Pediatric Acute Tubular Necrosis Medication

  • Author: Prasad Devarajan, MD; Chief Editor: Craig B Langman, MD   more...
 
Updated: Mar 29, 2011
 

Medication Summary

Diuretic treatment may convert oliguric acute tubular necrosis (ATN) to nonoliguric ATN, although diuretics do not appear to alter the course of acute renal failure (ARF).

Hyperkalemia in ATN is a medical emergency that may be managed by shifting potassium into cells with sodium bicarbonate, glucose/insulin infusion, or beta agonists; by increasing potassium excretion with exchange resins (sodium polystyrene) or loop diuretics (furosemide); or by dialysis. Protecting the myocardium from hyperkalemia is managed with intravenous (IV) calcium.

Hyperphosphatemia may be initially managed with oral calcium to bind dietary phosphate. Oral citrate salts may be used to manage mild metabolic acidosis, whereas IV sodium bicarbonate is needed for severe metabolic acidosis.

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Loop diuretics

Class Summary

In children with recent-onset oliguria from prerenal or toxic injury who are unresponsive to hydration, a trial of furosemide may convert the oliguric ATN to a nonoliguric type, which is managed more easily. These agents have a direct vasodilatory action and additionally may prevent tubular obstruction by increasing intratubular fluid flow.

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Furosemide (Lasix)

 

Furosemide increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. It is used for ATN prevention in children with oliguria duration less than 48 hours who have not responded to adequate hydration. It may also be considered for oliguria in the presence of volume overload. Furosemide is also used for hyperkalemia to increase potassium excretion in the urine.

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Alkalizing agents

Class Summary

Intravenous sodium bicarbonate and oral sodium citrate are used as buffers that break down to water and carbon dioxide after picking up free hydrogen ions, thus counteracting acidosis by raising blood pH. IV sodium bicarbonate is also used to manage hyperkalemia.

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Sodium bicarbonate

 

Sodium bicarbonate is used to treat hyperkalemia. It causes a rapid shift of potassium into cells. The magnitude of the potassium intracellular shift varies; thus, bicarbonate is not reliable in lowering the potassium level by itself. It is also used emergently to manage severe metabolic acidosis.

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Sodium citrate (Bicitra, Oracit)

 

Sodium citrate manages mild metabolic acidosis and is used as an alkalinizing agent when long-term maintenance of an alkaline urine is desirable.

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Myocardium stabilizers

Class Summary

Intravenous calcium is primarily used to protect the myocardium from the deleterious effects of hyperkalemia (ie, arrhythmias) by antagonizing the potassium actions on the myocardial cell membrane. It does not lower serum potassium levels.

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Calcium gluconate (Kalcinate)

 

Calcium gluconate is given intravenously to provide myocardial protection from hyperkalemia. It is indicated if hyperkalemia is accompanied by ominous electrocardiographic (ECG) changes beyond peaked T waves or if ECG changes persist after bicarbonate therapy.

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Intracellular transporters

Class Summary

Insulin and glucose (dextrose) cause a transcellular shift of potassium into muscle cells, thereby lowering (temporarily) potassium serum levels.

Dextrose and insulin infusion

 

Dextrose and insulin infusion is used as an adjunct to bicarbonate therapy to promote intracellular shift of potassium.

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Exchange resins

Class Summary

Sodium polystyrene sulfonate is an exchange resin that can be used to treat mild-to-moderate hyperkalemia. Each 1 mEq of potassium is exchanged for 1 mEq of sodium.

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Sodium polystyrene sulfonate (Kayexalate)

 

Sodium polystyrene sulfonate is indicated in all cases of hyperkalemia because it is the only modality (other than diuretics and dialysis) that actually removes excessive potassium from the body. It exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, and decreases total body potassium. Its onset of action after oral administration ranges from 2-12 hours and is longer when rectally administered.

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Phosphate binders

Class Summary

ATN is frequently complicated by hyperphosphatemia and hypocalcemia, which respond to calcium-containing oral phosphate binders.

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Calcium carbonate (Oystercal, Caltrate)

 

Calcium carbonate combines with dietary phosphate to form insoluble calcium phosphate, which is excreted in feces.

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Contributor Information and Disclosures
Author

Prasad Devarajan, MD  Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of Clinical Nephrology Laboratories, Chief Executive Officer of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

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.

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, Children's Memorial Hospital

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

Disclosure: Merck Grant/research funds None; NIH Grant/research funds None; Raptor Pharmaceuticals, Inc Grant/research funds None; Alexion Pharmaceuticals, Inc. Grant/research funds None

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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
ATNPrerenal
Urine specific gravity1010>1020
Urine sodium (mEq/L)>40< 10
Urine/plasma creatinine< 20>40
FENa (%)>2< 1
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