Acute kidney injury (AKI) is a syndrome characterized by an acute loss of renal function. The incidence of AKI is 208 per million population in Europe. There is no established therapy to accelerate the recovery and attempts at preventing AKI are not universally effective. The treatment of most forms of AKI is symptomatic and consists in substitution of renal function by dialysis if renal failure is severe. Despite the reversibility of the loss of renal function in most patients that survive, the mortality of AKI remains high (over 50%) [41].The tubular epithelium is a key cell in the renal injury. Indeed, tubular cell death plays an important role in the AKI and is the main histological correlation with the degree of renal failure [37, 51]. The tubular epithelium also contributes to renal failure by secreting pro-inflammatory cytokines and by the epithelium–mesenchymal differentiation originating fibroblasts and promoting tubular atrophy and interstitial fibrosis [40, 54]. These events are important contributors to progression of chronic kidney disease.