Summary
Albumin is the most abundant protein in the blood and is produced exclusively by the liver. It maintains oncotic pressure, transports hormones and drugs, and is the best single marker of liver synthetic function. Low albumin is a hallmark of chronic liver disease, malnutrition, and inflammatory states — and is one of the strongest predictors of mortality in hospitalised patients.
The liver produces approximately 10–15 grams of albumin per day. With a half-life of around 20 days, albumin reflects chronic rather than acute changes in liver synthetic function — making it a better marker of chronic liver disease than acute hepatitis.
Albumin falls in three main circumstances: (1) the liver cannot make enough (cirrhosis, chronic hepatitis); (2) it is lost from the body (nephrotic syndrome, protein-losing enteropathy, burns); or (3) production is suppressed by acute inflammation.
Albumin is also critical for interpreting calcium and drug levels. Low albumin causes a factitious fall in total calcium (corrected calcium accounts for albumin) and alters the free fraction of many protein-bound drugs.
What It Is
Albumin (Alb) is a 67 kDa non-glycosylated plasma protein synthesised by hepatocytes at a rate of 10–15 g/day. It serves as: (1) the main determinant of plasma oncotic pressure, preventing fluid from leaking out of capillaries into tissues; (2) a transport protein for bilirubin, fatty acids, thyroid hormones, cortisol, calcium, and many drugs; and (3) an antioxidant and free-radical scavenger.
Albumin has a half-life of 20 days, meaning serum levels only fall significantly over weeks of impaired synthesis or increased loss. This makes it a marker of chronic rather than acute liver disease. The Child-Pugh score — used to stage the severity of cirrhosis — includes albumin alongside bilirubin, PT, ascites, and encephalopathy.
Reference range in UK adults: 35–50 g/L. Levels below 30 g/L are associated with significant oedema and ascites.
Functions
Plasma oncotic pressure
Albumin generates the osmotic pressure that keeps fluid within blood vessels — low albumin causes oedema, ascites, and pleural effusions.
Liver synthetic function marker
Exclusively produced by the liver, albumin is the gold-standard marker of hepatic synthetic function in chronic liver disease.
Transport protein
Carries bilirubin, fatty acids, thyroid hormones, cortisol, calcium, and many drugs through the bloodstream — essential for drug pharmacokinetics.
Nutritional status indicator
Albumin reflects chronic protein and caloric adequacy — low albumin is a reliable marker of significant malnutrition in the absence of acute inflammation.
Reference Ranges
Serum Albumin
Measured in g/L| Status | Range (g/L) | Range (g/dL) | What it means |
|---|---|---|---|
| Low | < 35 | < 3.5 | Hypoalbuminaemia — investigate for liver disease, malnutrition, kidney loss, or inflammation. |
| Normal | 35–50 | 3.5–5.0 | Adequate liver synthetic function and protein status. |
| High | > 50 | > 5.0 | Elevated — usually from dehydration. Rarely clinically significant in isolation. |
Albumin is a negative acute phase reactant — it falls during inflammation regardless of liver function. Interpret in the context of CRP and clinical status. Half-life of 20 days means changes lag behind clinical events by weeks.
Symptoms of Imbalance
Low albumin produces symptoms related to loss of oncotic pressure and impaired protein transport.
- Peripheral oedema — swelling of the ankles and legs
- Ascites — fluid accumulation in the abdomen
- Pleural effusion — fluid around the lungs
- Poor wound healing and increased infection risk
- Fatigue and muscle weakness
- Altered drug responses — low albumin increases free fraction of many drugs
- High albumin is almost always from dehydration — symptoms relate to volume depletion
- Thirst, dark urine, and dizziness on standing
Causes of Imbalance
- Chronic liver disease (cirrhosis, chronic hepatitis)
- Malnutrition and protein deficiency
- Nephrotic syndrome — urinary albumin loss
- Protein-losing enteropathy (Crohn's, coeliac disease)
- Acute inflammation (negative acute phase reactant)
- Burns — massive protein loss
- Congestive heart failure (dilutional)
- Dehydration — haemoconcentration raises albumin
- Rare — no pathological cause of truly elevated albumin is well-recognised
FAQs
Not necessarily. Albumin falls in several circumstances: liver disease (reduced synthesis), malnutrition (insufficient protein substrate), nephrotic syndrome (urinary loss), protein-losing enteropathy (gut loss), and acute illness (negative acute phase response). The clinical context — alongside other liver markers, urinalysis, and CRP — determines the cause.
About 45% of calcium in the blood is bound to albumin. When albumin falls, total calcium appears low — but the biologically active ionised calcium may be normal. Corrected calcium = measured calcium + 0.02 × (40 − albumin in g/L). This adjustment is essential before acting on a ‘low’ calcium result in someone with low albumin.
Yes — particularly in acute illness or chronic inflammation. Albumin is a negative acute phase reactant: the liver diverts protein synthesis toward acute phase proteins (CRP, fibrinogen) in response to inflammation or injury, reducing albumin production. This means albumin can fall to 30 g/L within 24–48 hours of major surgery or serious infection, even with normal nutritional intake.
Albumin has a half-life of approximately 20 days, so recovery after the underlying problem is resolved is slow — it can take weeks to return to normal even after successful treatment. Prealbumin (transthyretin) has a much shorter half-life (2 days) and is a more sensitive marker of short-term nutritional recovery, though it is less commonly measured.
Yes — significantly. Many drugs are highly protein-bound (e.g. warfarin, phenytoin, diazepam, furosemide). Low albumin increases the free (active) drug fraction, potentially causing toxic effects at standard doses. This is particularly important in liver disease, where albumin is low and drug metabolism is also impaired. Always inform your doctor of any albumin abnormality when reviewing medications.
References
- Ballmer PE. Causes and mechanisms of hypoalbuminaemia. Clin Nutr. 2001;20(3):271–273. View source
- Don BR, Kaysen G. Serum albumin: relationship to inflammation and nutrition. Semin Dial. 2004;17(6):432–437. View source
- Pugh RN, et al. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg. 1973;60(8):646–649. View source