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Bilirubin in the urine

Medical expert of the article

Hematologist, oncohematologist
, medical expert
Last reviewed: 04.07.2025

Normally, bilirubin is not detected in urine, since unconjugated bilirubin is insoluble in water and is not excreted by the kidneys.

Conjugated bilirubin is excreted through the biliary pole of the hepatocyte into the intestine, where it is reduced by the action of dehydrogenases of the intestinal microbial flora into urobilinogen bodies. D-urobilinogen, I-urobilinogen, and L-urobilinogen are successively formed in the intestine. Most of the D- and I-urobilinogen formed in the upper sections of the large intestine is absorbed by the intestinal wall and again enters the liver through the portal vein, where it breaks down, and the products of this breakdown are again released into the intestine and, apparently, are involved in the reactions of hemoglobin synthesis. A fraction of L-urobilinogen (stercobilinogen), formed in the lower sections of the intestine, partially enters the general circulation through the lower hemorrhoidal veins and can be excreted with urine as urobilin; the larger part is excreted with feces as stercobilin, coloring it.

In children in the first months of life, due to the absence of putrefactive processes in the large intestine, stercobilin is not formed, and conjugated bilirubin is excreted unchanged.

It is known that a small amount of conjugated bilirubin in the intestine, under the influence of beta-glucuronidase, is hydrolyzed into unconjugated bilirubin and is reabsorbed via the enterohepatic pathway into the liver (enterohepatic circulation).

When plasma free bilirubin levels are high and renal excretion is low, the gradient for free bilirubin in plasma to that in the intestine is higher, and therefore in neonates a significant amount of free bilirubin can be excreted by diffusion through the intestine.

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Causes of bilirubin in urine

Obstruction of the extrahepatic bile ducts is a classic cause of bilirubinuria. Determination of bilirubin in urine (along with urobilinogen) is used in the differential diagnosis of jaundice. Bilirubinuria is observed in obstructive and parenchymatous jaundice, but is absent in hemolytic jaundice. In newborns and children of the first year of life, early urine testing helps with biliary atresia and allows early death to be avoided by timely surgical intervention, in some cases without transplantation. In viral hepatitis, bilirubin can be detected in urine before the development of jaundice. Bilirubin excretion increases with alkalosis,

Currently, diagnostic strips are more often used for qualitative determination of bilirubin in urine. In addition, oxidation methods according to Harrison and Fouchet are used, based on the ability of bilirubin to transform into biliverdin, which has an emerald-green color, under the influence of oxidants. Normally, qualitative methods for determining bilirubin in urine give a negative result.

To quantitatively determine the level of bilirubinuria, as well as to determine the level of bilirubin in the blood serum, diazo reaction followed by spectrophotometry is used.

In parenchymatous jaundice, the amount of conjugated (direct) bilirubin in the blood serum increases predominantly. Since conjugated bilirubin is soluble in water, it is easily excreted by the kidneys. The urine is colored dark. Qualitative reactions for bilirubin are sharply positive. The amount of stercobilinogen in the feces decreases, but its complete disappearance from the feces is observed only in mechanical jaundice. The intensity of bilirubinemia is higher, the higher the level of conjugated bilirubin in the blood. In severe parenchymatous jaundice, as well as in subhepatic jaundice, the amount of urobilin in the urine decreases. Qualitative reactions for urobilin may be negative. As the functional capacity of the liver and bile secretion are restored, the content of conjugated bilirubin in the blood serum decreases, the intensity of bilirubinuria falls, the amount of stercobilin in the feces increases, and qualitative reactions to urobilin again become positive.

In cases of jaundice caused by an increase in the level of free (unconjugated) bilirubin in the blood, qualitative reactions to bilirubin in the urine become negative, and to urobilin, on the contrary, positive, the amount of stercobilin in the feces increases.

Consequently, the determination of bilirubin in the blood serum, as well as qualitative reactions for bilirubin and stercobilin, have limited value for differentiating between parenchymatous and subhepatic jaundice. In some cases, the fact that with parenchymatous jaundice, especially with severe parenchymatous lesions, the blood serum contains more conjugated as well as unconjugated bilirubin may be significant, while with subhepatic jaundice, the blood contains more exclusively conjugated bilirubin. However, it should be borne in mind that even with parenchymatous jaundice occurring with pronounced cholestasis, almost exclusively conjugated bilirubin accumulates in the blood.

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