8.1 Procedural Definition: What Is This Test About?

The Azostix™ urea nitrogen reagent pad is a semiquantitative measurement of the urea nitrogen concentration in whole blood. The color change is the result of the action of the enzyme urease on urea in the blood. The urease acts on urea to release ammonium ions. The release of ammonium results in a pH change, resulting in the color change to increasingly darker green based on the reaction of the ammonium with the pH indicator in the reagent pad (bromothymol blue).

Urea is the waste product of protein catabolism. It is produced in the liver and excreted by the kidney. It can increase in the blood with decreased excretion due to a decrease in glomerular filtration rate (GFR). Increased protein intake can also increase the concentration of blood urea nitrogen (BUN). Since blood has a high protein content, hemorrhage into the gastrointestinal tract results in an increase in protein intake and can also cause an increase in BUN. The Azostix reagent pad does not replace the more accurate methodology used in clinical chemistry instrumentation. Nor can it be used alone to assess renal function. It does provide a good screening test for changes in BUN that indicate either decreased GFR or gastrointestinal hemorrhage.

8.2 Procedural Purpose: Why Should I Perform This Test?

Urea nitrogen is one of the two analytes used to assess glomerular filtration rate. Urea is produced in the liver as a result of protein catabolism and is both filtered and passively reabsorbed by the kidney. Creatinine is filtered with minimal secretion or reabsorption. Azotemia, the presence of an increase in one or both of these analytes in the blood due to decreased excretion by the kidney, can be caused by prerenal, renal, or postrenal disease. Urea is freely filtered by the kidney but can diffuse back into the blood as the urine filtrate moves through the nephron. The amount of urea reabsorbed depends on how quickly urine filtrate flows through the nephron. Creatinine is freely filtered by the kidney with minimal reabsorption or secretion making it a better indicator of total GFR.

The reagent pad urea nitrogen is a quick screening test for any patient with a history of polydipsia/polyuria, dehydration, or clinical evidence of uremia. The test is not a stand‐alone test for renal function. If increased concentration is found using the reagent pad test, the BUN concentration should always be interpreted in the context of clinical findings and urinalysis. A complete blood count, chemistry profile, and urinalysis are recommended as follow‐up.

Causes of increased BUN:

• any cause of decreased GFR (prerenal, renal, and postrenal)
  
• increased protein intake (high protein feed, gastrointestinal hemorrhage)
  
• increased protein catabolism unrelated to dietary intake (less common).

There are a few important caveats with regard to the interpretation of increased BUN concentration without an increase in creatinine concentration. Gastrointestinal hemorrhage will result in increased BUN with normal creatinine. This is due to the high protein content of blood making gastrointestinal hemorrhage a “high protein meal” as it is digested and the blood proteins are absorbed in the intestinal tract. The liver produces urea as a waste product of protein catabolism.

Decreased liver function occurs either by loss of hepatic mass (chronic liver disease) or shunting of blood past the liver (congenital or acquired portosystemic shunts). Patients with decreased liver function may have a significantly decreased BUN as a result of decreased hepatic production. In these patients, decreased GFR can result in a BUN concentration within the reference interval and increased creatinine.

Causes of decreased BUN:

• low protein diet
  
• decreased production by the liver
  
• increased renal excretion
  
  
  
  • increased urine filtrate flow through the nephron
    
    
    
    • osmotic diuresis
      
    • increased GFR.

Clinical indications for performing a reagent pad BUN include:

• clinical findings suggestive of renal disease
  
  
  
  • polydipsia/polyuria
    
  • weight loss
    
  • anorexia or hyporexia
    
  • vomiting
    
  • ammonia smell of breath
  
  
• clinical findings indicative of dehydration
  
  
  
  • pale tacky mucous membranes
    
  • tachycardia
    
  • decreased skin turgor
    
  • thin or thready pulses
    
  • sunken eyes.