eMedicine Specialties > Nephrology > Acute Kidney Failure

Acute Tubular Necrosis: Treatment & Medication

Author: Edgar V Lerma, MD, Clinical Associate Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Consulting Staff, Associates in Nephrology, SC
Coauthor(s): Brent Kelly, MD, Resident Physician, Department of Internal Medicine, University of Texas Medical Branch School of Medicine; Mahendra Agraharkar, MD, MBBS, FACP, FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine, President & CEO, Space City Associates of Nephrology
Contributor Information and Disclosures

Updated: Aug 28, 2009

Treatment

Medical Care

  • Prevention
    • Ischemic ATN: Be attentive to optimizing cardiovascular function as well as maintaining intravascular volume, especially in patients with preexisting risk factors or those taking nephrotoxic medications. Medicines that reduce systemic resistance (eg, afterload reducers) may cause renal vasoconstriction or affect the kidney's autoregulatory response (eg, ACE inhibitors, COX inhibitors) and also should be used with caution.
    • Nephrotoxic ATN
      • Aminoglycosides: Studies have demonstrated that once daily dosing of aminoglycosides decreases the incidence of nephrotoxicity.
      • Amphotericin B: Minimize the use of this drug and ensure that extracellular fluid (ECF) volume is adequate.
      • Cyclosporin and tacrolimus: Regular monitoring of blood levels can help maintain therapeutic levels and prevent nephrotoxicity.
      • Radiocontrast dye: Isotonic sodium chloride solution infusion has proven benefits in the prevention of CIN. Typically, isotonic sodium chloride solution (0.9%) administered at a rate of 1 mL/kg/h 12 hours before and 12 hours after the administration of the dye load is most effective, especially in the setting of prior renal insufficiency and diabetes mellitus. Nonionic contrast media is also protective in patients with diabetic nephropathy and renal insufficiency. NAC has been tried with success in high-risk patients to prevent contrast-induced nephrotoxicity.
  • Treatment
    • General treatment
      • The main goal of treatment is to prevent further injury to the kidney. ECF volume should be assessed promptly, either on clinical grounds or by invasive means (Swan-Ganz catheter), and repletion of any deficit should be initiated promptly. A renal ultrasound should be performed to exclude obstruction. All possible nephrotoxic drugs should be stopped. Despite some controversy in the literature, in general, if oliguria is present, make an attempt to increase urine output using intravenous loop diuretics. Only use diuretics if ECF volume and cardiac function are first carefully assessed and found adequate.
      • Intravenous furosemide or bumetanide in a single high dose (ie, 100-200 mg of furosemide) is commonly used, although little evidence indicates that it changes the course of ATN. The drug should be administered slowly because high doses can lead to hearing loss. If no response occurs, the treatment should be discontinued. Dopamine, a selective renal vasodilator, has also been used to increase urine output, but this treatment has little benefit and is no longer recommended.
      • Aggressively treat any complications that develop. For example, hyperkalemia can be treated with glucose and insulin, binding resins, or, if necessary, dialysis. Metabolic acidosis may be treated with bicarbonate or dialysis as well. Anemia can be corrected with blood transfusions.
      • Recall that sepsis is a common cause of death with severe ARF, so aggressive treatment of infections is prudent.
      • Also, adjust doses of all medications if the kidney eliminates them.
    • Dialysis treatment
      • In general, no clear consensus is established on when or how often to perform hemodialysis in the setting of ARF. Some studies have suggested that early initiation may be beneficial, but, in one prospective trial, aggressive dialysis did not improve recovery or survival rates. However, hemodialysis is still considered standard therapy in severe ARF. In addition, continuous hemodialysis (continuous venovenous hemodiafiltration [CVVHD] and continuous arteriovenous hemofiltration with dialysis [CAVHD]) and peritoneal dialysis are also available. No compelling studies suggest that one mode is better than another. In general, patients with multiorgan failure and hemodynamic instability may benefit from a continuous mode because it is typically less taxing on the hemodynamics.
      • Some studies suggest that the use of biocompatible membranes instead of cuprophane membranes may improve the recovery rate and decrease the mortality rate in ARF.
    • Treatment of nephrotoxic ATN: Generally, the treatment of choice is to stop all nephrotoxic agents to prevent further damage to the kidney. Of note, calcium channel blockers may have some use in cyclosporine toxicity, where they may reduce the vasoconstrictive action of the drug. However, their use is typically avoided because of possible hypotension.

