Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (1265 page)

   Limitations

   cTnT may be increased in some patients with skeletal muscle injury and myotonic dystrophy but not in third-generation assays. cTnI is not increased by skeletal muscle injury, making it more highly specific for myocardial injury.

   Heterophile antibodies are one of the most common reasons for false-positive results due to interference with the immunoassay. Human antimouse antibodies, autoantibodies, rheumatoid factor also may cause false-positive results in addition to hemolysis of sample or fibrin clots in the specimen.

   Unfortunately, most point-of-care assays are not as sensitive as those performed in central laboratories. If a single value is out of proportion to others, it is recommended to respin the point-of-care sample and reanalyze.

   As troponin is able to detect very early stages of disease and confer a worse prognosis if elevated, if confounding factors for laboratory analysis of troponin are suspected, the use of other cardiac biomarkers in addition to direct cardiac imaging (or biopsy for transplant recipients) is strongly recommended.

Suggested Readings

Apple FS, Jesse RL, Newby LK, et al. National Academy of Clinical Biochemistry. National Academy of Clinical Biochemistry and IFCC Committee for Standardization of Markers of Cardiac Damage Laboratory Medicine Practice Guidelines: Analytical issues for biochemical markers of acute coronary syndromes.
Clin Chem.
2007;53(4):547–551.

Jaffe AS. The clinical impact of the universal diagnosis of myocardial infarction.
Clin Chem Lab Med.
2008;46(11):1485–1488.

Morrow DA, Cannon CP, Jesse RL, et al. National Academy of Clinical Biochemistry. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical characteristics and utilization of biochemical markers in acute coronary syndromes.
Circulation.
2007;115(13):e356–e375.

Roongsritong C, Warraich I, Bradley C. Common causes of troponin elevations in the absence of acute myocardial infarction incidence and clinical significance.
Chest.
2004;125(5):1877–1884.

Starrow AB, Apple FS, Wu AH, et al. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: point of care testing, oversight, and administration of cardiac biomarkers for acute coronary syndromes.
Point Care.
2007;6(4):215–222.

Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF Task Redefinition myocardial infarction.
Eur Heart J.
2007;28:2525–2538;
Circulation
. 2007;116:2634–2653;
J Am Coll Cardiol
. 2007;50:2173–2195.

Vafaie M, Biener M, Mueller M, et al. Analytically false or true positive elevations of high sensitivity cardiac troponin: a systematic approach.
Heart.
Online April 25. Doi: 10.1136/heart jnl-2012-303202

UREA NITROGEN, URINE

   Definition

   Urea is a low molecular weight substance that is freely filtered by glomeruli, and the majority is excreted into the urine, although variable amounts are reabsorbed along the nephron. Urine urea nitrogen is a measure of protein breakdown in the body. Urea is excreted by the kidneys, so excretion of urea can reflect kidney function. Approximately 50% of urinary solute excretion and 90–95% of total nitrogen excretion is composed of urea under normal conditions.

   
Normal range:

   Twenty-four–hour urine: 2–20 g/day

   Random urine: