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Bilirubinuria

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Dibyajyoti Banerjee – 1st expert on this subject based on the ideXlab platform

  • Reduction of urinary thiols in nephrotic syndrome–a possible effect of free iron.
    Clinica chimica acta; international journal of clinical chemistry, 2020
    Co-Authors: Indrajit Sinha, Sandip Ghosh, Jose Jacob, Dibyajyoti Banerjee

    Abstract:

    Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual.
    We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls.
    We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33+/-4.2 micromol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45+/-10.6 micromol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7+/-0.05 micromol/l), a parameter undetectable in the healthy controls.
    We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no Bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.

  • Reduction of urinary thiols in nephrotic syndrome–a possible effect of free iron.
    Clinica Chimica Acta, 2005
    Co-Authors: Indrajit Sinha, Sandip Ghosh, Jose Jacob, Dibyajyoti Banerjee

    Abstract:

    Abstract Background Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual. Methods We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls. Result We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33±4.2 μmol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45±10.6 μmol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7±0.05 μmol/l), a parameter undetectable in the healthy controls. Conclusion We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no Bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.

Hisao Hayashi – 2nd expert on this subject based on the ideXlab platform

  • Preliminary study of spontaneous hepatitis in Long-Evans Cinnamon rats: a blood exchange may improve fetal hepatitis.
    Nagoya journal of medical science, 2020
    Co-Authors: Jun Ueyama, Shinya Wakusawa, Yasuyuki Tatsumi, Ai Hattori, Motoyoshi Yano, Hisao Hayashi

    Abstract:

    Long-Evans Cinnamon rats are a Wilson disease model highly susceptible to fulminant hepatitis around the age of 20 weeks, and hepatoma over the age of one year. Although prophylaxis has been established for the otherwise fatal hepatitis, effective treatment remains unknown. A blood exchange was tested to determine whether the prognosis of spontaneous hepatitis could be modified in icteric female rats. When Bilirubinuria appeared, the rats immediately underwent surgery. Rats under anesthesia were first cannulated into the right atrium via the carotid vein, followed by 2.5 mL of blood exchange with heparinized fresh blood from Long-Evans agouti rats. Treated rats and controls were then observed for 2 months. Compared to the 50% mortality of untreated rats, all icteric rats that received a blood exchange survived the acute episode. We confirmed that Wilson disease animals are highly susceptible to acute hepatitis and show a poor prognosis. However, a single blood exchange improved spontaneous hepatitis in this animal model. This would serve as a first step for establishing a treatment for fatal hepatitis in animals. A blood exchange may improve fulminant hepatitis of Wilson disease model rats.

  • Preliminary Study on Spontaneous Hepatitis in Long-Evans Cinnamon Rats: A Blood Exchange May Improve the Fetal Hepatitis
    Nagoya Journal of Medical Science, 2010
    Co-Authors: Jun Ueyama, Shinya Wakusawa, Yasuyuki Tatsumi, Ai Hattori, Motoyoshi Yano, Hisao Hayashi

    Abstract:

    : Long-Evans Cinnamon rats are a Wilson disease model highly susceptible to fulminant hepatitis around the age of 20 weeks, and hepatoma over the age of one year. Although prophylaxis has been established for the otherwise fatal hepatitis, effective treatment remains unknown. A blood exchange was tested to determine whether the prognosis of spontaneous hepatitis could be modified in icteric female rats. When Bilirubinuria appeared, the rats immediately underwent surgery. Rats under anesthesia were first cannulated into the right atrium via the carotid vein, followed by 2.5 mL of blood exchange with heparinized fresh blood from Long-Evans agouti rats. Treated rats and controls were then observed for 2 months. Compared to the 50% mortality of untreated rats, all icteric rats that received a blood exchange survived the acute episode. We confirmed that Wilson disease animals are highly susceptible to acute hepatitis and show a poor prognosis. However, a single blood exchange improved spontaneous hepatitis in this animal model. This would serve as a first step for establishing a treatment for fatal hepatitis in animals. A blood exchange may improve fulminant hepatitis of Wilson disease model rats.

Indrajit Sinha – 3rd expert on this subject based on the ideXlab platform

  • Reduction of urinary thiols in nephrotic syndrome–a possible effect of free iron.
    Clinica chimica acta; international journal of clinical chemistry, 2020
    Co-Authors: Indrajit Sinha, Sandip Ghosh, Jose Jacob, Dibyajyoti Banerjee

    Abstract:

    Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual.
    We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls.
    We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33+/-4.2 micromol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45+/-10.6 micromol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7+/-0.05 micromol/l), a parameter undetectable in the healthy controls.
    We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no Bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.

  • Reduction of urinary thiols in nephrotic syndrome–a possible effect of free iron.
    Clinica Chimica Acta, 2005
    Co-Authors: Indrajit Sinha, Sandip Ghosh, Jose Jacob, Dibyajyoti Banerjee

    Abstract:

    Abstract Background Albumin is a potent antioxidant as it chelates transitional metals and contains antioxidants like thiol and bilirubin. In neprotic syndrome, the defining parameter is proteinuria with hypoalbuminemia. Therefore albuminuria in nephrotic syndrome may increase toxic transitional metal ions and also can cause loss of albumin associated antioxidants causing oxidative stress to the individual. Methods We investigated this possibility and estimated some markers of oxidative stress in 20 nephrotic syndrome patients and healthy controls along with urinary thiols, urinary bilirubin and plasma free iron in both cases and in the controls. Result We found oxidative stress in 20 nephrotic syndrome patients and the markers of oxidative stress correlated significantly with proteinuria, but the urine of nephrotic syndrome patients (28.33±4.2 μmol/g creatinine)contained significantly less thiols compared to the healthy controls (88.45±10.6 μmol/g creatinine) and no biliribin. The patients plasma also showed free iron (0.7±0.05 μmol/l), a parameter undetectable in the healthy controls. Conclusion We suggest that oxidative stress and presence of free iron in the patients were responsible for less thioluria and no Bilirubinuria. A detailed study of oxidative biology in a large cohort of nephrotic syndrome patients is necessary to confirm the presence of free iron as appropriate chelation of free iron may benefit the long-term prognosis of the disease.