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The clinical course of acute tubular necrosis is often divided into three phases: initial injury, maintenance, and recovery The maintenance phase is expressed as either oliguric (urinary output < 500 mL/d) or nonoliguric Nonoliguric acute tubular necrosis has a better outcome Conversion from oliguric to nonoliguric states may be attempted but has not been shown to change the prognosis Drugs such as dopamine and diuretics are sometimes used for this purpose but have not been shown to improve outcomes In numerous studies, dopamine use in this setting has been shown to have no benefit Average duration of the maintenance phase is 1 3 weeks but may be several months Cellular repair and removal of tubular debris occur during this period The recovery phase is heralded by diuresis GFR begins to rise; BUN and serum creatinine fall Other treatments for acute tubular necrosis, such as atrial natriuretic peptide use, have not proven beneficial Ongoing randomized controlled studies are looking at the usefulness of intensive versus conventional renal replacement therapy for a survival benefit The mortality rate from acute renal failure is 20 50% in medical illness and up to 70% in a surgical setting Increased mortality is associated with advanced age, severe underlying disease, and multisystem organ failure Leading causes of death are infections, fluid and electrolyte disturbances, and worsening of underlying disease Mortality rates have not changed significantly over 20 years, making prevention of acute renal failure a high priority
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Treatment is aimed at hastening recovery and avoiding complications Preventive measures should be taken to avoid volume overload and hyperkalemia Loop diuretics have been used in large doses (eg, furosemide in doses ranging from 20 mg to 160 mg orally or intravenously twice daily, or as a continuous infusion) to effect adequate diuresis and may help convert oliguric to nonoliguric renal failure Such a conversion has never been shown to affect outcomes such as mortality, though One retrospective study has shown potentially worse outcomes in patients who receive doses of furosemide, including nonrecovery of renal function and an increased risk of death A more recent prospective randomized controlled trial has shown no difference between the administration of large doses of diuretics versus placebo on either recovery from acute renal failure or death Widespread use of diuretics in critically ill patients with acute renal failure should be discouraged Side effects of supranormal dosing include deafness This is mainly due to peak furosemide levels and can be avoided by the use of a furosemide drip A starting dose of 02 06 mg/kg/h is appropriate, increasing to a maximum of 1 mg/ kg/h A bolus of the hourly dose should be administered at the beginning of treatment Intravenous thiazide diuretics can be used to augment urinary output; chlorothiazide, 500 mg intravenously every 8 12 hours, is a reasonable choice Shortterm effects also include activation of the renin angiotensin system Nutritional support should maintain adequate intake
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A patient with acute renal failure should be referred to a nephrologist when the etiology is unclear or renal function continues to worsen despite intervention Also, referral is appropriate if fluid, electrolyte, and acidbase abnormalities are recalcitrant
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before resolution Patients rarely progress to ESRD Those with prolonged courses of oliguric failure and advanced age have a worse prognosis Treatment consists of supportive measures and removal of the inciting agent If renal failure persists after these steps, a short course of corticosteroids can be given Short-term, high-dose methylprednisolone (05 1 g/d for 1 4 days) or prednisone (60 mg/d for 1 2 weeks) followed by a prednisone taper can be used in these more severe cases of drug-induced interstitial nephritis
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