urea nitrogen in serum/plasma
Reference interval
- Male & Female: 6 - 18 mg/dL
Principle
Clinical significance
Urea, formed in the liver by the deamination of amino acids, is the primary method of nitrogen excretion. Urea, then, is the end product of protein metabolism & is formed in the liver. After synthesis, urea travels through the blood & is excreted in the urine.
Acute or chronic renal failure is the most common cause of high BUN levels. In prerenal failure, a low renal blood supply, such as occurs with hypovolemia or congestive heart failure, leads to reduced glomerular filtration & therefore an elevated BUN. In renal failure, damage to the nephrons, particularly such as occurs with glomerulonephritis or pyelonephritis, leads to decreased glomerular filtration & excretion. As a result, the blood urea nitrogen begins to rise when the glomerular filtration rate falls below 50 mL/min due to increased resorption of urea in the proximal tubules (the normal GFR in an average size manis approximately 125 mL/min). The BUN/creatinine ratio increases as well (> 20).
Postrenal failure resulting from urinary tract obstructions can also cause uremia. Prostatic enlargement is probably the most common cause of urinary tract obstruction.
Other causes of borderline elevated levels of BUN are usually high protein intake & excessive body protein catabolism such as occurs with sepsis or fever, glucocorticoid administration, tetracyclines & gastrointestinal bleeding.
Increases
- acute renal failure
- chronic renal failure
- prerenal azotemia (poor renal perfusion)
- intrinsic renal failure
- post obstructive uropathy
- gastrointestinal bleeding
- hyperalimentation
- albumin infusions[11]
- catabolic states[11], glucocorticoids
- pharmaceutical agents:
- in vivo effects
- alkaline antacids, antimony salts, arsenicals, cephaloridine, furosemide, gentamicin, kanamycin, methyldopa, neomycin, tetracyclines[11]
- chemical interferences
- chloral hydrate, chlorobutanol, guanethidine
- in vivo effects
Decreases
- muscle atrophy
- protein malnutrition
- cirrhosis[11]
Specimen
- no special patient preparation is required
- collect whole blood & allow to clot according to manufacturer's instructions
- specimens are collected in a red top vacutainer & should be separated immediately from the cells after collection
- minimum sample size 0.5 mL: with an optimum size of 1.0 mL or larger
More general terms
Additional terms
Component of
- chemistry 7 panel (Chem-7 SMA7)
- chemistry 8 panel (basic metabolic panel, BMP, basic chemistry panel)
- chemistry 8 panel with ionized calcium; basic metabolic panel (BMP) with ionized calcium
- chemistry 14 panel (comprehensive metabolic panel, CMP, chem 12, SMA12, SMA20)
References
- ↑ Kodak Ektachem 700 Analyzer Operator's Manual, Kodak Clinical Products, Rochester, New York.
- ↑ Kodak Ektachem Slide Package Inserts, Kodak Clinical Products Rochester, New York.
- ↑ Kodak Ektachem Training Manual, Kodak Clinical Products, Rochester, New York.
- ↑ Tilkian, Conover, & Tilkian: Clinical Implications of Laboratory Tests, C. V. Mosby Company, St. Louis, Mo, p. 18, 1979.
- ↑ Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 620.
- ↑ Clinical Diagnosis & Management by Laboratory Methods, 19th edition, J.B. Henry (ed), W.B. Saunders Co., Philadelphia, PA. 1996, pg 12.
- ↑ Urea Nitrogen, Serum or Plasma Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0020023.jsp
- ↑ Panel of 11 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0020144.jsp
- ↑ Panel of 9 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0020399.jsp
- ↑ Panel of 15 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0020408.jsp
- ↑ 11.0 11.1 11.2 11.3 11.4 11.5 Medical Knowledge Self Assessment Program (MKSAP) 16, 17. American College of Physicians, Philadelphia 2012, 2015