ReviewRenal failure2026
Lactate in acute kidney injury: pathobiology, risk stratification, and clinical interpretation.
Review in Renal failure, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lactate is frequently measured in patients with acute kidney injury (AKI), but its interpretation remains challenging because circulating lactate reflects systemic metabolic stress rather than kidney injury. Although elevated lactate levels are associated with adverse outcomes in critically ill patients with AKI, its biological and clinical significance varies according to disease context, timing, and the clinical question being addressed. This structured expert narrative review integrates mechanistic insights and clinical evidence to establish a context-dependent framework for interpreting lactate in AKI. We summarize the role of the kidney in lactate metabolism and discuss how impaired renal function, altered perfusion, mitochondrial dysfunction, and immune-metabolic remodeling contribute to lactate accumulation. We further evaluate clinical evidence regarding lactate in AKI risk assessment, severity evaluation, organ-support requirement, and mortality prediction, while emphasizing limitations related to confounding factors and clinical heterogeneity. Emerging clinical contexts, including extracorporeal membrane oxygenation-supported patients, are also considered. Overall, this framework supports a more precise interpretation of lactate as a context-dependent risk marker and metabolic signal rather than a kidney-specific biomarker.
Indexed as
Identifiers
What 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.