ArticleTranslational stroke research2026
Beyond Acute Kidney Injury : Direct Pathways Implicate Inflammatory Mechanisms in Serum NGAL's Mortality Effect in Acute Brain Injury.
Article in Translational stroke research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Neutrophil gelatinase-associated lipocalin (NGAL) is associated with mortality in critically ill patients, conventionally attributed to its role in acute kidney injury (AKI) detection. However, NGAL is a neutrophil granule protein released during innate immune activation-a process central to acute brain injury (ABI) pathophysiology. Whether the association between NGAL and mortality in neurocritical care operates through AKI-mediated or alternative pathways has not been evaluated. In this prospective cohort of 274 adults with ABI (98 intracerebral hemorrhage, 60 ischemic stroke, 46 subarachnoid hemorrhage, 70 traumatic brain injury) admitted to a neurocritical care unit, serum NGAL was measured within 24 h of admission. Causal mediation analysis with time-varying AKI status decomposed NGAL's mortality effect into direct and AKI-mediated components. High NGAL (≥ 150 ng/mL) was independently associated with in-hospital mortality (adjusted hazard ratio [aHR] 2.94, 95% confidence interval [CI] 1.57-5.51; absolute risk difference 15.0% at 28 days), ICU mortality, 6-month mortality, and worse functional outcomes. Pathway decomposition revealed a significant direct effect not mediated through AKI (aHR 2.15, 95% CI 1.04-4.62, P=.04), whereas the AKI-mediated component was not significant (P=.33). Effects were consistent across injury types. Admission NGAL correlated with subsequent 72-hour systemic inflammatory burden (Spearman ρ = 0.38, P<.001), and within-subject NGAL and interleukin-6 showed concordant temporal trajectories (repeated-measures r = .29, P<.001). These findings indicate that the NGAL-mortality association in ABI includes a significant direct effect not mediated through AKI, implying that NGAL elevation reflects systemic innate immune activation rather than impending renal dysfunction.
Indexed as
Identifiers
42635685What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.