Objective: From day 3 after bilateral or unilateral ischemia-reperfusion injury (BIRI or UIRI) operation, control diet, high-salt diet (HSD), or low-salt diet (LSD) were provided to each cohort of 9-week-old male C57BL/6 mice. Mice were sacrificed on day 14 and 42 after BIRI and on day 42 and 84 after UIRI. HK-2 cells were treated with additional NaCl. Methods: Compared to the control diet group, body weight tended to be lower in the HSD group, but blood pressure was similar between the groups. There was no difference in creatinine between groups after BIRI and UIRI, but cystatin-C and total cholesterol were higher in the HSD and LSD group and blood urea nitrogen was lower in the HSD group after UIRI. The intrarenal regulatory T cells were lower in the HSD and LSD group in BIRI. The intrarenal total T cells, major subtypes of T cells, total B cells, and NK T cells were higher in the HSD group after UIRI. Intrarenal VEGF was lower in the HSD group after BIRI, and intrarenal RANTES and TNF-α were higher in the HSD group after UIRI. Renal tubular damage after UIRI was more severe and the extent of fibrosis after BIRI was larger in the HSD group. High NaCl concentration suppressed proliferation in hypoxic HK-2 cells. Results: The HSD impaired the repair process in ischemia AKI by inducing prolonged proinflammatory changes in the post-ischemic kidneys. There may be no benefit from strict LSD during the recovery phase of ischemic AKI. Conclusions: Objective: Intrarenal immunologic micromilieu alteration through dietary modification and the subsequent effects on the repair after ischemic acute kidney injury (AKI) are unclear. The effects of salt intake on intrarenal immunologic micromilieu and the repair of tubular damage after ischemic AKI using murine ischemic AKI and human kidney-2 (HK-2) cell hypoxia models were investigated. Methods: From day 3 after bilateral or unilateral ischemia-reperfusion injury (BIRI or UIRI) operation, control diet, high-salt diet (HSD), or low-salt diet (LSD) were provided to each cohort of 9-week-old male C57BL/6 mice. Mice were sacrificed on day 14 and 42 after BIRI and on day 42 and 84 after UIRI. HK-2 cells were treated with additional NaCl. Results: Compared to the control diet group, body weight tended to be lower in the HSD group, but blood pressure was similar between the groups. There was no difference in creatinine between groups after BIRI and UIRI, but cystatin-C and total cholesterol were higher in the HSD and LSD group and blood urea nitrogen was lower in the HSD group after UIRI. The intrarenal regulatory T cells were lower in the HSD and LSD group in BIRI. The intrarenal total T cells, major subtypes of T cells, total B cells, and NK T cells were higher in the HSD group after UIRI. Intrarenal VEGF was lower in the HSD group after BIRI, and intrarenal RANTES and TNF-α were higher in the HSD group after UIRI. Renal tubular damage after UIRI was more severe and the extent of fibrosis after BIRI was larger in the HSD group. High NaCl concentration suppressed proliferation in hypoxic HK-2 cells. Conclusions: The HSD impaired the repair process in ischemia AKI by inducing prolonged proinflammatory changes in the post-ischemic kidneys. There may be no benefit from strict LSD during the recovery phase of ischemic AKI.