Acute Tubular Necrosis Medication
- Author: Edgar V Lerma, MD, FACP, FASN, FAHA, FASH, FNLA, FNKF; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...
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.
Antioxidants may prevent reperfusion damage as well as improve renal hemodynamics.
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.
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.
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.
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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|Finding||Prerenal Azotemia||ATN and/or Intrinsic Renal Disease|
|Fractional excretion of sodium (FENa)
|Fractional excretion of urea
|Urine sediment||Bland and/or nonspecific||May show muddy brown granular casts|