Nephrol Dial Transplant (2004) 19: 596-601
Nephrol Dial Transplant Vol. 19 No. 3 (c) ERA-EDTA 2004; all rights reserved
Original Article
No association of the –2518 MCP-1 A/G promoter polymorphism with incidence and clinical course of IgA nephropathy
1Medizinische Klinik IV, Universitätsklinikum Hamburg Eppendorf, 2Abteilung für Nephrologie und Klinische Immunologie, Universitätsklinikum Aachen and 3Institut für Pathologie, Universitätsklinikum Hamburg Eppendorf, Germany
Correspondence and offprint requests to: Oliver M. Steinmetz, MD, Zentrum für Innere Medizin, Medizinische Klinik IV, University of Hamburg, Martinistraße 52, D-20246 Hamburg, Germany. Email: o.steinmetz{at}uke.uni-hamburg.de
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 
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.
Keywords: CCL2; chemokine; IgA nephropathy; inflammation; MCP-1
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors.