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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2018  |  Volume : 29  |  Issue : 6  |  Page : 1498-1501
Bile cast nephropathy causing acute kidney injury in a patient with nonfulminant acute hepatitis A

1 Department of Nephrology, Kerala Institute of Medical Sciences, Thiruvananthapuram, Kerala, India
2 Department of Pathology, Kerala Institute of Medical Sciences, Thiruvananthapuram, Kerala, India

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Date of Submission09-Nov-2017
Date of Decision01-Jan-2018
Date of Acceptance06-Jan-2018
Date of Web Publication27-Dec-2018


Hepatitis A is usually a benign self-limiting disease with few or no extrahepatic manifestations. Acute hepatitis A causing severe renal dysfunction is not very common, although described. Patients developing renal dysfunction post hepatitis A infection usually have prerenal acute kidney injury (AKI) or acute tubular necrosis due to vomiting, diarrhea, and poor fluid replacement. However, if renal dysfunction persists, other causes need to be evaluated. The term cholemic nephrosis or more specifically bile cast nephropathy has been described in the setting of cholestatic jaundice and decompensated liver failure where bilirubin levels reach above 20 mg/dL. Herein, we describe the clinical course of a patient who developed acute hepatitis A with severe liver dysfunction and subsequently AKI which persisted for six weeks. Renal biopsy showed the evidence of bile cast nephropathy. After six weeks of hemodialysis, urine output improved. He slowly recovered both hepatic and renal functions.

How to cite this article:
Ravi R, Suthar K, Murlidharan P, Lakshmi K, Balan S, Safeer M. Bile cast nephropathy causing acute kidney injury in a patient with nonfulminant acute hepatitis A. Saudi J Kidney Dis Transpl 2018;29:1498-501

How to cite this URL:
Ravi R, Suthar K, Murlidharan P, Lakshmi K, Balan S, Safeer M. Bile cast nephropathy causing acute kidney injury in a patient with nonfulminant acute hepatitis A. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2022 Jan 16];29:1498-501. Available from: https://www.sjkdt.org/text.asp?2018/29/6/1498/248305

   Introduction Top

Acute viral hepatitis causing renal injury is not very common. In patients with hepatitis A with renal dysfunction, other factors such as sepsis, shock, bacterial infections, drug toxicity, and rhabdomyolysis are more likely to cause renal dysfunction. Acute tubular necrosis and acute interstitial nephritis complicating hepatitis A are described.[1] Furthermore, the jaundice of hepatitis A can be compounded by drug-induced liver injury causing cholestatic jaundice. Here, the bilirubin may be elevated more than that expected in uncomplicated hepatitis A infection, and alkaline phosphatase may also be elevated. Bile cast nephropathy is a rare entity where tubular injury is caused by the direct effect of bile casts.

   Case Report Top

Informed consent was obtained from the patient before reporting the case. A 25-year-old gentleman, with no known co-morbidities and normal creatinine one week prior to admission, was admitted with a history of fever for one week, associated with jaundice, vomiting, and diarrhea for two days. On examination, he was found to be icteric and hypotensive, with no response to intravenous fluid challenge. Laboratory evaluation revealed total bilirubin of 40 mg/dL, aspartate amino-transferase (AST) of 1753 U/L, alanine amino-transferase (ALT) of 2066 U/L, and serum creatinine (SCr) of 8.5 mg/dL. There was no active sediment and no significant proteinuria on urine examination. IgM hepatitis A virus was 3.13 (>0.5 being positive). Ultrasono-graphy of the abdomen showed an enlarged liver with increased echogenicity and normal spleen with normal-sized kidneys and no features of urinary obstruction. His renal function further deteriorated to a serum creatinine (SCr) of 11 mg/dL with anuria for which he was initially started on continuous renal replacement therapy (CRRT) as he was hemo-dynamically unstable and then later switched over to conventional hemodialysis (HD) once his clinical condition improved. In view of vomiting and diarrhea with hypotension, he was given supportive therapy with fluid status optimization and HD as per requirement. Even after four weeks of (HD), however, he continued to be anuric. In addition, during this period, he developed accelerated hypertension with generalized tonic-clonic seizures. Magnetic resonance imaging of the brain was suggestive of posterior reversible encephalopathy syndrome. In view of persistent dialysis-dependent renal failure, renal biopsy was performed. This showed normal glomeruli and interstitial edema, with tubules containing pigment casts [Figure 1], [Figure 2], [Figure 3]. Immunofluorescence was negative for IgA, IgG, IgM, C1q, fibrinogen, kappa, and lambda. Fouchet stain of the tubular casts was positive, supporting the diagnosis of bile cast nephropathy. Supportive therapy was continued. Steroid was tapered and stopped. Six weeks after starting dialysis, the patient’s renal failure started improving. Dialysis was stopped. Urine output was adequate. At present, the patient is on follow-up with a SCr of 2 mg/dL and bilirubin of 1.1 mg/dL with AST 273 U/L and ALT 175 U/L.
Figure 1: Light microscopy -low-power image showing normal glomeruli with interstitial edema.

