Blood Urea Nitrogen
The term blood urea nitrogen (BUN) is ingrained in the veterinary literature, despite the fact that urea nitrogen determinations usually are performed on serum (SUN) or plasma samples.
Causes of Decreased Blood Urea Nitrogen
Common Causes
Liver failure
Neonatal animals (blood urea nitrogen is normally lower than in adults)
Uncommon Causes
Low-protein diet
Anabolic steroid administration
This is of little consequence because the actual difference in urea concentrations of whole blood and serum or plasma is relatively small; instead of urea nitrogen, in some parts of the world, urea is measured as the whole molecule. Urea concentration in serum is approximately twice that of the BUN. Urea provides a nontoxic means of excreting ammonia generated by amino acid catabolism and the intestinal microflora. It is distributed throughout the body water. In the intestine, urea is broken down by urease, which is produced by the intestinal microflora, and the nitrogen, as ammonium ion, is recycled to the liver. Urea is excreted by the kidneys, primarily by glomerular filtration, intestine (in high concentration in horses), saliva, and sweat. Ruminants excrete urea into the gastrointestinal tract, where it is converted to ammonia and amino acids that result in protein production.
Urea production occurs almost exclusively in the liver and is synthesized by hepatocytes from ammonia derived from amino acid catabolism. Blood or serum urea is dependent on hepatic urea production and renal tubular flow rate. Urea excretion is not solely determined by GFR because once in the tubules, at rapid flow rates, 40% of the urea is reabsorbed. However, at slow flow rates, as occurs in hypovolemia, 60% is reabsorbed, thus increasing urea levels in serum or blood. Liver failure is frequently associated with a decrease in BUN (Box 22.22).
Urea nitrogen tends to be low in nursing animals because of their high fluid intake and urine output and their anabolic state of rapid growth. Urea nitrogen may be reduced slightly in animals given anabolic steroids or fed diets low in protein but of adequate calorie content.Starvation or other processes that result in rapid tissue catabolism such as fever, burns, exercise, and increased protein digestion (e.g., hemorrhage in the gastrointestinal tract) decrease GFR, or corticosteroid administration may result in modest increases in BUN (Box 22.23). BUN, along with creatinine, provides a crude index of altered renal function in most animal species. BUN is influenced more directly by dietary factors than is creatinine, and creatinine is generally a better guide to renal failure. This is particularly true in ruminants, in which BUN may remain within normal limits in animals with marked impairment of renal function.
The BUN-to-creatinine ratio has been used to try to aid in differentiating prerenal azotemia and intrinsic renal azotemia based on the proportion of increases of each substance in the ratio. However, given the wide variation in BUN and creatinine concentration along with the differences of species, it is not a reliable indicator. In the horse a BUN-to-creatinine ratio of less than 10 : 1 is expected with ARF; when it exceeds 15 : 1, CRF is more likely. With these considerations in mind, the discussion of prerenal, renal, and obstructive causes of azotemia in the creatinine section apply to BUN.