For mannitol, arabitol, threitol, and pinitol, little difference was detected from sham at 2 hours post ischemia but significant elevation was evident in both plasma and kidney tissue by 48 hour Fusidate Sodium reperfusion time. This kind of polyol elevation was sustained to the 1 week reperfusion time in kidney. The change of those polyols was unlike the osmolytes described above, but similar to the change patterns of diet-derived compounds. As the origin, function, and metabolic fates for many of those polyols remained poorly understood, it remains unclear if their change contributes to the osmolality regulation in renal IRI. The metabolic signatures of inflammation associated with renal ischemia/reperfusion were evident in plasma and kidney tissue which is consistent with other studies showing the accumulation of immune cells in kidney after ischemic AKI. Metabolic pathways reporting on inflammation in this study included the generation of prostaglandins from omega-6 fatty acid precursors, the inflammatory cytokine-responsive kynurenine pathway for tryptophan degradation, and the generation of nitric oxide from arginine with citrulline as a byproduct. However, the elevation of tissue levels for multiple prostaglandins was a relatively late event, appearing strongest at the 1 wk reperfusion time in kidney. Although the precursor arachidonate did not show significant induction, prostaglandin E1, prostaglandin B2, prostaglandin D2, prostaglandin E2, and prostaglandin A2 were elevated over time during reperfusion, a pattern consistent with the known inflammation component of the ischemia/ reperfusion injury. The late induction of prostaglandins at one week reperfusion time suggests that they may exert more protective or wound Gabapentin HCl healing role in ischemic AKI instead of promoting cell death and the cytoprotective effects of prostaglandins in ischemic AKI has been reported before. Likewise, in both plasma and kidney tissue, the increased levels of the tryptophan metabolite kynurenine and its metabolite kynurenate with a more complex pattern further supported a pro-inflammatory environment, potentially systemically, following kidney ischemia and reperfusion.