@article{oai:soar-ir.repo.nii.ac.jp:00003814,
 author = {Li,  Gang and Hu,  Rui and Kamijo,  Yuji and Nakajima,  Takero and Aoyama,  Toshifumi and Ehara,  Takashi and Shigematsu,  Hidekazu and Kannagi,  Reiji and Kyogashima,  Mamoru and Hara,  Atsushi},
 issue = {7},
 journal = {NEPHROLOGY},
 month = {Oct},
 note = {We recently proposed serum sulfatides as a novel biomarker for cardiovascular disease in patients with end-stage renal failure (ESRF), based on the possible antithrombotic properties of this molecule. In this earlier study, the level of serum sulfatides was gradually decreased in parallel with kidney dysfunction; however the precise mechanism underlying this decrease was unknown. The aim of the present study was to investigate the mechanism underlying the decrease in serum sulfatide levels caused by kidney dysfunction in an experimental animal model. To produce a kidney dysfunction animal model, we prepared a mouse model of protein overload nephropathy. Using high-throughput analysis combined with matrix-assisted laser desorption ionisation time-of-flight mass spectrometry, we measured the levels of sulfatides in the sera, livers, small intestines and kidneys of protein overload nephropathy mice. As the disease progressed, the levels of sulfatides in sera decreased. Also, the levels in livers and small intestines decreased in a similar manner to those in sera, to approximately 60% of the original levels. On the contrary, those in kidneys increased by approximately 1.4-fold. Our results indicate that kidney dysfunction affects the levels of sulfatides in lipoprotein-producing organs, such as livers and small intestines, and lowers the levels of sulfatides in sera., Article, NEPHROLOGY. 14(7):658-662 (2009)},
 pages = {658--662},
 title = {Kidney dysfunction induced by protein overload nephropathy reduces serum sulfatide levels in mice},
 volume = {14},
 year = {2009}
}