ischemic and nephrotoxic ATN are frequently used synonymously with ischemic or nephrotoxic ARF.[11] The focus of this article is ischemic and nephrotoxic ATN. Other important causes of intrinsic ARF in children, such as hemolytic-uremic syndrome (HUS) and immunologic glomerular diseases, are not discussed.

Pathologically, ATN is characterized by varying degrees of tubule cell damage (see Pathophysiology) and by cell death that usually results from prolonged renal ischemia, nephrotoxins, or sepsis. Its clinical course may be divided into initiation, maintenance, and recovery phases.

Patients with hospital-acquired ATN frequently have no specific symptoms. Careful evaluation of the hospital course usually reveals the cause of ATN. In patients with community-acquired ATN, a thorough history and physical examination are invaluable in pinpointing the etiology (see Clinical Presentation).

Laboratory evaluation confirms the diagnosis; ultrasonography of the kidneys and bladder with Doppler flow is essential. Serum creatinine is the current criterion standard for the diagnosis of ARF; however, important limitations are noted (see Workup).

Treatment of pediatric patients with ATN requires correction of imbalances in fluid volume, electrolytes, and acid-base balance. Dialysis may be indicated. Patients must be monitored for the development of complications, including infection and hematologic, neurologic, and metabolic disorders (see Treatment and Management).

Furosemide may convert the oliguric ATN to a nonoliguric type, which is managed more easily. In addition, ATN is frequently complicated by hyperphosphatemia and hypocalcemia, which respond to calcium-containing oral phosphate binders (see Medication).

Go to Acute Tubular Necrosis for more complete information on this topic.



The current understanding of the pathophysiology of acute tubular necrosis (ATN) is the result of intensive scientific studies performed over many decades. Despite the nomenclature, frank necrosis of tubule cells is relatively inconspicuous in ischemic ATN, whereas it can be more extensive in heavy metal–induced nephrotoxic ATN.[12, 13, 14]

The typical findings in humans 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 Henle loop
  • 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.

The clinical course of ATN may be divided into the following 3 phases:

  • Initiation
  • Maintenance
  • Recovery

Initiation phase

The initiation phase corresponds to the period of exposure to ischemia or nephrotoxins. Renal tubule cell damage begins to evolve (but is not yet established) during this phase. The glomerular filtration rate (GFR) starts to fall, and urine output decreases.

Maintenance phase

During the maintenance phase, renal tubule injury is established, the GFR stabilizes at the level well below normal, and the urine output is low or absent. Although oliguria (or anuria) is one of the clinical landmarks of ATN, it is absent in a minority of patients with so-called nonoliguric ATN. Acute renal failure (ARF) due to nephrotoxins is typically nonoliguric. The second phase of ATN usually lasts for 1-2 weeks but may extend to a few months.

Recovery phase

The recovery phase of ATN is characterized by polyuria and gradual normalization of the GFR. This phase involves the restitution of cell polarity and tight junction integrity in sublethally injured cells, removal of dead cells by apoptosis, removal of intratubular casts by reestablishment of tubular fluid flow, and regeneration of lost renal epithelial cells.

In the absence of multiorgan failure, most patients with ATN regain most renal function. However, when ATN occurs (as it often does) in the context of multiorgan dysfunction, regeneration of renal tissue may be severely impaired and renal function may not return. Morbidity and mortality in such situations remains dismally high despite significant scientific and technological advances.

Following ischemia-reperfusion, a marked up-regulation of numerous genes that play important roles in renal tubule cell proliferation occurs, including epidermal growth factor (EGF), insulinlike growth factor-1 (IGF-1), fibroblast growth factor (FGF), and hepatocyte growth factor (HGF).

In animals, exogenous administration of several of these growth factors has been shown to accelerate recovery from ischemic ARF[15] ; however, in a single human trial, IGF-1 did not prove to be beneficial when given to adults with ARF of various etiologies.[16] Additional human studies with growth factors are currently under way.

Heat shock proteins (HSPs) are a group of highly conserved proteins that are expressed constitutively in normal cells and markedly induced in cells injured by heat, hypoxia, or toxins. They act as intracellular chaperones, allowing proper folding, targeting, and assembly of newly synthesized and denatured proteins.

