Home  |  Rus  |   Ask a question  Contact
Articles  |  Facebook  |  Links

Bilirubinuria, urobilinogenuria



Bilirubinuria is the presence of bilirubin in urine. Bilirubin is the end product of the metabolism of bile pigments. Normal bilirubin in urine is not detected. The appearance in the urine in conjugated form precedes hyperbilirubinemia.

Bilirubin refers to a group of chromoproteins and the end product breakdown of hemoglobin, myoglobin, cytochrome, catalase, and other substances. bilirubin formation occurs mainly in reticuloendothelial system spleen, liver and bone marrow. The plasma bilirubin is bound to albumin, forming a complex compound (unconjugated, free or indirect bilirubin), which does not pass kidney filter.

Unconjugated bilirubin is absorbed by hepatocytes. In hepatocyte unconjugated bilirubin is connected to an activated glucuronic acid.

Formation of bilirubin mono-and bilirubin-diglyukuronidy, which are conjugated bilirubin (BC). BC is water soluble and pass kidney filter. BC is derived from bile in the bile capillaries in series, strokes, gall bladder, small intestine, where there is a further transformation of bilirubin to form urobilinogen, mezobilirubinogena, hydrobilirubin and other compounds.

Urobilinogen in duodenal enterocytes and absorbed with the current portal venous blood returns to the liver where it is completely oxidized to dipirrolov. Other derivatives of bilirubin in the colon under the influence of the reducing intestinal flora become sterkobilinogen and excreted in the feces. A small part of sterkobilinogena in the colon is absorbed into the bloodstream and through the hemorrhoidal veins and inferior vena cava enters the kidneys and excreted in urine.

Thus, in normal urine contains small amounts (traces) stercobilinogen (stercobilin), which is in the urine called urobilinogen (urobilin) because modern methods used in clinical diagnostic laboratories do not allow to differentiate sterkobilinogen of urobilinogen.

Increased stercobilin in feces and urine (bilirubinuria causes):

  • elevated intracellular hemolysis of red blood cells
  • resorption of massive hematoma
  • diseases of the colon associated with an increased reabsorption of stercobilinogen

Conjugated bilirubin is detected in urine at bilirubinemia of approximately 30-34 mmol/l or 20 mg/L. In this concentration of conjugated bilirubin in the blood appears yellowness of the mucous membranes and sclera.

The metabolism of bilirubin is accompanied by hyperbilirubinemia, bilirubinuriey, urobilinuria and jaundice. Identify several pathogenic mechanisms of these disorders:

  • increased, mainly intracellular, the destruction of red blood cells
  • damage to the liver parenchyma (any etiology)
  • obturation of the bile duct or bile duct
  • congenital (hereditary) and acquired defects in the exchange of bile pigments



Urobilinogenuria (stercobilinogenuria) - is revealing urobilinogen in the urine, possibly caused by metabolic impairments in hepatocyte, in which the urobilinogen is not oxidized in the liver cell to dipirrolov. Unoxidized urobilinogen returned to the blood and out of it - in the urine. Urobilinogenuria may be an early sign of lesion of liver parenchyma. It is revealed during an infectious prodrome (serum) hepatitis.

The increase of stercobilin (urobilin) in the feces and urine is caused by the enhanced intracellular hemolysis of erythrocytes. Formed an unconjugated bilirubin entering the intestine, gives a large number of stercobilinogen (urobilinogen). Last absorbed into the blood and passes into the urine.

Urobilinuria may develop in the amplification of the direct pathway of bilirubin, resulting in splitting gemsoderzhaschih pigments (shunt hyperbilirubinemia). Urobilinogenuria causes:

  • pernicious anemia
  • gunther porphyria
  • thalassemia
  • aplastic anemia
  • hemorrhages

Increase stercobilinogen (urobilin) is accompanied by physiological jaundice of newborn due to high excess erythrocyte hemolysis and transient immaturity of hepatocytes, due to lack of activity of liver enzymes, including glyukuroniltransferazy.

A similar pathogenetic mechanism is observed at eritremii and dismielopoeze (ineffective erythropoiesis), when the conjugation produced large amounts of unconjugated bilirubin requires high activity glyukuroniltransferazy. Exceeding the limit of its activity is accompanied by hyperbilirubinemia, increased sterkobilinogena in feces and its appearance in the urine (urobilin).

Increasing stercobilinogen in feces and urine (urobilin) is observed as a result of impaired ability of hepatocytes to bind bilirubin blood at its normal output. Unconjugated bilirubin, the number is usually low, was escorted into the clinic subikterichnostyu sclera. The mechanism of bilirubin metabolism disorders, apparently due to lack of enzyme systems to capture and transport of bilirubin through the cell membrane in the hepatocyte (postgepatitnaya giperbulirubinemiya Kalk, congenital anomaly of Gilbert's, Crigler-Najjar syndrome).


If you have any questions about the diagnosis or treatment or bilirubinuria and urobilinogenuria, you can specify them with our urologist or a nephrologist on the phone: +7 (926) 988-14-23



Neurology, Neurosurgery
+7 (926) 988-14-23
Surgery, Traumatology
+7(903) 167-99-20
+7(909) 994-94-66
Mon...Fri 10:00–20:00
Sat 09:00–15:00