title: Increased urinary excretion of monocyte chemoattractant protein-1 in proteinuric renal diseases.
abstract: Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that is produced mainly by tubular epithelial cells in kidney and contributes to renal interstitial inflammation and fibrosis. More recently, we have demonstrated that urinary MCP-1 excretion is increased in proportion to the degree of albuminuria (proteinuria) and positively correlated with urinary N-acetylglucosaminidase (NAG) levels in type 2 diabetic patients. Based on these findings, we have suggested that heavy proteinuria, itself, probably aggravates renal tubular damage and accelerates the disease progression in diabetic nephropathy by increasing the MCP-1 expression in renal tubuli. In the present study, to evaluate whether urinary MCP-1 excretion is increased in the proteinuric states not only in diabetic nephropathy but also in other renal diseases, we examined urinary MCP-1 levels in IgA nephropathy patients with macroalbuminuria (IgAN group; n = 6), and compared the results with the data obtained from type 2 diabetic patients with overt diabetic nephropathy (DN group; n = 23) and those without diabetic nephropathy (non-DN group; n = 27). Urinary MCP-1 excretion levels in non-DN, DN, IgAN groups were 157.2 (52.8-378.5), 346.1 (147.0-1276.7), and 274.4 (162.2-994.5) ng/g creatinine, median (range), respectively. Expectedly, urinary MCP-1 and NAG excretion levels in DN and IgAN groups were significantly elevated as compared with non-DN group. Therefore, we suggest that MCP-1 expression in renal tubuli is enhanced in proteinuric states,irrespective of the types of renal disease, and that increased MCP-1 expression probably contributes to renal tubular damage in proteinuric states.
authors.affiliation: Department of Geriatric Medicine, Akita University School of Medicine, Hondo, Akita, Japan. morii@med.akita-u.ac.jp
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Morii
authors.forename: Hiroki
authors.initials: H
authors.lastname: Fujita
authors.forename: Takuma
authors.initials: T
authors.lastname: Narita
authors.forename: Jun
authors.initials: J
authors.lastname: Koshimura
authors.forename: Takashi
authors.initials: T
authors.lastname: Shimotomai
authors.forename: Hiromi
authors.initials: H
authors.lastname: Fujishima
authors.forename: Naomi
authors.initials: N
authors.lastname: Yoshioka
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Imai
authors.forename: Masafumi
authors.initials: M
authors.lastname: Kakei
authors.forename: Seiki
authors.initials: S
authors.lastname: Ito
mesh_terms: D000118:Acetylglucosaminidase / Q000652:urine; D000328:Adult; D000368:Aged; D000419:Albuminuria / Q000378:metabolism*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D018932:Chemokine CCL2 / Q000652:urine*; D003404:Creatinine / Q000097:blood / Q000652:urine; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism; D003928:Diabetic Nephropathies / Q000378:metabolism; D005260:Female; D005922:Glomerulonephritis, IGA / Q000378:metabolism*; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000378:metabolism; D008297:Male; D008875:Middle Aged
chemical_list: D000118:Acetylglucosaminidase; D015415:Biomarkers; D018932:Chemokine CCL2; D003404:Creatinine; D006442:Glycated Hemoglobin