As shown previously (Nakajima et al., 1994; Geleilete et al., 2002; Volpini et al., 2004), GT rats developed nephrotoxic AKI, with limited body growth, marked creatinine retention, and tubular damage, characterized by clear histologic evidence of cellular necrosis, along with marked increase in the renal content of KIM-1. This evidence concerns the gene HAVCR1 and acute kidney injury.