Preclinical subtractive hybridization screens identified kidney injury molecule 1 （Kim-1） as a gene that is markedly up-regulated in ischemic rat kidneys. Downstream proteomic studies have also shown KIM-1 to be one of the most highly induced proteins in the kidney after AKI in animal models. KIM-1 is a transmembrane protein that is not expressed in normal kidney but is specifically upregulated in dedifferentiated proximal tubule cells after ischemic or nephrotoxic AKI. It has been identified as a phosphatidylserine receptor that transforms epithelial cells into phagocytes by recognizing cell surface-specific epitopes expressed by apoptotic tubular epithelia. A proteolytically processed extracellular domain of KIM-1 is detectable in the urine soon after AKI. KIM-1 represents a promising biomarker for the early diagnosis of AKI and its clinical outcomes. The recent availability of a rapid urine dipstick test for KIM-1 will facilitate its further evaluation in preclinical and clinical studies.