Selenium and zinc in acute kidney injury: A systematic scoping review of speciation-resolved mechanisms, analytical validation, and translational biomarkers.

PURPOSE: To assess selenium (Se) and zinc (Zn) Status, mechanisms, analytical methods and biomarker potential in acute kidney injury (AKI).

METHODS

The search was conducted in PubMed, Embase, Web of Science, and Scopus databases, according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) up to February 2026. Only primary experimental, clinical and analytical studies that reported quantitative data for Se or Zn in AKI were included. Design-specific tools were used for methodological quality and risk of bias assessment.

RESULTS

Low plasma Se (<70 µg/L; <0.89 µmol/L) and Zn (<60 µg/dL; <9.2 µmol/L) was associated with increased incidence, severity, and mortality of AKI in clinical cohorts (n = 453-11,238); however, these relationships may be confounded by inflammation, acute-phase redistribution, and disease severity. Although preclinical evidence points to a role for glutathione peroxidase 4 (GPX4)-regulated ferroptosis, and for the zinc importer/zinc exporter (ZIP/ZnT)-nuclear factor kappa B (NF-κB)-NOD-, leucine-rich repeat- and pyrin domain-containing protein 3 (NLRP3) signalling, these have not yet been validated in humans.

CONCLUSION

Selenoprotein P (SELENOP), glutathione peroxidase 3 (GPX3) and urinary Zn(II) and metallothionein (MT) constitute a proposed panel for clinical implementation, which needs to be analytically validated, discriminated and calibrated, externally validated, incrementally valued and clinically utility evaluated in prospective multicentre studies.