Kidney injury molecule-1 is an early biomarker of cadmium nephrotoxicity. Prozialeck, W. C., Vaidya, V. S., Liu, J., Waalkes, M. P., Edwards, J. R., Lamar, P. C., Bernard, A. M., Dumont, X., & Bonventre, J. V. Kidney International, 72(8):985–993, October, 2007.
doi  abstract   bibtex   
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.
@article{prozialeck_kidney_2007,
	title = {Kidney injury molecule-1 is an early biomarker of cadmium nephrotoxicity},
	volume = {72},
	issn = {0085-2538},
	doi = {10.1038/sj.ki.5002467},
	abstract = {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.},
	language = {eng},
	number = {8},
	journal = {Kidney International},
	author = {Prozialeck, W. C. and Vaidya, V. S. and Liu, J. and Waalkes, M. P. and Edwards, J. R. and Lamar, P. C. and Bernard, A. M. and Dumont, X. and Bonventre, J. V.},
	month = oct,
	year = {2007},
	pmid = {17687258},
	pmcid = {PMC2747605},
	keywords = {Animals, Biomarkers, Body Weight, Cadmium, Cell Adhesion Molecules, Dose-Response Relationship, Drug, Kidney Tubules, Proximal, Male, Membrane Proteins, Metallothionein, Proteinuria, Rats, Rats, Sprague-Dawley, Uteroglobin},
	pages = {985--993},
}

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