Kidney injury molecule-1 is an early biomarker of cadmium nephrotoxicity
(2007) Kidney International — Vol. 72, n° 8, p. 985-993 (2007)
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- Cadmium ( Cd) exposure results in injury to the proximal tubule characterized by polyuria and proteinuria. Kidney injury molecule-1 ( Kim-1) is a transmembrane glycoprotein not normally detected in the mature kidney, but is upregulated and shed into the urine following nephrotoxic injury. In this study, we determine if Kim-1 might be a useful early biomarker of Cd nephrotoxicity. Male Sprague-Dawley rats were given daily injections of Cd for up to 12 weeks. Weekly urine samples were analyzed for Kim-1, protein, creatinine, metallothionein, and Clara cell protein CC-16. Significant levels of Kim-1 were detected in the urine by 6 weeks and continued to increase throughout the treatment period. This appearance of Kim-1 occurred 4-5 weeks before the onset of proteinuria, and 1-3 weeks before the appearance of metallothionein and CC-16. Higher doses of Cd gave rise to higher Kim-1 excretion. Reverse transcriptase-polymerase chain reaction ( RT-PCR) expression analysis showed that Kim-1 transcript levels were increased after 6 weeks at the low dose of Cd. Immunohistochemical analysis showed that Kim-1 was present in proximal tubule cells of the Cd-treated rats. Our results suggest that Kim-1 may be a useful biomarker of early stages of Cd-induced proximal tubule injury.
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Prozialeck, W. C., Vaidya, V. S., Liu, J., Waalkes, M. P., Edwards, J. R., Lamar, P. C., Bernard, A., Dumont, X., & Bonventre, J. V. (2007). Kidney injury molecule-1 is an early biomarker of cadmium nephrotoxicity. Kidney International, 72(8), 985-993. https://doi.org/10.1038/sj.ki.5002467 (Original work published 2007)