#Bun blood urea nitrogen normal range series

The clinical usefulness of the BUN to creatinine 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. Low circulatory states such as heart failure, dehydration and hypovolemic shock may be associated with a mild increase in plasma urea, despite a normal GFR. Kidneys increase the reabsorption of urea to conserve water. Postrenal diseases, such as urinary tract obstruction, also increase the ratio above 10. 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. The ratio of BUN to creatinine can be used to determine the etiology of acute renal failure. Normally, the ratio is 10 to 1. 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. Since BUN accounts for only the nitrogen content of urea (molecular weight 28) and urea accounts for the whole molecule (molecular weight 60), urea is approximately two times higher (60/28 = 2.14) than BUN. Urea consists of two amino (NH2) groups and a carbamyl (C-O) group. Although urea nitrogen is measured in plasma or serum, the test is called blood urea nitrogen (BUN). The unit of measurement is mg/dL. In the United States, plasma or serum urea concentration is expressed as the amount of urea nitrogen. Glomerular filtration rate (GFR) must be reduced by around 50% before plasma urea increases above the upper limit of the reference range. By itself, urea is a rather poor measure of renal function. Urea concentration is also affected by protein intake (malnutrition or hyperalimentation), endogenous protein metabolism, and liver disease. Urea 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 urea concentration. Plasma urea concentration reflects the balance between urea production in the liver and urea elimination by the kidneys. Urea is filtered freely by the glomeruli and reabsorbed by the proximal and distal tubules.

Most of the urea produced in the liver is transported in blood to the kidneys where it is eliminated in urine. Urea is easily diffusible and exists in all body fluids in practically the same concentration.

#Bun blood urea nitrogen normal range series

Ammonia, which is toxic, is then converted to urea, which is nontoxic, in a series of five linked enzymatic reactions that comprise the urea cycle. Proteins are first degraded to amino acids, which are then deaminated with the production of ammonia (NH3). Urea is the major end product of protein and amino acid catabolism in the liver.