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Figure 2: High-power image showing bile casts.

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Figure 3: H & E stain with bile casts.

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   Discussion Top

Renal dysfunction is rare in nonfulminant hepatitis. In a review of case reports in 1996, 26 patients with acute hepatitis A and acute renal failure were reviewed.[2] Out of the 14 patients who underwent renal biopsies, eight showed acute tubular necrosis, two each were suggestive of interstitial nephritis and mesan-gioproliferative glomerulonephritis, one revealed membranoproliferative glomerulonephritis, and histology was normal in one case. None showed bile cast nephropathy. In our patient, as renal failure persisted despite correction of prerenal factors, and since the patient had anuric renal failure, a biopsy was performed to ascertain the cause of such severe renal dysfunction.

Chronic liver dysfunction causes renal dysfunction much more commonly. In a post mortem study conducted by Slambrouck et al in 2006 on patients with liver dysfunction and renal failure, bile casts were found in 24 out of 44 cases. They, therefore, postulated that bile cast nephropathy is a common pathological finding in patients with severe liver dysfunction. Of note, patients with hepatitis C causing chronic liver disease did not have bile casts.[3] Our patient was nonalcoholic and had no features of cirrhosis or cholestasis on ultra-sonography. Other reports of bile cast nephro-pathy include reports in patients with obstructive jaundice[4] and with the use of anabolic steroids causing severe cholestatic injury.[5] Very few cases have been reported describing bile cast nephropathy as a complication of hepatitis A. In another case of hepatitis A with bile cast nephropathy reported in 2017, the renal recovery showed a prolonged course and required dialysis support.[6]

The term cholemic nephrosis includes injury due to both bile casts and tubular injury from bilirubin. Bile cast nephropathy has been described as far back as 1922.[7] However, most reports of this condition are associated with cirrhosis. The presence of bile casts corresponds to a higher severity of liver dysfunction as well as higher creatinine.[3] Mechanism of acute kidney injury in bile cast nephropathy is analogous to that of renal injury due to myeloma and myoglobin casts. Excretion of high levels of bile acids causes oxidative damage to the tubules. Once excretion is saturated, cast formation and tubular obstruction occur. A direct correlation between the severity of hepatic dysfunction (as measured by ALT) with the severity of renal dysfunction was ascertained by a mouse model study.[8] In the present case, total bilirubin as well as AST and ALT were very high, leading to the precipitation of bile in the tubules and bile cast nephropathy.

There are no guidelines or consensus regarding the treatment for bile cast nephropathy. There are case reports of patients being treated with plasmapheresis for bile cast nephropathy as in multiple myeloma. However, similar to our patient, most patients seem to improve with supportive therapy alone once liver dysfunction recovers.

Conflict of interest: None declared.

   References Top

Sarawgi S, Gupta AK, Arora DS, Jasuja A. Acute renal failure associated with non-fulminant acute viral hepatitis A. Indian J Nephrol 2008;18:77-9.  Back to cited text no. 1
[PUBMED]  [Full text]  
Lin CC, Chang CH, Lee SH, Chiang SS, Yang AH. Acute renal failure in non-fulminant hepatitis A. Nephrol Dial Transplant 1996;11: 2061-6.  Back to cited text no. 2
van Slambrouck CM, Salem F, Meehan SM, Chang A. Bile cast nephropathy is a common pathologic finding for kidney injury associated with severe liver dysfunction. Kidney Int 2013; 84:192-7.  Back to cited text no. 3
Betjes MG, Bajema I. The pathology of jaundice-related renal insufficiency: Cholemic nephrosis revisited. J Nephrol 2006;19:229-33.  Back to cited text no. 4
Luciano RL, Castano E, Moeckel G, Perazella MA. Bile acid nephropathy in a bodybuilder abusing an anabolic androgenic steroid. Am J Kidney Dis 2014;64:473-6.  Back to cited text no. 5
Jung JH. Bile cast nephropathy associated with acute hepatitis A. Chonnam Med J 2017;53: 170.  Back to cited text no. 6
Haessler H, Rous P, Broun GO. The renal elimination of bilirubin. J Exp Med 1922;35: 533-52.  Back to cited text no. 7
Lee HT, Park SW, Kim M, D’Agati VD. Acute kidney injury after hepatic ischemia and reperfusion injury in mice. Lab Invest 2009; 89:196-208.  Back to cited text no. 8

Correspondence Address:
Dr. Ranjani Ravi
Department of Nephrology, Kerala Institute of Medical Sciences, Anayara PO, Thiruvananthapuram -695 029, Kerala
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DOI: 10.4103/1319-2442.248305

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