PMID- 12505750
OWN - NLM
STAT- MEDLINE
DCOM- 20030702
LR  - 20220311
IS  - 1056-8727 (Print)
IS  - 1056-8727 (Linking)
VI  - 17
IP  - 1
DP  - 2003 Jan-Feb
TI  - Association of monocyte chemoattractant protein-1 with renal tubular damage in 
      diabetic nephropathy.
PG  - 11-5
AB  - Monocyte chemoattractant protein-1 (MCP-1), is a chemokine that mediates renal 
      interstitial inflammation, tubular atrophy, and interstitial fibrosis by 
      recruiting monocytes/macrophages into renal tubulointerstitium. Recent studies 
      have demonstrated that protein overload in renal tubular cells up-regulates MCP-1 
      gene and its protein expression. Therefore, we hypothesized that increased 
      expression of MCP-1 in renal tubuli, probably triggered by an increase in the 
      leakage of plasma protein from glomerular capillary to tubular fluid, may 
      contribute to renal tubular damage and accelerate the progression of diabetic 
      nephropathy. To test this hypothesis, we examined urinary excretion levels of 
      MCP-1 and N-acetylglucosaminidase (NAG), a sensitive marker of renal tubular 
      damage, in Japanese Type II diabetic patients with normoalbuminuria (n=29), 
      microalbuminuria (n=25), and macroalbuminuria (n=18). The median urinary 
      excretion level of MCP-1 in patients with macroalbuminuria (394.4 ng/g 
      creatinine) was significantly elevated compared to the levels in patients with 
      normoalbuminuria and microalbuminuria (159.6 and 193.9 ng/g creatinine, 
      respectively). Furthermore, the urinary MCP-1 excretion level was positively 
      correlated with urinary excretion levels of albumin (r=.816, P<.001) and NAG 
      (r=.569, P<.001) in all subjects. These results suggest that MCP-1 is produced in 
      renal tubular cells and released into urine in proportion to the degree of 
      proteinuria (albuminuria), and that increased MCP-1 expression in renal tubuli 
      contributes to renal tubular damage. Therefore, we conclude that heavy 
      proteinuria itself may accelerate the progression of diabetic nephropathy by 
      increasing the MCP-1 expression in renal tubuli.
FAU - Morii, Tsukasa
AU  - Morii T
AD  - Department of Geriatric Medicine, Akita University School of Medicine, 1-1-1 
      Hondo, Japan. morii@med.akita-u.ac.jp
FAU - Fujita, Hiroki
AU  - Fujita H
FAU - Narita, Takuma
AU  - Narita T
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  - Journal Article
PL  - United States
TA  - J Diabetes Complications
JT  - Journal of diabetes and its complications
JID - 9204583
RN  - 0 (Chemokine CCL2)
RN  - AYI8EX34EU (Creatinine)
RN  - EC 3.2.1.52 (Acetylglucosaminidase)
SB  - IM
MH  - Acetylglucosaminidase/urine
MH  - Aged
MH  - Albuminuria/metabolism
MH  - Chemokine CCL2/*urine
MH  - Creatinine/blood
MH  - Diabetes Mellitus, Type 2/metabolism/*urine
MH  - Diabetic Nephropathies/metabolism/*urine
MH  - Female
MH  - Humans
MH  - Kidney Tubules/*metabolism
MH  - Male
MH  - Middle Aged
MH  - Proteinuria/metabolism
EDAT- 2002/12/31 04:00
MHDA- 2003/07/03 05:00
CRDT- 2002/12/31 04:00
PHST- 2002/12/31 04:00 [pubmed]
PHST- 2003/07/03 05:00 [medline]
PHST- 2002/12/31 04:00 [entrez]
AID - S1056872702001769 [pii]
AID - 10.1016/s1056-8727(02)00176-9 [doi]
PST - ppublish
SO  - J Diabetes Complications. 2003 Jan-Feb;17(1):11-5. doi: 
      10.1016/s1056-8727(02)00176-9.