At least 2 families of HSPs, namely HSP-70 and HSP-25, have been shown to be overexpressed in renal tubule cells following ischemia-reperfusion injury in animals. HSP-70 may play a role in the restitution of cell polarity, and HSP-25 is an actin-capping protein that may assist in the repair of actin microfilaments in sublethally injured cells. The role for HSPs in human ATN remains to be elucidated.

Go to Pathophysiologic Mechanisms of Pediatric Acute Tubular Necrosis for more complete information on this topic.



The following are prevalent causes of ATN in neonates[17] :

  • Ischemia - Perinatal asphyxia, respiratory distress syndrome, hemorrhage (eg, maternal, twin-twin transfusion, intraventricular), congenital cyanotic heart disease, shock/sepsis
  • Exogenous toxins - Aminoglycosides, amphotericin B, maternal ingestion of angiotensin-converting enzyme (ACE) inhibitors or nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Endogenous toxins - Hemoglobin following hemolysis, myoglobin following seizures
  • Kidney disease - Renal venous thrombosis, renal artery thrombosis, renal hypoplasia and dysplasia, autosomal recessive polycystic kidney disease, bladder outlet obstruction

Causes of ATN in older children

The following are prevalent causes of ATN in older children:

  • Ischemia - Severe dehydration, hemorrhage, shock/sepsis, burns, third-space losses in major surgery, trauma, nephrotic syndrome, cold ischemia in cadaveric kidney transplant, near drowning, severe cardiac or pulmonary disease
  • Exogenous toxins - Drugs that impair autoregulation (eg, cyclosporine, tacrolimus, ACE inhibitors, NSAIDs), direct nephrotoxins (eg, aminoglycosides, amphotericin B, cisplatin, contrast agents, cyclosporine, tacrolimus)
  • Endogenous toxins - Hemoglobin release (eg, transfusion reactions, malaria, snake and insect bites, glucose 6-phosphate dehydrogenase deficiency, extracorporeal circulation, cardiac valvular prostheses), myoglobin release (eg, crush injuries, prolonged seizures, malignant hyperthermia, snake and insect bites, myositis, hypokalemia, hypophosphatemia, influenza)


Frequency varies widely, depending on the clinical context. ATN is the most frequent cause of hospital acquired ARF.[18] In adults, prevalence of ATN is approximately 1% at admission, 2-5% during hospitalization, and 4-15% after cardiopulmonary bypass. ATN occurs in approximately 5-10% of newborn patients in the ICU and 2-3% of pediatric patients in the ICU.[19] Prevalence in children undergoing cardiac surgery is 5-8%. ATN is more common in neonates than in other pediatric populations because of the high frequency of comorbid conditions.[20, 21, 22, 23]



The prognosis for children with ATN from prerenal causes or in the absence of significant comorbid conditions is usually quite good if appropriate therapy is instituted in a timely fashion. Most patients recover adequate renal function to lead normal lives. Some are left with permanent renal damage. In those left with mild-to-moderate renal damage, further deterioration in kidney function may occur later in childhood; therefore, long-term follow-up is required in these patients.

Mortality rates widely vary according to the underlying cause and associated medical condition. The most common causes of death are sepsis,[24] cardiovascular and pulmonary dysfunction, and withdrawal of life support measures.

For patients with community-acquired ATN without other serious comorbid conditions, mortality is approximately 5% and has decreased over the past decades because of the availability of efficient renal replacement therapies.[25] Mortality jumps to 80% in patients in the ICU with multiorgan failure, although death is almost never caused by renal failure.

Despite significant advances in supportive care and renal replacement therapy, the high mortality rates with multiorgan failure have not improved in the past few decades. Patients die not because of renal failure but because of serious involvement of other systems during the period of ATN.

A review of United States Renal Data System data (n = 1,070,490) for 2001 through 2010 found that  although the incidence of end-stage renal disease (ESRD) attributed to ATN increased during that period, the prospects for renal recovery and survival also increased. Recovery of renal function was more likely in patients with ATN than in matched controls (cumulative incidence 23% vs. 2% at 12 weeks, 34% vs. 4% at 1 year), as was death (cumulative incidence 38% vs. 27% at 1 year). Hazards ratios for death declined in stepwise fashion to 0.83 in 2009-2010.[26]


Patient Education

For patient education information, see eMedicine’s Diabetes Center, as well as Acute Kidney Failure.

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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