title: Fibrocytes are involved in the pathogenesis of human chronic kidney disease.
abstract: The presence of chronic kidney disease in humans is associated with a risk of kidney function loss as well as the development of cardiovascular disease. Fibrocytes have been shown to contribute to organ fibrosis. In this study, the presence of fibrocytes was investigated immunohistochemically in kidney biopsy specimens from 100 patients with chronic kidney disease. In addition, 6 patients with thin basement membrane disease were studied as a disease control. In patients with chronic kidney disease, the infiltration of fibrocytes was observed mainly in the interstitium. The number of interstitial fibrocytes in patients with chronic kidney disease was higher than that in patients with thin basement membrane disease. The number of infiltrated fibrocytes in the interstitium correlated well with the severity of tubulointerstitial lesions, such as interstitial fibrosis, in patients with chronic kidney disease. In addition, there were significant correlations between the number of interstitial fibrocytes and the number of CD68-positive macrophages in the interstitium as well as urinary monocyte chemoattractant protein-1/CCL2 levels. In particular, there was an inverse correlation between the number of interstitial fibrocytes and kidney function at the time of biopsy. Finally, the numbers of interstitial fibrocytes and macrophages as well as urinary CCL2 levels were significantly decreased during convalescence induced by glucocorticoid therapy. These results suggest that fibrocytes may be involved in the pathogenesis of chronic kidney disease through the interaction with macrophages as well as CCL2.
authors.affiliation: Division of Blood Purification, Kanazawa University Hospital, Kanazawa 920-8641, Japan.
authors.forename: Norihiko
authors.initials: N
authors.lastname: Sakai
authors.forename: Kengo
authors.initials: K
authors.lastname: Furuichi
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Shinozaki
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yamauchi
authors.forename: Tadashi
authors.initials: T
authors.lastname: Toyama
authors.forename: Shinji
authors.initials: S
authors.lastname: Kitajima
authors.forename: Toshiya
authors.initials: T
authors.lastname: Okumura
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kokubo
authors.forename: Motoo
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Kazuya
authors.initials: K
authors.lastname: Takasawa
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Takeda
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Yoshimura
authors.forename: Shuichi
authors.initials: S
authors.lastname: Kaneko
authors.forename: Takashi
authors.initials: T
authors.lastname: Wada
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D018925:Chemokines / Q000378:metabolism; D002908:Chronic Disease; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005355:Fibrosis / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D007674:Kidney Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D007676:Kidney Failure, Chronic / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D008264:Macrophages / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index
chemical_list: D018925:Chemokines