PMID- 14767014
OWN - NLM
STAT- MEDLINE
DCOM- 20040713
LR  - 20221207
IS  - 0931-0509 (Print)
IS  - 0931-0509 (Linking)
VI  - 19
IP  - 3
DP  - 2004 Mar
TI  - No association of the -2518 MCP-1 A/G promoter polymorphism with incidence and 
      clinical course of IgA nephropathy.
PG  - 596-601
AB  - BACKGROUND: The clinical course of IgA nephropathy is highly variable, ranging 
      from complete remission to progression with end-stage renal disease. Although the 
      mechanisms involved in disease progression are not characterized in detail, loss 
      of renal function is positively correlated with mononuclear cell infiltration. In 
      general, chemokines play an important role in the directional recruitment of 
      inflammatory cells. Recently, a polymorphism in the distal 5' regulatory region 
      of the chemokine monocyte chemoattractant protein-1 (MCP-1), which affects gene 
      expression, has been described (A/G at position -2518). The aim of our study was 
      to evaluate a possible association of this polymorphism with disease progression 
      in patients with IgA nephropathy, as well as susceptibility to this form of 
      glomerulonephritis. METHODS: Blood samples from 207 patients with biopsy proven 
      IgA nephropathy and 140 ethnically, age and sex-matched healthy controls were 
      collected and genomic DNA was extracted. MCP-1 -2518 genotype was assessed by 
      PCR, followed by restriction fragment length polymorphism analysis. Genotype 
      distribution between the two groups was compared by chi(2) test. Cumulative renal 
      survival was assessed by Kaplan-Meier plot and log-rank analysis. RESULTS: 111 
      (53.6%) patients had the MCP-1 -2518 wild-type A/A, 83 (40.1%) were heterozygous 
      for the G allele and 13 (6.3%) patients showed homozygosity. The allelic 
      distribution was not significantly different in the control group of 140 healthy 
      blood donors (P = 0.71). Renal survival analysis of patients did not reveal 
      statistically significant differences in cumulative survival (P = 0.32), median 
      survival time and 5 year survival rate between the wild-type group and carriers 
      of the G allele. Furthermore, the number of infiltrating CD68-positive 
      monocytes/macrophages into the kidneys of patients with IgA nephropathy was not 
      statistically different between the groups. CONCLUSION: Our data indicate that no 
      association exists between the -2518 A/G polymorphism and susceptibility to IgA 
      nephropathy or its clinical course.
FAU - Steinmetz, Oliver M
AU  - Steinmetz OM
AD  - Medizinische Klinik IV, Universitatsklinikum Hamburg Eppendorf, Germany. 
      o.steinmetz@uke.uni-hamburg.de
FAU - Panzer, Ulf
AU  - Panzer U
FAU - Harendza, Sigrid
AU  - Harendza S
FAU - Mertens, Peter R
AU  - Mertens PR
FAU - Ostendorf, Tammo
AU  - Ostendorf T
FAU - Floege, Jurgen
AU  - Floege J
FAU - Helmchen, Udo
AU  - Helmchen U
FAU - Stahl, Rolf A K
AU  - Stahl RA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Nephrol Dial Transplant
JT  - Nephrology, dialysis, transplantation : official publication of the European 
      Dialysis and Transplant Association - European Renal Association
JID - 8706402
RN  - 0 (Chemokine CCL2)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Case-Control Studies
MH  - Chemokine CCL2/*genetics
MH  - Child
MH  - DNA/genetics
MH  - Female
MH  - Genetic Predisposition to Disease/genetics
MH  - Glomerulonephritis, IGA/*genetics/*physiopathology
MH  - Humans
MH  - Kidney Failure, Chronic/genetics
MH  - Male
MH  - Middle Aged
MH  - *Polymorphism, Genetic
MH  - Regulatory Sequences, Nucleic Acid/*genetics
MH  - Retrospective Studies
MH  - White People/genetics
EDAT- 2004/02/10 05:00
MHDA- 2004/07/14 05:00
CRDT- 2004/02/10 05:00
PHST- 2004/02/10 05:00 [pubmed]
PHST- 2004/07/14 05:00 [medline]
PHST- 2004/02/10 05:00 [entrez]
AID - 10.1093/ndt/gfg577 [doi]
PST - ppublish
SO  - Nephrol Dial Transplant. 2004 Mar;19(3):596-601. doi: 10.1093/ndt/gfg577.