Diet

Clearly, the maintenance of fluid and electrolyte balance is critical. Aggressive and early nutritional support also improves survival rates. Adequate protein and caloric intake is essential because marked increase in protein catabolism is often observed, especially in patients with shock, sepsis, or rhabdomyolysis. The risks of this catabolism include malnutrition and an impaired immune system.

Medication

Medications have not been effective in treating ATN. Therapeutic mainstays are prevention, avoidance of further kidney damage, treatment of underlying conditions, and aggressive treatment of complications.

Antioxidants

May prevent reperfusion damage as well as improve renal hemodynamics.


N-acetylcysteine (Mucomyst, Mucosil)

Used for acetaminophen toxicity. 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 CIN. May work by improving renal hemodynamics and by preventing direct oxidative tissue damage.

Adult

600 mg PO bid for 2 d (administer 1 day before and on the day of exposure to radiocontrast dye)

Pediatric

Not established

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

GI distress may occur

Diuretics

Help maintain a nonoliguric state, which has a better overall survival rate.


Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. Individualize dose to the patient. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg per dose increments until a satisfactory effect is achieved.

Adult

20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states

Pediatric

1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h
1 mg/kg IV/IM slowly, under close supervision; not to exceed 6 mg/kg

Decreased furosemide concentrations with concomitant metformin; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; possible hearing loss of varying degrees may occur; possible enhancement of anticoagulant activity of warfarin when taken concurrently; increased plasma lithium levels and toxicity possible when taken concurrently

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, CO2, glucose, creatinine, uric acid, calcium, and BUN determinations during first few mo of therapy and periodically thereafter

More on Acute Tubular Necrosis

Overview: Acute Tubular Necrosis
Differential Diagnoses & Workup: Acute Tubular Necrosis
Treatment & Medication: Acute Tubular Necrosis
Follow-up: Acute Tubular Necrosis
Multimedia: Acute Tubular Necrosis
References
Further Reading
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References

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  5. Mishra J, Mori K, Ma Q, et al. Amelioration of ischemic acute renal injury by neutrophil gelatinase-associated lipocalin. J Am Soc Nephrol. Dec 2004;15(12):3073-82. [Medline].

  6. Mishra J, Ma Q, Kelly C, et al. Kidney NGAL is a novel early marker of acute injury following transplantation. Pediatr Nephrol. Jun 2006;21(6):856-63. [Medline].

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Further Reading

Related eMedicine topics:
Acute Renal Failure
Acute Tubular Necrosis [Pediatrics: General Medicine]
Azotemia
Kidney Transplantation, Surgical Complications
Kidney, Trauma
Oliguria
Renal Failure, Acute

Clinical guidelines:
ACR Appropriateness Criteria® renal failure. American College of Radiology - Medical Specialty Society.  1995 (revised 2005).  8 pages. [NGC Update Pending] NGC:004615

Clinical trials:
Allogeneic Multipotent Stromal Cell Treatment for Acute Kidney Injury Following Cardiac Surgery

Sensitivity and Specificity of NGAL in an Emergency Room Population

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Keywords

acute tubular necrosis, renal failure, kidney failure, acute renal failure, tubular necrosis, end-stage renal disease, acute kidney failure, intrinsic renal disease, acute ischemic nephropathy, ischemic acute tubular necrosis, nephrotoxic acute tubular necrosis

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Contributor Information and Disclosures

Author

Edgar V Lerma, MD, Clinical Associate Professor of Medicine, Section of Nephrology, Department of Medicine, University of Illinois at Chicago College of Medicine; Consulting Staff, Associates in Nephrology, SC
Edgar V Lerma, MD 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)

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.

Mahendra Agraharkar, MD, MBBS, FACP, FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine, President & 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

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

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.

 
 
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