Acute kidney injury (AKI) is a widespread clinical syndrome directly associated with patient short-term and long-term morbidity and mortality. During the last decade, the incidence rate of AKI has been increasing, the repeated and severe episodes of AKI have been recognized as a major risk factor chronic kidney diseases (CKD) and end-stage kidney disease (ESRD) leading to global disease burden. Proposed pathological processes and risk factors that add to the transition of AKI to CKD and ESRD include severity and frequency of kidney injury, older age, gender, genetics and chronic health conditions like diabetes, hypertension, and obesity. Therefore, there is a great interest in learning about the mechanism of AKI leading to renal fibrosis, the ultimate renal lesions of CKD. Over the last several years, a significant attention has been given to the field of renal fibrosis with impressive progression in knowing the mechanism of renal fibrosis to detailed cellular characterization and molecular pathways implicated in tubulointerstitial fibrosis. Research and clinical trial are underway for emerging biomarkers detecting early kidney injury, predicting kidney disease progression and developing strategies to efficiently treat AKI and to minimize AKI progression to CKD and ESRD. Specific interventions to prevent renal fibrosis are still experimental. Potential therapeutic advances based on those molecular mechanisms will hopefully offer promising insights into the development of new therapeutic interventions for patients in the near future.
Keywords: Acute kidney injury; Fibrosis; Inflammation; Maladaptive repair; Proximal tubular cell.