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as well as (iii) forkhead box O transcription factors.11 Experimental evidence supports these observations, showing H₂-rich saline ability to attenuate renal inflammation and preserve endothelial glycocalyx integrity in sepsis-induced AKI.12 Moreover, novel solid-state H₂ sources demonstrated efficacy against toxin-induced kidney injury by inhibiting critical inflammatory pathways.8 Additionally, high-concentration H₂ inhalation has been reported to reduce mitochondrial dysfunction in septic AKI models by promoting mitochondrial biogenesis and fusion processes.13 Beyond conventional delivery methods, advanced H₂-generating nanomaterials have been explored to achieve targeted reactive oxygen species modulation in renal conditions.9 Clinical case reports have shown improved renal function and reduced fatigue in diabetic nephropathy,14 while preclinical research also indicates protective effects in crush syndrome–associated AKI.15 Despite these promising results, the existing literature on H₂ therapies is marked by considerable methodological heterogeneity