http://www.arabslab.com/vb/showthread.php?t=6210

Urea is a relatively nontoxic substance made by the liver as a means of disposing of ammonia from protein metabolism.
*Urea has MW 60, of which 28 comes from the two nitrogen atoms.
Clinical chemists used to measure only the nitrogen in urea, hence the "urea nitrogen" measurement on lab reports.
The real concentration of urea is BUN x (60/28), or BUN x 2.14. But everyone thinks in terms of BUN units.
Normal blood urea nitrogen is 8-25 mg/dL (2.9-8.9 mmol/L).


Increased BUN is, by definition, azotemia. It is due either to increased protein catabolism or impaired kidney function.
Increased protein catabolism results from:
 a really big protein meal (Kansas City steak, etc.)
 severe stress (myocardial infarction, high fever, etc.)
 upper GI bleeding (blood being digested and absorbed)
Impaired kidney function may be "prerenal", "renal", or "postrenal".
 Prerenal azotemia results from underperfusion of the kidney:
dehydration, hemorrhage, shock, congestive heart failure (review: NEJM 320: 397, 1989; but a poor guide to therapy, at least in kids: Ann. Emerg. Med. 18; 755, 1989); glomerulonephritis is likely also to be "prerenal" if mild, since it comprmises renal blood flow more than tubular function
 Renal azotemia has several familiar causes:
acute tubular necrosis, chronic interstitial nephritis, some glomerulonephritis, etc.
 Postrenal azotemia results from obstruction of urinary flow:
prostate trouble, stones, surgical mishaps, tumors
See below for some ways to distinguish these causes of azotemia.
In acute renal failure, BUN increases around 20 mg/dL each day (*estimates vary; range of increase is 10-50 mg/dL daily).
Decreased BUN
Lack of protein (celiac disease, some patients with nephrotic syndrome)
Severe liver disease (end-stage cirrhosis, yellow atrophy, really bad hepatitis, halothane or acetaminophen toxicity, enzyme defects)
Overhydration (iatrogenic, psychogenic water-drinking)