ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: TH-PO056

Bile Cast Nephropathy-Retrospective Cohort of Hyperbilirubinemia Associated Nephropathy

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical‚ Outcomes‚ and Trials

Authors

  • Abu Amer, Nabil, Chaim Sheba Medical Center, Rmat Gan, Israel
  • Erman, Orit, Chaim Sheba Medical Center, Rmat Gan, Israel
  • Kukuy, Lesya, Chaim Sheba Medical Center, Rmat Gan, Israel
  • Kunin, Margarita, Chaim Sheba Medical Center, Rmat Gan, Israel
  • Mini-Goldberger, Sharon, Chaim Sheba Medical Center, Rmat Gan, Israel
  • Beckerman, Pazit, Chaim Sheba Medical Center, Rmat Gan, Israel
Background

Bile cast nephropathy (BCN) represents kidney dysfunction in the setting of severe hyperbilirubinemia. The proposed pathogenesis includes direct bile toxicity and obstructive tubular cast formation. BCN remains controversial despite typical findings on kidney pathology. The aim of this study is clinical characterization and risk factor identification of hyperbilirubinemia associated nephropathy.

Methods

A retrospective cohort study of patients admitted to surgery departments between January 2007 and January 2020 with total bilirubin above 10 mg/dl. Hyperbilirubinemia associated acute kidney injury (AKI) were identified, after carefully excluding all other etiologies of AKI. Data collected included demographic parameters, medical background, etiology of hyperbilirubinemia, lab tests, vital signs and nephrotoxic agents given during the hospitalization period.

Results

A total of 1,181 patients with serum bilirubin above 10 mg/dl were enrolled. 672 patients with other known kidney insults were excluded. The remaining 509 patients had a mean maximal bilirubin of 14.7 mg/d (SD±5.8). Of which, eighty-eight patients (17%) developed AKI, defined as bile cast nephropathy. They were mostly female (78%) and had a lower baseline estimated glomerular filtration rate compared to patients with hyperbilirubinemia who did not develop AKI (66 mL/min per 1.73 m2 (IQR 60.8-99.7) and 81 mL/min per 1.73 m2 (IQR 48.7- 80.4), respectively). Most of the patients (63%) had AKI stage 1 and there was no linear correlation between bilirubin level and AKI event.
Renal recovery occurred after a decrease in serum bilirubin to a nadir of 4.19 mg/dl (IQR 1.4-6.8).

Conclusion

The diagnosis of bile cast nephropathy should be considered in patients with hyperbilirubimenia who develop AKI. In most cases AKI is mild and resolves following a decrease in bilirubin levels. This finding suggests that reduction in bilirubin levels may be beneficial among patients who develop AKI, even when no definitive treatment of hyperbilirubinemia is available.