Bile cast nephropathy in obstructive jaundice: a case report
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The present case has been reported in the journal KI Reports.
Acute kidney injury (AKI) is common in patients with severe hepatic failure and is associated with significant morbidity and mortality. Ischemia and inflammation are the hallmarks of the pathophysiology of kidney injury in cirrhosis. Additionally, an important nonvasomotor mechanism of AKI in cirrhosis is the toxicity of cholephiles, often known as bile cast nephropathy, with histological evidence of tubular bile cast formation and tubular epithelial injury.

Learning Points:-
• Bile cast nephropathy has been a largely forgotten diagnosis as a cause of acute kidney injury and is diagnosed via a kidney biopsy.

• Bile cast nephropathy is promoted by associated kidney ischemia, but severe isolated cholestasis is sufficient to induce its occurrence.

• Bile cast nephropathy represents a spectrum of renal injury from proximal tubulopathy to intrarenal bile cast formation found in patients with severe liver dysfunction.

• The management of bile cast nephropathy is through normalization of bilirubinemia, which may require time on renal replacement therapy.

A 61-year-old man was admitted with fatigue, anorexia, and severe jaundice. He had a background of T3N0 transitional cell bladder carcinoma, bilateral retinoblastoma, and multiple malignant melanomas. Before his admission, his baseline kidney function was normal with a serum creatinine of 86 μmol/l (normal 60 μmol/l to 120 μmol/l). His skin was markedly jaundiced and scleral icterus was present, but he demonstrated no peripheral stigmata of chronic liver disease.

Laboratory tests revealed a cholestatic picture with increased total bilirubin (260 mg/dl) (normal <20 mg/dl), alkaline phosphatase (1070 IU/l) (normal 30–110 IU/l), and γ-glutamyltranspeptidase (450 IU/l) (normal <38 IU/l) levels. Serum creatinine level was elevated at 463 μmol/l. C-reactive protein level was 4.5 mg/l (normal <5 mg/l). Autoimmune and infectious causes were excluded. Proteinuria was measured at protein excretion of 1.1 g per 24 hours (normal <15 mg per 24 hours).

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