Albumin is a protein produced by the liver, circulating in the bloodstream. Its primary function is maintaining oncotic pressure, which helps keep fluid within blood vessels, preventing leakage into surrounding tissues. Albumin also serves as a transporter for various substances, including hormones, fatty acids, and medications, moving them throughout the body. Hypoalbuminemia is a condition of abnormally low levels of this protein in the blood.
When the Liver Can’t Make Enough
The liver is the sole site of albumin synthesis, producing 9-12 grams of albumin daily. When the liver is damaged or diseased, its capacity to produce this protein diminishes, leading to reduced circulating levels. Chronic liver diseases, such as cirrhosis, severely impair the liver’s synthetic function. Cirrhosis involves extensive scarring of liver tissue, disrupting the normal architecture and function of hepatocytes, the cells responsible for albumin production.
Chronic hepatitis, whether caused by viral infections (like hepatitis B or C), alcoholic liver disease, or non-alcoholic steatohepatitis (NASH), can also progressively damage liver cells. Over time, this sustained injury reduces the number of functional hepatocytes available for albumin synthesis. Severe acute liver failure, involving rapid and widespread destruction of liver cells, can precipitously drop albumin production, leading to a sudden and pronounced decrease in blood albumin levels.
When the Body Loses Too Much
Albumin levels can also become low due to excessive loss. Kidney disease, particularly nephrotic syndrome, is a prominent example where the kidneys’ filtration barriers become damaged. Normally, these barriers prevent large proteins like albumin from escaping into the urine. In nephrotic syndrome, however, the impaired glomeruli allow significant amounts of albumin to leak from the bloodstream into the urine, a condition known as proteinuria.
Severe burns are another major cause of albumin loss. When extensive skin surfaces are burned, the integrity of capillaries and blood vessels is compromised. This damage leads to increased vascular permeability, allowing large quantities of albumin-rich plasma to seep out of the circulation into the burned tissues or onto the body surface. This direct leakage can result in substantial and rapid depletion of circulating albumin.
Albumin can also be lost through the gastrointestinal tract in protein-losing enteropathies. Disorders such as inflammatory bowel disease, severe celiac disease, or lymphatic obstruction can lead to increased permeability of the intestinal lining. This allows albumin and other plasma proteins to leak into the digestive tract, where they are degraded or excreted, rather than reabsorbed into the bloodstream.
When You Don’t Get Enough
Insufficient dietary intake or impaired protein absorption can lead to low albumin levels, as the body lacks the necessary building blocks for synthesis. Albumin is constructed from amino acids derived from dietary protein. Prolonged and severe malnutrition, such as starvation or severe protein-calorie malnutrition, directly limits the availability of these amino acids. Without adequate raw materials, the liver cannot produce sufficient albumin to meet the body’s demands.
Malabsorption conditions further complicate this process by preventing the body from effectively absorbing ingested proteins. Diseases like inflammatory bowel disease (Crohn’s disease or ulcerative colitis) can damage the intestinal lining, reducing its ability to absorb nutrients and amino acids. Celiac disease, an autoimmune disorder triggered by gluten, causes damage to the small intestine’s villi, impairing nutrient absorption. Certain bariatric surgeries, which alter the digestive tract, can also lead to malabsorption, limiting the availability of amino acids for albumin synthesis.
Inflammation and Fluid Shifts
Systemic inflammation and critical illness are significant contributors to reduced albumin levels through several mechanisms. During severe inflammatory states, such as sepsis, major surgery, or severe infections, metabolic priorities shift. The liver, while still capable of producing albumin, prioritizes the synthesis of “acute phase proteins” (like C-reactive protein) involved in the immune response, leading to a down-regulation of albumin production.
Inflammation also increases the breakdown rate of existing albumin and causes increased vascular permeability, known as capillary leak syndrome. This allows albumin to leak out of blood vessels and accumulate in the interstitial spaces or tissues, reducing its concentration within the circulation. This redistribution, combined with reduced synthesis, significantly lowers plasma albumin levels during inflammatory conditions.
Fluid overload can dilute the albumin concentration in the blood, leading to a seemingly low reading. In severe heart failure, the heart’s inability to pump blood effectively can lead to fluid retention and increased total body water. This excess fluid expands the plasma volume, effectively diluting circulating albumin without necessarily reducing the total amount of albumin in the body. While the absolute amount of albumin might not have decreased, its concentration per unit volume of blood appears lower.