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Do not Attempt to Convert Oliguric to Nonoliguric Renal Failure with Diuretics

Brandon R. Bruns MD

Heidi L. Frankel MD

Oliguria, recently defined as urine output of less than 0.3 mL/kg/h for a 24-hour period, is a common problem in the intensive care unit (ICU). Oliguria is an important harbinger of acute renal failure. Nearly 70% of ICU patients who develop acute renal failure are oliguric. Classically, renal failure has been ascribed to three causes: prerenal, renal, and postrenal.

Prerenal

  • Absolute decrease in intravascular volume
    • Hemorrhage
    • Fluid sequestration (e.g., pancreatitis, after an exploratory laparotomy, burns, diarrhea, and vomiting)
  • Renal perfusion impairment
    • Thrombosis of renal vasculature
    • Emboli to the renal artery
    • Abdominal compartment syndrome
    • Dissection of a renal artery
  • Relative decrease in intravascular volume
    • Vasodilatation associated with sepsis
    • Severe right-sided heart failure
    • Cirrhosis
    • Nephrosis

Renal

  • Acute tubular necrosis
    • Myoglobin
    • Aminoglycosides
    • Intravenous contrast
  • Acute interstitial nephritis, which can be caused by a wide variety of drugs (e.g., antibiotics)

Postrenal

  • Prostatic hypertrophy

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  • Ureteral obstruction
  • Foley catheter malfunction

Other than the avoidance of unnecessary toxins or attention to the appropriate volume resuscitation of the ICU patient, there are few modalities that can prevent incipient acute renal failure. In general, patients with nonoliguric renal failure are easier to manage than patients with oliguric renal failure. However, the use of loop diuretics in an attempt to convert from oliguric to nonoliguric renal failure is associated with an increased mortality and a decreased rate of recovery of renal function. Similarly, agents such as dopamine and fenoldopam have been unsuccessful.

A new renal failure grading system—RIFLE—uses glomerular filtration rate (GFR) criteria or urine output to predict whether acute renal failure will result in chronic deficits. The categories include risk, injury, failure, and the subcategories of loss and end-stage renal disease. In general, the longer it takes for renal function to return, the less the chance it ever will. After 6 months of acute renal failure, there is little hope for recovery. Thus, whereas avoidance of nephrotoxins (and intravenous contrast) is critical in those with incipient or acute renal failure of short standing, there is little need to withhold these therapies in those with chronic renal failure; thus the old saying “You can't kill a nephron twice.â€

Treatment for acute renal failure involves resolution of the underlying cause, for example, restoring intravascular volume in a trauma patient or removal of an offending nephrotoxic agent. Other options include mechanical means of renal replacement—dialysis. Recovery from the effects of renal failure depends on the severity of the underlying damage.

Suggested Readings

Bell M, Liljestam E, Granath F, et al. Optimal follow-up time after continuous renal replacement therapy in acute renal failure patients stratified by the RIFLE criteria. Nephrol Dial Transplant. 2005;20:354–360.

Civetta JM, Taylor RW, Kirby RR. Critical Care. 3rd ed. Philadelphia: Lippincott– Raven Publishers; 1997:2081–2091.

Fink MP, Abraham E, Vincent JL, eds. Textbook of Critical Care. 5th ed. Philadelphia: Elsevier Saunders; 2005

 

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