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dc.contributor.authorNakagawa, Shunsakuja
dc.contributor.authorNishihara, Kumikoja
dc.contributor.authorMiyata, Hitomija
dc.contributor.authorShinke, Harukaja
dc.contributor.authorTomita, Erija
dc.contributor.authorKajiwara, Motoja
dc.contributor.authorMatsubara, Takeshija
dc.contributor.authorIehara, Noriyukija
dc.contributor.authorIgarashi, Yoshinobuja
dc.contributor.authorYamada, Hiroshija
dc.contributor.authorFukatsu, Atsushija
dc.contributor.authorYanagita, Motokoja
dc.contributor.authorMatsubara, Kazuoja
dc.contributor.authorMasuda, Satohiroja
dc.contributor.alternative中山, 俊作ja
dc.contributor.alternative宮田, 仁美ja
dc.contributor.alternative松原, 雄ja
dc.contributor.alternative柳田, 素子ja
dc.contributor.alternative松原, 和夫ja
dc.description.abstractIn chronic kidney disease (CKD), progressive nephron loss causes glomerular sclerosis, as well as tubulointerstitial fibrosis and progressive tubular injury. In this study, we aimed to identify molecular changes that reflected the histopathological progression of renal tubulointerstitial fibrosis and tubular cell damage. A discovery set of renal biopsies were obtained from 48 patients with histopathologically confirmed CKD, and gene expression profiles were determined by microarray analysis. The results indicated that hepatitis A virus cellular receptor 1 (also known as Kidney Injury Molecule-1, KIM-1), lipocalin 2 (also known as neutrophil gelatinase-associated lipocalin, NGAL), SRY-box 9, WAP four-disulfide core domain 2, and NK6 homeobox 2 were differentially expressed in CKD. Their expression levels correlated with the extent of tubulointerstitial fibrosis and tubular cell injury, determined by histopathological examination. The expression of these 5 genes was also increased as kidney damage progressed in a rodent unilateral ureteral obstruction model of CKD. We calculated a molecular score using the microarray gene expression profiles of the biopsy specimens. The composite area under the receiver operating characteristics curve plotted using this molecular score showed a high accuracy for diagnosing tubulointerstitial fibrosis and tubular cell damage. The robust sensitivity of this score was confirmed in a validation set of 5 individuals with CKD. These findings identified novel molecular markers with the potential to contribute to the detection of tubular cell damage and tubulointerstitial fibrosis in the kidney.ja
dc.publisherPublic Library of Scienceja
dc.rights© 2015 Nakagawa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedja
dc.titleMolecular markers of tubulointerstitial fibrosis and tubular cell damage in patients with chronic kidney diseaseja
dc.type.niitypeJournal Articleja
dc.identifier.jtitlePLOS ONEja
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