Diagnostic Use
Urea is synthesised mainly in the liver as the final degradation product arising from nitrogen containing amino acids and pyrimidine catabolism. More than 90% of urea are excreted through the kidneys.
Like plasma creatinine, urea is an imperfect endogenous marker of glomerular filtration, indirectly reflecting kidney filtration function. While urea is freely filtered by glomeruli, about 40-70% is passively reabsorbed, a process dependent on the urine flow rate (low flow increase reabsorption). Urea level is also affected by non-renal factors including amount of protein intake and rate of hepatic synthesis.
Increase in plasma urea disproportional to a normal or raised creatinine may suggest catabolic state of tissue breakdown, post gastrointestinal bleed, pre-renal azotaemia e.g. from dehydration or shock, high protein intake especially in uraemic patients, or post-renal obstruction. In primary adrenal insufficiency, urea is usually raised. In secondary adrenal insufficiency, there may be a normal urea (as renin-angiotensin-aldosterone system still intact) or even low urea with dilutional hyponatremia as glucocorticoids are required to excrete water load.
Low plasma urea can be found in patients with low protein intake or severe liver disease with impaired synthesis.
Urea clearance [i.e. Urine urea concentration (in mmol/L) * volume of urine (in ml/min) divided by plasma urea (in mmol/L)] tend to underestimate glomerular filtration due to passive reabsorption of urea in the renal tubules. In chronic renal failure, osmotic diuresis at the remaining functioning nephrons reduce reabsorption of urea and thus urea clearance more closely reflect inulin clearance.
Urea is featured in some composite scoring systems (e.g. PSI, CURB-65, APACHE II, BAR, GBS) that aid prognosticating e.g. respiratory infections, gastrointestinal bleeding and patients in critical care.
Test Method
Principle: Kinetic test with urease and glutamate dehydrogenase.
Analyser: Roche Diagnostics Cobas c703
Reagent: UREAL