LAUSR

Kidney injury molecule‐1 (KIM‐1) is a membrane receptor upregulated in the proximal tubule cells following various types of kidney injuries. Notably, studies have suggested a correlation between KIM‐1 expression and extracellular signal‐regulated kinase (ERK) activation. In this study, we aimed to investigate the association between the kidney overexpression pattern of cytoplasmic phosphorylated‐ERK (p‐ERK) protein and increased urinary KIM‐1 levels in rats exposed to gentamicin or lead acetate, both at the end of toxic exposure and after a 4‐week recovery period. Although other proteins were evaluated, only kidney overexpression of cytoplasmic p‐ERK protein correlated with increased urinary KIM‐1 levels. For both toxic substances, the increased urinary KIM‐1 levels corresponded with kidney inflammation. Our results suggest that KIM‐1 and p‐ERK share a common mechanism in kidney injury mediated by both toxic substances that induce proximal tubule damage.