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Mechanistic insights and protocol standardization Initial studies on H₂-based renal therapies emphasized H₂ selective antioxidant properties: it scavenges hydroxyl radicals while preserving other reactive oxygen species involved in normal signaling.2,21 This duality underpins H₂ therapeutic potential, as it helps maintain endogenous antioxidants (such as catalase, superoxide dismutase) and inhibits proinflammatory cytokine release, thereby reducing apoptosis and tissue damage.21,22,23,24,25 Subsequent work broadened these findings to include anti-inflammatory and antifibrotic effects, with H₂ influencing key transcription factors, such as Nrf2, NF-κB, and sirtuin 1 (SIRT1), which modulate redox balance, fibrosis, and inflammation.9,11,27,28 Recent approaches, such as blood oxygen level–dependent magnetic resonance imaging and H₂-generating nanomaterials, suggest that H₂ renoprotection extends beyond radical scavenging, engaging multifaceted cellular networks critical for renal homeostasis.9,27,29 Despite these mechanistic advances, studies still employ diverse administration methods (inhalation, oral, dialysate) and outcome endpoints.7,9,11,30 Additionally, at the molecular level, H₂ targets inflammatory and apoptotic pathways, such as NF-κB and nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3), in AKI,8,9,12,13,23,31,32 and exhibits antifibrotic potential in CKD by downregulating transforming growth factor-beta 1 and supporting SIRT1.10,26,29,33,34,35 Clarifying whether short-term protection differs from longer-term antifibrotic effects is essential for guiding patient selection and dosing strategies