Tubular dysfunction in the deeply jaundiced patient with hepatorenal syndrome

Rector, William G.; Kanel, Gary C.; Rakela, Jorge; Reynolds, Telfer B.

doi:10.1002/hep.1840050229

Cited by 25 publications

(12 citation statements)

References 10 publications

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“…However, no evaluation of the proximal tubular function was attempted, whereas a threshold serum bilirubin concentration of about 23 mg/dL (393 mol/L) differentiated patients with normal and high urine ␤ 2 -microglobulin concentrations. 18 Even though there was a correlation between the markers of proximal tubular dysfunction and serum bilirubin levels in our study, no evidence of a threshold serum bilirubin concentration was noticed, because renal tubular abnormalities were observed even in patients with lower serum bilirubin levels. Furthermore, hypouricemia and hyperuricosuria resulting from defective postsecretory reabsorption of uric acid has been previously described in patients with primary biliary cirrhosis.…”

Section: Discussioncontrasting

confidence: 80%

Partially reversible renal tubular damage in patients with obstructive jaundice

et al. 2001

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Decreased serum uric acid levels resulting from renal urate wasting have been occasionally encountered in jaundiced patients. However, in these cases, there are no data concerning the underlying renal tubular defects. In the present study, we investigated the renal tubular function in 35 patients with obstructive jaundice of various severity and causes (11 with lithiasis, 17 with carcinoma, and 7 with intrahepatic cholestasis). A detailed study of the renal tubular function was performed. Beyond the conventional methods, 1 H-NMR spectroscopy of urine was used to evaluate noninvasively renal damage by the characteristic perturbation in the excretion pattern of low-molecular weight endogenous metabolites. On admission, patients with obstructive jaundice had significantly lower serum uric acid and phosphate levels and higher bile acid concentrations compared with 40 age-and sex-matched controls. Serum uric acid levels presented a negative correlation with the total and direct bilirubin as well as the fractional excretion of uric acid. Furthermore, a great number of the patients studied developed one or more proximal tubular dysfunction manifestations beyond uricosuria, such as renal glucosuria, phosphaturia, and increased excretion of ␣ 1 -microglobulin. 1 H-NMR spectroscopy of the urine showed decreased levels of citrate and hippurate and increased levels of 3-hydroxybutyrate and acetate. In 12 patients partial or complete remission of jaundice was followed by an improvement of the proximal renal tubular damage. In conclusion, obstructive jaundice can cause a partially reversible generalized proximal tubular dysfunction. (HEPATOLOGY 2001;33:1365-1369.)It has been occasionally reported that jaundiced patients, particularly those suffering from cancer, develop decreased serum uric acid levels resulting from inappropriate uricosuria. 1-6 However, no detailed evaluation of the underlying tubular abnormalities leading to the hypouricemia has been undertaken yet. In the present study, we examined the renal tubular function in patients with obstructive jaundice of various severity and causes to explore whether the urate wasting, commonly encountered in such cases, is an isolated lesion or part of a generalized proximal tubular defect. Beyond the conventional methods, we used 1 H-NMR spectroscopy to evaluate noninvasively the underlying renal damage by the characteristic perturbation in the excretion pattern of low molecular weight endogenous metabolites. In fact, urinalysis by NMR spectroscopy has led to the detailed investigation of the excretion pattern in various physiological and pathological situations and allowed the detection of unexpected constituents related to disease or tissue damage. 7-9 PATIENTS AND METHODSWe studied 35 patients with obstructive jaundice (21 male, 14 female, mean age 40 Ϯ 11 years) during their hospitalization. The patients had jaundice with predominantly conjugated bilirubinemia in combination with prominent elevations of the alkaline phosphatase, 5-nucleotidase, and gamma-glutamyltranspept...

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Section: Discussioncontrasting

confidence: 80%

Partially reversible renal tubular damage in patients with obstructive jaundice

et al. 2001

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“…Extreme hyperbilirubinemia has been reported to exert multiple cellular toxic effects, including effects on cellular respiration, membrane integrity, and transport functions, and excessive accumulation of bilirubin has been incriminated as causing renal tubular damage, thereby contributing to persistence of renal failure (6). Variable degrees of renal tubular dysfunction have been demonstrated in patients with jaundice due to biliary obstruction or liver failure (2,16). Removal of serum bilirubin by plasma separation or bilirubin adsorption has led to favorable clinical outcomes in patients with severe hyperbilirubinemia after liver transplantation (15).…”

mentioning

confidence: 99%

Potential Benefit of Plasma Exchange in Treatment of Severe Icteric Leptospirosis Complicated by Acute Renal Failure

Tse¹,

Yip²,

Hui³

et al. 2002

Clin Vaccine Immunol

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Leptospirosis is a common zoonosis seen worldwide, but it is rare in our locality (Hong Kong). Clinical manifestations of leptospirosis are variable and may range from subclinical infection to fever, jaundice, hemorrhagic tendency, and fulminant hepato-renal failure. Severe hyperbilirubinemia and acute renal failure have been associated with high mortality. We report our experience with a patient who developed severe Weil's syndrome with marked conjugated hyperbilirubinemia and oliguric acute renal failure. These complications persisted despite treatment with penicillin and hemodiafiltration. Plasma exchange was instituted in view of the severe hyperbilirubinemia (970 mol/liter). This was followed by prompt clinical improvement, with recovery of liver and renal function. The beneficial effects of plasma exchange could be attributed to amelioration of the toxic effects of hyperbilirubinemia on hepatocyte and renal tubular cell function. We conclude that plasma exchange should be considered as an adjunctive therapy for patients with severe icteric leptospirosis complicated by acute renal failure who have not shown rapid clinical response to conventional treatment.

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“…She, however, failed to respond to midodrine and octreotide. In the face of persistent hypotension, HRS can evolve into acute tubular necrosis that will not respond to vasoconstrictors . The urine analysis suggested the possibility of intrinsic renal disease.…”

Section: Discussionmentioning

confidence: 99%

Bile cast nephropathy: An often forgotten diagnosis

Sequeira

2014

Hemodialysis International

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High bilirubin levels are nephrotoxic. Bilirubin can cause a functional proximal tubulopathy or may precipitate into casts associated with acute tubular injury. This condition is known as bile cast nephropathy. The kidney injury is generally reversible if bilirubin levels are decreased early. We present a case wherein an alcoholic patient presented with high bilirubin levels and anuric acute kidney injury. The initial urine analysis suggested intrinsic renal disease. A kidney biopsy, performed a few days after the initiation of dialysis, demonstrated the presence of bile casts along with acute tubular injury. The patient however continued to be dialysis dependent inspite of initiating prednisolone to treat acute alcoholic hepatitis.

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Tubular dysfunction in the deeply jaundiced patient with hepatorenal syndrome

Cited by 25 publications

References 10 publications

Partially reversible renal tubular damage in patients with obstructive jaundice

Partially reversible renal tubular damage in patients with obstructive jaundice

Potential Benefit of Plasma Exchange in Treatment of Severe Icteric Leptospirosis Complicated by Acute Renal Failure

Bile cast nephropathy: An often forgotten diagnosis

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