Urobilinogen is a colorless byproduct formed during the body’s natural process of breaking down old red blood cells. Its presence or absence is routinely checked during a standard urinalysis as a diagnostic marker. This compound reflects how effectively your liver and red blood cells are functioning. Understanding urobilinogen levels in a urine test can provide important clues about potential health conditions.
The Origin Story: How Urobilinogen is Formed
The metabolic journey begins when red blood cells reach the end of their lifespan, typically around 120 days, and are broken down. This releases hemoglobin, which is converted into the yellow pigment bilirubin. This initial form, unconjugated bilirubin, is not water-soluble and must be transported to the liver bound to the protein albumin.
Once in the liver, unconjugated bilirubin is chemically altered, or conjugated, to become water-soluble. This conjugated bilirubin is secreted by the liver as a component of bile, which is released into the small intestine. The majority of the bilirubin then continues its journey into the large intestine, where it encounters resident gut bacteria.
These intestinal bacteria use enzymes to chemically reduce the conjugated bilirubin, transforming it into the colorless compound, urobilinogen. Most of this newly formed urobilinogen (approximately 80 to 90%) is further reduced into stercobilinogen and stercobilin, which gives feces its characteristic brown color upon oxidation.
Normal Excretion and Testing in Urine
Following its creation in the gut, a small portion of the urobilinogen (about 10 to 20%) is reabsorbed into the bloodstream. The majority of this reabsorbed urobilinogen travels back to the liver for reprocessing and re-excretion into the bile, a cycle known as the enterohepatic circulation.
A small fraction of the reabsorbed urobilinogen bypasses the liver and travels through the bloodstream to the kidneys. The kidneys filter this small amount, which is then excreted in the urine. This urinary urobilinogen is converted into urobilin, the pigment responsible for urine’s yellow color.
Since it is a normal byproduct of metabolism, a small amount of urobilinogen is expected in urine. The normal range is typically a trace amount, often between 0.1 and 1.8 milligrams per deciliter (mg/dL). Levels are usually measured using a reagent strip, or dipstick, as part of a routine urinalysis.
Interpreting High Levels
Elevated levels of urobilinogen (generally above 2.0 mg/dL) indicate that either too much bilirubin is being produced or the liver’s processing capacity is overwhelmed. A primary cause is an increased rate of red blood cell destruction, known as hemolytic anemia. When red blood cells break down rapidly, the resulting surge in bilirubin leads to a greater amount being converted into urobilinogen in the intestine.
This excess urobilinogen is reabsorbed into the blood, overwhelming the liver’s ability to clear it and causing more to spill into the urine. High levels can also signal a problem with the liver itself, such as early or mild hepatitis or cirrhosis. In these cases, the liver may struggle to efficiently re-excrete the reabsorbed urobilinogen from the enterohepatic circulation back into the bile. This impaired re-excretion allows more urobilinogen to remain in the bloodstream and be eliminated by the kidneys.
Interpreting Low or Absent Levels
A low or absent reading of urobilinogen can be significant, suggesting a problem with either its production or transport. The most common reason for complete absence is an obstruction of the bile duct, which prevents conjugated bilirubin from reaching the intestine. If bilirubin cannot enter the gut, intestinal bacteria cannot convert it into urobilinogen, causing the urine level to drop.
Low levels can also occur in people taking broad-spectrum antibiotics. These medications reduce or eliminate the gut bacteria responsible for converting bilirubin to urobilinogen, effectively stopping the compound’s production. Additionally, severe liver failure can lead to low urobilinogen because the damaged liver may be unable to effectively conjugate bilirubin in the first place. If this initial conversion step is impaired, insufficient conjugated bilirubin is available to be sent to the intestine for urobilinogen formation.