PMID- 12803507
OWN - NLM
STAT- MEDLINE
DCOM- 20031211
LR  - 20221207
IS  - 0886-022X (Print)
IS  - 0886-022X (Linking)
VI  - 25
IP  - 3
DP  - 2003 May
TI  - Increased urinary excretion of monocyte chemoattractant protein-1 in proteinuric 
      renal diseases.
PG  - 439-44
AB  - 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.
FAU - Morii, Tsukasa
AU  - Morii T
AD  - Department of Geriatric Medicine, Akita University School of Medicine, Hondo, 
      Akita, Japan. morii@med.akita-u.ac.jp
FAU - Fujita, Hiroki
AU  - Fujita H
FAU - Narita, Takuma
AU  - Narita T
FAU - Koshimura, Jun
AU  - Koshimura J
FAU - Shimotomai, Takashi
AU  - Shimotomai T
FAU - Fujishima, Hiromi
AU  - Fujishima H
FAU - Yoshioka, Naomi
AU  - Yoshioka N
FAU - Imai, Hirokazu
AU  - Imai H
FAU - Kakei, Masafumi
AU  - Kakei M
FAU - Ito, Seiki
AU  - Ito S
LA  - eng
PT  - Comparative Study
PT  - Evaluation Study
PT  - Journal Article
PL  - England
TA  - Ren Fail
JT  - Renal failure
JID - 8701128
RN  - 0 (Biomarkers)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glycated Hemoglobin A)
RN  - AYI8EX34EU (Creatinine)
RN  - EC 3.2.1.52 (Acetylglucosaminidase)
SB  - IM
MH  - Acetylglucosaminidase/urine
MH  - Adult
MH  - Aged
MH  - Albuminuria/*metabolism
MH  - Biomarkers/blood/urine
MH  - Chemokine CCL2/*urine
MH  - Creatinine/blood/urine
MH  - Diabetes Mellitus, Type 2/metabolism
MH  - Diabetic Nephropathies/metabolism
MH  - Female
MH  - Glomerulonephritis, IGA/*metabolism
MH  - Glycated Hemoglobin/metabolism
MH  - Humans
MH  - Hypertension/metabolism
MH  - Male
MH  - Middle Aged
EDAT- 2003/06/14 05:00
MHDA- 2003/12/12 05:00
CRDT- 2003/06/14 05:00
PHST- 2003/06/14 05:00 [pubmed]
PHST- 2003/12/12 05:00 [medline]
PHST- 2003/06/14 05:00 [entrez]
AID - 10.1081/jdi-120021156 [doi]
PST - ppublish
SO  - Ren Fail. 2003 May;25(3):439-44. doi: 10.1081/jdi-120021156.