Which lab studies are performed in the evaluation of prerenal azotemia?

Updated: Apr 24, 2020
  • Author: Moro O Salifu, MD, MPH, FACP; Chief Editor: Vecihi Batuman, MD, FASN  more...
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In prerenal azotemia, hemoconcentration results in elevation of the hematocrit and total protein/albumin, calcium, bicarbonate, and uric acid levels from baseline values.

Oliguria (urine volume < 500 mL/day) or anuria (< 100 mL/day), high urine specific gravity (>1.015), normal urinary sediment, and low urinary sodium (< 20 mEq/L; fractional excretion of sodium [FENa] < 1%) are seen.

When volume depletion is predominant, exaggerated proximal tubular reabsorption results in azotemia, hypernatremia, and elevated levels of calcium, uric acid, and bicarbonate, whereas hemoconcentration results in elevation of total protein, albumin, and hematocrit levels from baselines. When hypoperfusion due to decreased cardiac output or effective arterial volume is present, patients exhibit edema, hyponatremia, and hypoalbuminemia. Hematocrit and calcium, uric acid, and bicarbonate levels vary widely. These patients often are critically ill.

The FENa has traditionally been used to differentiate prerenal azotemia from ATN. An FENa below 1% suggests a prerenal cause (eg, volume depletion), whereas an FENa above 2% suggests acute tubular necrosis (ATN). Because the FENa is based on the fact that sodium reabsorption is enhanced in the setting of volume depletion, active use of diuretics may elevate the FENa even when volume depletion is present, yielding misleading values.

Alternatives to the FENa in this setting include the fractional excretion of urea or urea nitrogen (FEUrea) and the fractional excretion of uric acid (FEUA); excretion of urea and uric acid excretion is not influenced by diuretics. An FEUrea below 35% or an FEUA below 9-10 % suggests a prerenal etiology of acute kidney injury (AKI), whereas an FEUrea above 50% or an FEUA above 10-12 % suggests acute tubular necrosis (ATN). [9]

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