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Background <p>Hyperbilirubinemia-associated acute kidney injury (AKI) is characterized by kidney dysfunction in&#xa0;the context of severe hyperbilirubinemia. The proposed pathogenesis involves direct bile acid toxicity and obstructive tubular cast formation. Even though there are typical morphological findings at the kidney biopsy, the risk factors and clinical features of hyperbilirubinemia-associated AKI remain poorly understood.</p> Methods <p>This is a retrospective cohort study that&#xa0;included 1183 patients admitted with total bilirubin levels above 10&#xa0;mg/dl. We assessed the clinical characteristics and risk factors of hyperbilirubinemia-associated AKI after excluding patients with AKI due to other medical conditions. Risk factors for hyperbilirubinemia-associated AKI were assessed using logistic regression analysis. Survival among&#xa0;patients with hyperbilirubinemia-associated AKI and other groups was compared using the Kaplan–Meier method.</p> Results <p>Eighty-eight patients (7.4%) developed hyperbilirubinemia-associated AKI, while 255 (21.5%) developed non-hyperbilirubinemia associated AKI.</p> <p>Patients with hyperbilirubinemia-associated AKI had a lower baseline estimated glomerular filtration rate (<i>P</i> &lt; 0.001). Chronic kidney disease, congestive heart failure, serum bilirubin &gt; 20 mg/dL, male sex, and older age were associated with a higher risk of developing&#xa0;hyperbilirubinemia-associated AKI. Renal recovery occurred at a median of 4.1 days following a decrease in serum bilirubin to a median nadir of 4.19 mg/dL (IQR 1.4–6.8). The survival of patients with hyperbilirubinemia-associated AKI was significantly lower than that of patients with AKI due to other causes&#xa0;(<i>P</i> &lt; 0.001).</p> Conclusion <p>The diagnosis of hyperbilirubinemia-associated AKI should be considered in all&#xa0;patients with hyperbilirubinemia and AKI. Lowering bilirubin levels may result in AKI resolution even when no definitive treatment for hyperbilirubinemia is available.</p> Graphical Abstract <p></p>

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Hyperbilirubinemia-associated kidney injury: a retrospective analysis of clinical features, risk factors, and mortality

  • 期刊论文

  • 发表日期：

    2025年8月4日

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  • Nabil Abu-Amer,
  • Margarita Kunin,
  • Orit Erman,
  • Olga Kukuy,
  • Sharon Mini,
  • Abhijat Kitchlu,
  • Pazit Beckerman

摘要

Background

Hyperbilirubinemia-associated acute kidney injury (AKI) is characterized by kidney dysfunction in the context of severe hyperbilirubinemia. The proposed pathogenesis involves direct bile acid toxicity and obstructive tubular cast formation. Even though there are typical morphological findings at the kidney biopsy, the risk factors and clinical features of hyperbilirubinemia-associated AKI remain poorly understood.

Methods

This is a retrospective cohort study that included 1183 patients admitted with total bilirubin levels above 10 mg/dl. We assessed the clinical characteristics and risk factors of hyperbilirubinemia-associated AKI after excluding patients with AKI due to other medical conditions. Risk factors for hyperbilirubinemia-associated AKI were assessed using logistic regression analysis. Survival among patients with hyperbilirubinemia-associated AKI and other groups was compared using the Kaplan–Meier method.

Results

Eighty-eight patients (7.4%) developed hyperbilirubinemia-associated AKI, while 255 (21.5%) developed non-hyperbilirubinemia associated AKI.

Patients with hyperbilirubinemia-associated AKI had a lower baseline estimated glomerular filtration rate (P < 0.001). Chronic kidney disease, congestive heart failure, serum bilirubin > 20 mg/dL, male sex, and older age were associated with a higher risk of developing hyperbilirubinemia-associated AKI. Renal recovery occurred at a median of 4.1 days following a decrease in serum bilirubin to a median nadir of 4.19 mg/dL (IQR 1.4–6.8). The survival of patients with hyperbilirubinemia-associated AKI was significantly lower than that of patients with AKI due to other causes (P < 0.001).

Conclusion

The diagnosis of hyperbilirubinemia-associated AKI should be considered in all patients with hyperbilirubinemia and AKI. Lowering bilirubin levels may result in AKI resolution even when no definitive treatment for hyperbilirubinemia is available.

Graphical Abstract