Everything you need to know about albumin and liver function

Click here to learn about albumin metabolism, and how it is used to assess liver function in your patients.
Last update26th Jan 2021

In addition to bilirubin, albumin is another mainstay on a typical liver function panel. Let’s review how albumin is formed, its functions, and what serum albumin levels can tell us about your patients’ health.

Where is albumin formed and what does it do?

Albumin is the most abundant circulating protein found in the plasma. It represents half of the total protein content in the plasma of a healthy patient. A normal plasma albumin concentration in a healthy patient is 3.5–5.0 g / dL.

Albumin is synthesized by liver hepatocytes, but very little albumin is stored in the liver. It is rapidly excreted into the bloodstream at the rate of 10–15 g / day in people with normally functioning livers.

In humans, serum albumin functions as a significant modulator of plasma oncotic pressure and as a transporter of endogenous and exogenous ligands (e.g., drugs).

Figure 1. Functions of serum albumin include the modulation of plasma oncotic pressure and the transportation of endogenous and exogenous ligands.

What can serum albumin measurements tell us?

In clinical medicine, serum albumin measurements are a highly sensitive marker of a patient's nutritional status. Low albumin levels may indicate malnutrition, chronic liver disease, or inflammatory disease.

The half-life of albumin is approximately three weeks. When liver function is impaired over a prolonged period, albumin synthesis is also impaired, which results in low levels of albumin. For this reason, hypoalbuminemia is a common finding in chronic liver disease. However, a significant reduction in serum albumin levels is not observed in patients with acute liver failure.

Figure 2. Low serum albumin can indicate malnutrition, chronic liver disease (not acute), or inflammatory disease.

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Recommended reading

  • Chalasani, N, Younossi, Z, Lavine, JE, et al. 2012. The diagnosis and management of non-alcoholic fatty liver disease: practice guideline by the American Gastroenterological Association, American Association for the Study of Liver Diseases, and American College of Gastroenterology. Gastroenterology142: 1592–1609. PMID: 22656328
  • Fuchs, S, Bogomolski-Yahalom, V, Paltiel, O, et al. 1998. Ischemic hepatitis: clinical and laboratory observations of 34 patients. J Clin Gastroenterol26: 183–186. PMID: 9600366
  • Lok, ASF and McMahon, BJ. 2007. Chronic hepatitis B. Hepatology45: 507–539. PMID: 17256718
  • Moussavian, SN, Becker, RC, Piepmeyer, JL, et al. 1985. Serum gamma-glutamyl transpeptidase and chronic alcoholism. Influence of alcohol ingestion and liver disease. Dig Dis Sci30: 211–214. PMID: 2857631
  • Myers, RP, Cerini, R, Sayegh, R, et al. 2003. Cardiac hepatopathy: clinical, hemodynamic, and histologic characteristics and correlations. Hepatology37: 393–400. PMID: 12540790
  • Rej, R. 1978. Aspartate aminotransferase activity and isoenzyme proportions in human liver tissues. Clin Chem24: 1971–1979. PMID: 213206
  • van de Steeg, E, Stránecký, V, Hartmannová, H, et al. 2012. Complete OATP1B1 and OATP1B3 deficiency causes human Rotor syndrome by interrupting conjugated bilirubin reuptake into the liver. J Clin Invest122: 519–528. PMID: 22232210

About the author

Amer Wahed, MD FRCPath
Amer is a Professor and Vice Chair (Clinical Pathology) and Associate Residency Program Director in the Department of Pathology and Laboratory Medicine at the University of Texas, Health Science Center at Houston, USA.
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