Pediatric Acute Tubular Necrosis Clinical Presentation

Updated: Aug 09, 2018
  • Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD  more...
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Presentation

History

Patients with hospital-acquired acute tubular necrosis (ATN) frequently have no specific symptoms. The diagnosis is, at times, suspected when urine output diminishes and is usually made by the documentation of successive elevations in blood urea nitrogen (BUN) and serum creatinine levels. 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.

In children, the most common form is ischemic ATN caused by severe hypovolemia, shock, trauma, sepsis, burns, and major surgery. Nephrotoxic ATN is also common and is caused by various drugs. Their deleterious effect is markedly enhanced by hypovolemia, renal ischemia, or other renal insults. [28]

Conditions resulting in fluid loss

Severe vomiting and/or diarrhea are common causes of renal hypoperfusion in children. Significant fluid loss may also result from hemorrhage or burns. Loss of intravascular volume into the interstitial compartment accompanies major surgery, shock syndromes, and the nephrotic syndrome.

Children with fluid losses may complain of thirst, dizziness, palpitations, and fatigue. A history of acute weight loss and oliguria may be documented; however, ATN resulting from nephrotoxic drugs and from perinatal events are frequently nonoliguric. Refer to the illustration shown below.

Common causes of oliguric versus nonoliguric acute Common causes of oliguric versus nonoliguric acute renal failure in children.

Medication use

In the presence of mild prerenal insufficiency, ingestion of seemingly innocuous medications that impair renal autoregulation can precipitate oliguric ATN; for example, nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the renal synthesis of vasodilator prostaglandins and can precipitate ATN when administered to febrile children with intercurrent dehydration.

Cyclosporine, tacrolimus, and contrast agents are afferent arteriolar constrictors. Their nephrotoxicity is potentiated by preexisting hypovolemia because they inhibit the myogenic response of the afferent arteriole to renal hypoperfusion.

Drugs that induce direct tubule cell damage include aminoglycosides, amphotericin B, cyclosporine, tacrolimus, antineoplastic agents (eg, cisplatin, methotrexate), and contrast agents.

Acyclovir and sulfonamides can precipitate and obstruct the tubular lumens, especially in children with diminished tubular fluid flow.

Conditions associated with release of endogenous tubular toxins

Myoglobinuric ATN may be encountered in various clinical situations, including muscle trauma, prolonged seizures, malignant hyperthermia, snake and insect bites, myositis, severe hypokalemia and hypophosphatemia, and infections such as severe influenza.

Hemoglobinuric ATN can accompany various states of hemolysis, including transfusion reactions, malaria, snake and insect bites, glucose 6-phosphate dehydrogenase deficiency, and mechanical causes such as extracorporeal circulation and cardiac valvular prostheses.

Hyperuricosuric ATN is primarily observed during treatment of lymphoproliferative or myeloproliferative malignancies and presents as tumor lysis syndrome.

Hypoxia

In infants, ATN frequently complicates severe perinatal asphyxia, respiratory distress syndrome, hemorrhage, and cyanotic congenital heart disease. Older children with severe pulmonary or cardiac disease are also prone to ATN.

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Physical Examination

Signs of acute renal failure (ARF) include hypertension, edema, anemia, and signs of heart failure, such as hepatomegaly, gallop rhythm, and pulmonary edema.

Signs of intravascular volume depletion include tachycardia, orthostatic hypotension, decreased skin turgor, dry mucous membranes, and changes in sensorium.

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Complications

Infections develop in 30-70% of patients with ATN. These include infections of the respiratory system, urinary tract, and indwelling catheters. Impaired defenses due to uremia and excessive use of antibiotics and invasive maneuvers may contribute to the high rate of infectious complications.

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

Other complications include the following:

  • GI (eg, anorexia, nausea, vomiting, ileus, bleeding)

  • Hematologic (eg, anemia, platelet dysfunction)

  • Neurologic (eg, confusion, asterixis, somnolence, seizures)

  • Electrolyte disturbances (eg, hyponatremia, hyperkalemia, hypocalcemia, hyperphosphatemia)

  • Metabolic acidosis

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