The kidney injury molecule-1 (designated as Kim-1 in rodents, KIM-1 in humans) is expressed, at much lower levels, in lymphocytes and has also been referred to as T-cell immunoglobulin mucin (TIM)-1 and HAVCR-1, hepatitis A virus cellular receptor-1. The protein has also been reported to be expressed in the cochlea in response to cisplatin-induced injury [8]. The KIM/TIM family consists of eight members in mice, six in rats and three in humans.
KIM-1 is a type I cell membrane glycoprotein which contains, in its extracellular portion, a novel six-cysteine immunoglobulin-like domain, two N-glycosylation sites and a T/SP rich domain characteristic of mucin-like O-glycosylated proteins.

KIM-1 is a phosphatidylserine receptor that recognizes apoptotic cells directing them to lysosomes. It also serves as a receptor for oxidized lipoproteins and hence is adept at recognizing apoptotic cell ‘eat me’ signals. Given these properties KIM-1 is unique in being the first non-myeloid phosphatidylserine receptor that transforms epithelial cells into semi-professional phagocytes [13,14].

A number of characteristics of KIM-1 show that the protein is an ideal biomarker of kidney injury: the absence of KIM-1 expression in the normal kidney; its marked upregulation and insertion into the apical membrane of the proximal tubule; its persistence in the epithelial cell until the cell has completely recovered; the rapid and robust cleavage of the ectodomain and the ex vivo room temperature stability of the ectodomain.