Hyperbilirubinemia-associated kidney injury: a retrospective analysis of clinical features, risk factors, and mortality
Bibliographic record
Abstract
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.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.002 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".