Acute Tubular Necrosis Medication

  • Author: Edgar V Lerma, MD, FACP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN   more...
 
Updated: Jun 28, 2011
 

Medication Summary

Medications have only an ancillary role in the treatment of acute tubular necrosis (ATN). Antioxidants and diuretics may be helpful in specific circumstances. Therapeutic mainstays are prevention, avoidance of further kidney damage, treatment of underlying conditions, and aggressive treatment of complications.

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Antioxidants

Class Summary

Antioxidants may prevent reperfusion damage as well as improve renal hemodynamics.

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N-acetylcysteine (Mucomyst, Mucosil)

 

N-acetylcysteine is used for acetaminophen toxicity. It has been shown to prevent renal deterioration in patients with acetaminophen toxicity and hepatorenal syndrome. This finding led to its study in the prevention of contrast-induced nephropathy (CIN). It may work by improving renal hemodynamics and by preventing direct oxidative tissue damage. The use of N-acetylcysteine (NAC) is believed to have antioxidant properties that potentially counteract the effects of ROS.

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Diuretics

Class Summary

Diuretics help maintain a nonoliguric state, which has a better overall survival rate. Loop diuretics work to increase urine output. Diuretics should only be used if ECF volume and cardiac function are first carefully assessed and found to be adequate.

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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 the distal renal tubule. Individualize the dose to the patient. Depending on the response, administer furosemide at increments of 20-40 mg, no sooner than 6-8 hours after the previous dose, until the desired diuresis occurs. When treating infants, titrate with 1 mg/kg per dose increments until a satisfactory effect is achieved.

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Bumetanide

 

Bumetanide is a loop diuretic that increases the excretion of water by interfering with the chloride-binding co-transport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle. These effects increase urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs following administration, renal vascular resistance decreases, and renal blood flow is enhanced.

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Contributor Information and Disclosures
Author

Edgar V Lerma, MD, FACP, FASN, FAHA  Clinical Associate Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Research Director, Internal Medicine Training Program, Advocate Christ Medical Center; Consulting Staff, Associates in Nephrology, SC

Edgar V Lerma, MD, FACP, FASN, FAHA is a member of the following medical societies: American Heart Association, American Medical Association, American Society of Hypertension, American Society of Nephrology, Chicago Medical Society, Illinois State Medical Society, National Kidney Foundation, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP, FASN  Clinical Associate Professor of Medicine, Baylor College of Medicine; President and CEO, Space City Associates of Nephrology

Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology, and National Kidney Foundation

Disclosure: South Shore DaVita Dialysis Center Ownership interest Other

Brent Kelly, MD  Resident Physician, Department of Internal Medicine, University of Texas Medical Branch School of Medicine

Brent Kelly, MD is a member of the following medical societies: Alpha Omega Alpha and American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

F John Gennari, MD  Associate Chair for Academic Affairs, Robert F and Genevieve B Patrick Professor, Department of Medicine, University of Vermont College of Medicine

F John Gennari, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Federation for Medical Research, American Heart Association, American Physiological Society, American Society for Clinical Investigation, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

George R Aronoff, MD  Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN  Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

References

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  14. du Cheyron D, Daubin C, Poggioli J, et al. Urinary measurement of Na+/H+ exchanger isoform 3 (NHE3) protein as new marker of tubule injury in critically ill patients with ARF. Am J Kidney Dis. Sep 2003;42(3):497-506. [Medline].

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A photomicrograph of renal biopsy shows renal medulla, which is composed mainly of renal tubules. Patchy or diffuse denudation of the renal tubular cells is observed, suggesting acute tubular necrosis (ATN) as the cause of acute kidney injury (AKI).
Acute tubular necrosis (ATN). Flattening of the renal tubule cells due to tubular dilation.
Acute tubular necrosis. Intratubular cast formation.
Acute tubular necrosis. Intratubular obstruction due to the denuded epithelium and cellular debris. Note that the denuded tubular epithelial cells clump together due to rearrangement of intercellular adhesion molecules (ICAM).
Sloughing of cells, which is responsible for the formation of granular casts, a feature of acute tubular necrosis (ATN).
Table. Laboratory Findings Used to Differentiate Prerenal Azotemia From ATN
Finding Prerenal Azotemia ATN and/or Intrinsic Renal Disease
Urine osmolarity



(mOsm/kg)



>500< 350
Urine sodium



(mmol/d)



< 20>40
Fractional excretion of sodium (FENa)



(%)



< 1>2
Fractional excretion of urea



(%)



< 35>50
Urine sedimentBland and/or nonspecificMay show muddy brown granular casts
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