Loading
Life sciences · Journal article
Renal Failure · September 14, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Occupational heatstroke frequently causes acute kidney injury (AKI). Myoglobin, released by exertional rhabdomyolysis, is the central nephrotoxic amplifier and may be physically removable by extracorporeal techniques. Yet the trials governing purification timing enrolled general intensive care populations whose injury biology differs. We aimed to integrate heatstroke-specific renal pathophysiology, novel AKI biomarker performance, and evidence on extracorporeal modalities. We then mapped the temporal cascade onto a biomarker-augmented framework for initiating blood purification during a narrative State-of-the-Art Review. Ten search blocks were run in PubMed/MEDLINE to 16 August 2026, yielding 16,443 unique records. Eligible sources reported human or animal data, consensus statements, or mechanistic evidence bearing on three questions: (i) how does heat injure kidneys? (ii) which biomarkers detect injury? and (iii) when blood purification should begin? Records without an English-language abstract or without retrievable full text were excluded and, ultimately, 95 discreate sources were retained. Four pathways operate on distinct timescales: direct thermal cytotoxicity, myoglobin-driven ferroptosis, inflammatory-coagulation amplification, and gut-derived endotoxemia. L-FABP has the only prospective heat-specific human data; [TIMP-2]·[IGFBP7] has the strongest critical care record but none in heatstroke. No biomarker is validated for predicting later chronic kidney disease in this population. No modality has been shown superior in a heatstroke-specific population, and only one clinical study reports outcomes in exertional heatstroke. We propose a provisional three-tier initiation framework anchored to myoglobin concentration and tubular injury biomarkers rather than creatinine alone. It is a structured hypothesis rather than validated guidance, and prospective biomarker-stratified trials in occupational settings are needed.