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Blood Urea Nitrogen (BUN)

Urea is the major end product of protein and amino acid catabolism and is produced in the liver in the urea cycle. Urea is easily diffusible and exists in all body fluids in practically the same concentration. Urea is filtered freely by the glomeruli and reabsorbed by the proximal and distal tubules. BUN concentration is primarily regulated by renal tubular reabsorption, which is highly dependent on urine flow rate. Increased tubular flow, due to blood volume expansion, decreases absorption and BUN concentration. Decreased tubular flow, due to volume depletion or congestive heart failure, increases absorption and BUN concentration. BUN concentration is also affected by protein intake (malnutrition or hyperalimentation), endogenous protein metabolism, and liver disease. These variables make BUN a rather poor measure of renal function.

Most clinicians agree that creatinine is a more specific indicator of glomerular function than BUN.However, the BUN to creatinine ratio may be used as an indirect estimate of renal function. It is commonly used to determine the etiology of acute renal failure. The ratio of BUN to creatinine can be used to determine the etiology of acute renal failure. Normally, the ratio is 10 to 1. The ratio usually exceeds 20 in prerenal failure due to decreased renal perfusion, such as occurs with hypertension, hemorrhage, or dehydration. It is normal in intrinsic renal disease because BUN and creatinine rise proportionately. Postrenal diseases, such as urinary tract obstruction, also increase the ratio above 10.

The clinical usefulness of this ratio is limited by nonrenal factors that increase BUN such as GI bleed, parenteral nutrition, and glucocorticoid therapy. A GI bleed increases BUN more than creatinine because of the increased amino acid absorption from digested blood and hypovolemia.

Several diseases may cause a decreased BUN to creatinine ratio of less than 8 to 1. Rhabdomyolysis results in increased production of creatinine. Liver disease and malnutrition can decrease the production of urea. Hemodialysis and peritoneal dialysis remove urea more efficiently than creatinine. Some medications may elevate serum creatinine by blocking tubular secretion. The most common examples are cimetidine, trimethoprim, and pyrimethamine.

BUN concentration can be used in patients with chronic renal failure to determine the timing of dialysis. BUN correlates with uremic symptoms better than serum creatinine concentration. BUN levels fall more rapidly than creatinine following dialysis and can be used to assess the adequacy of dialysis.

In summary, increased BUN may be associated with renal failure, urinary tract obstruction, dehydration and gastrointestinal hemorrhage. Decreased BUN may be associated with hepatic failure and decreased protein intake.

Reference range is 5 - 20 mg/dL.

Specimen requirement is one SST tube of blood. Hemolysis should be avoided.

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