Abstract: Objective To investigate the effects of short-term high salt diet on the interstitial transformation（EMT） of renal tubular epithelial cells and renal fibrosis in C57 BL6/J mice. Methods Twenty male C57 BL/6 J mice were randomly divided into control group（fed with 0.5% NaCl pellet feed） and high salt group（fed with 8% NaCl pellet feed）, 10 mice in each group. The tail artery blood pressure was measured once a week for 3 weeks. 24-hour urine was collected by metabolic cage. The serum creatinine, urea nitrogen, 24-hour urinary microalbumin（MAU）, urinary sodium and potassium were measured 3 weeks after intervention. Creatinine clearance rate（Ccr） and 24-hour urinary sodium/potassium ratio were calculated. The renal morphology and fibrosis were observed by HE（hematoxylin-eosin）, PAS（periodic acid-Schiff） and Masson staining. The protein distribution and expression of E-cadherin, Vimentin, α-smooth muscle actin（α-SMA） and kidney injury molecule-1（Kim-1） in the kidneys of mice was detected with immunohistochemistry and Western blot. Results After 3 weeks of high-salt diet, there was no significant difference in blood pressure among two groups（P＞0.05）. Compared with the control group, the 24-hour MAU （0.39±0.09） vs（0.07±0.01）mg, Ccr （1.99±0.46） vs（1.25±0.58）L/（g·min）, 24-hour urinary sodium （0.62±0.28） vs（0.01±0.01）mmol, 24-hour urinary potassium （0.29±0.04） vs（0.05±0.01）mmol and 24-hour urinary sodium/potassium ratio（4.31±1.80 vs 0.08±0.03） increased in the high salt group（P＜0.05）. The glomerular sclerosis index, glomerular fibrosis index and renal interstitial fibrosis index were also increased（P＜0.05）. As compared with control, the expression of Vimentin, α-SMA and Kim-1 increased while E-cadherin decreased（all P＜0.05） in the high salt as indicated by immunohistochemistry and Western blot analysis. Conclusion Short term high salt diet may induce renal tubule EMT and promote renal fibrosis in C57 BL/6 J mice with normal blood pressure through blood pressure independent pathway.