Acute kidney injury(AKI) has higher perioperative mortality and morbidity as well as high medical expense. Ischemia-reperfusion injury (I/R) is one of the most common causes of AKI.The molecular mechanism underlying I/R induced AKI is still unclarified, and there is a lack of early diagnosis markers. Herein, we demonstrated that mmu-lncRNA129814 was triggered by ischemic AKI in BUMPT cells and C57BL/6J mice. The knockdown of mmu-lncRNA129814 attenuated I/R-stimulated BUMPT cell death, and its overexpression had an opposite effect. Mechanistically, mmu-lncRNA129814 could sponge miRNA-494-5p and upregulated IL-1α expression to promote cell apoptosis. Furthermore, knockdown of mmu-lncRNA129814 ameliorated the I/R-induced progression of AKI via targeting miRNA-494-5p/IL-1α pathways. Interestingly, hsa-lncRNA582795, a homology with mmu-lncRNA129814, also promoted I/R-stimulated HK-2 cell apoptosis and AKI progression by regulating the miRNA-494-5p/IL-1α axis. Finally, we found that I/R-induced AKI patients exhibited remarkably elevated plasma and urinary levels of hsa-lncRNA582795 compared to those after Ischemia-reperfusion without AKI. Spearman’s test demonstrated a significant correlation between serum creatinine and plasma hsa-lncRNA582795 in I/R patients (r = 0.824),while urinary hsa-lncRNA582795 and urinary [TIMP2]*[IGFBP7]( r = 0.789). The AUC values of plasma and urinary hsa-lncRNA582795 were 0.889 and 0.804, respectively. The plasma hsa-lncRNA 582795 had a low specificity (86.7%) and high sensitivity (76.7%) compared to urinary hsa-lncRNA 582795 (93.3% and 63.3%, respectively). Collectively, the mmu-lncRNA129814/hsa-lncRNA582795/miRNA-494-5p/IL-1α axis was found to modulate the progression of ischemic AKI, and hsa-lncRNA582795 could act as a diagnosis biomarker and potential therapy target of I/R induced AKI.