Bilirubinuria and urobilinogenuria

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Bilirubinuria is the presence of bilirubin in the urine. Bilirubin is the end product of the exchange of bile pigments. Normally, bilirubin is not detected in the urine. Its appearance in urine in conjugated form is preceded by hyperbilirubinemia.

Bilirubin belongs to the group of chromoproteins and is the end product of the breakdown of hemoglobin, myoglobin, cytochrome, catalase, and other substances. Bilirubin is formed mainly in the RES of the spleen, liver, and bone marrow. In plasma, bilirubin binds to albumin, forming a complex compound (unconjugated, free, or indirect bilirubin) that does not pass the renal filter.

Unconjugated bilirubin is taken up by hepatocytes. In the hepatocyte, unconjugated bilirubin combines with activated glucuronic acid.

Bilirubin-mono- and bilirubin-diglucuronides are formed, which are conjugated bilirubin (BC). BC is water-soluble and passes the renal filter. BC is excreted with bile sequentially into the bile capillaries, ducts, gall bladder, small intestine, where the further transformation of bilirubin occurs with the formation of urobilinogen, mesobilirubinogen, mesobilirubin, and other compounds.

Urobilinogen in the duodenum is absorbed by enterocytes and returns to the liver with the portal vein blood flow, where it is completely oxidized to dipyrroles. The rest of the derivatives of bilirubin in the colon under the influence of reducing intestinal flora are converted into stercobilinogen and excreted in the feces. A small part of stercobilinogen in the colon is absorbed into the bloodstream and through the hemorrhoidal veins and the inferior vena cava enters the kidneys and excreted in the urine.

Thus, normal urine contains a small amount (traces) of stercobilinogen (stercobilin), which in urine is usually called urobilinogen (urobilin), because modern methods used in clinical diagnostic laboratories do not allow differentiating stercobilinogen from urobilinogen.

An increase in stercobilin in feces and urine is possible with:

  • increased intracellular hemolysis of erythrocytes
  • resorption of massive hematomas
  • diseases of the colon, accompanied by an increase in stercobilinogen reabsorption

Conjugated bilirubin is found in urine with bilirubinemia, which is approximately 30-34 μmol / L or 20 mg / L. At this concentration of conjugated bilirubin in the blood, yellowness of the mucous membranes and sclera appears.

Disruption of bilirubin metabolism is accompanied by hyperbilirubinemia, bilirubinuria, urobilinuria, and jaundice. There are several pathogenetic mechanisms of these disorders:

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



Urobilinogenuria is the detection of urobilinogen in urine, possible due to metabolic disorders in the hepatocyte, in which urobilinogen is not oxidized in the hepatic cell to dipyrroles. The unoxidized urobilinogen is returned to the bloodstream, and from it to the urine. Urobilinogenuria may be an early sign of liver parenchymal damage. It is detected during the prodrome of infectious (serum) hepatitis.

An increase in stercobilinogen (urobilin) in feces and urine is observed due to increased intracellular hemolysis of erythrocytes. The formed unconjugated bilirubin, entering the intestine, gives large amounts of stercobilinogen. The latter is absorbed into the bloodstream and passes into the urine.

Urobilinuria can develop when the direct pathway of bilirubin formation is enhanced, as a result of the cleavage of heme-containing pigments (shunt hyperbilirubinemia). Urobilinuria occurs when:

  • pernicious anemia
  • Gunther porphyria
  • thalassemias
  • aplastic anemia
  • hemorrhages

An increase in stercobilinogen (urobilin) is accompanied by physiological jaundice of newborns, caused by high hemolysis of excess erythrocytes and transient immaturity of hepatocytes, due to insufficient activity of liver enzymes, including glucuronyl-transferase.

A similar pathogenetic mechanism is observed in erythremia and dysmyelopoiesis (ineffective erythropoiesis) when high glucuronyl transferase activity is required for the conjugation of the large amounts of unconjugated bilirubin formed. Exceeding the limit of its activity is accompanied by hyperbilirubinemia, an increase in stercobilinogen in feces, and its appearance in the urine (urobilin).

An increase in stercobilinogen in feces and urine (urobilin) is observed as a result of an impaired ability of hepatocytes to bind blood bilirubin during normal production. Bilirubin is unconjugated, its amount is usually low, accompanied in the clinic by subicteric sclera. The mechanism of disruption of bilirubin metabolism is apparently due to a deficiency of enzyme systems that ensure the capture and transport of bilirubin across the cell membrane into the hepatocyte (post-hepatitis hyperbulirubinemia Kalk, congenital Gilbert's anomaly, Crigler-Nayyard syndrome).