Open Access Research article

UMOD polymorphism rs12917707 is not associated with severe or stable IgA nephropathy in a large Caucasian cohort

Miriana Dinic1, Lidia Ghisdal2, Judith Racapé3, Lise Thibaudin1, Philippe Gatault4, Marie Essig5, Yann Le Meur6, Christian Noël7, Guy Touchard8, Pierre Merville9, Zineb Ajarchouh10, Christophe Mariat1, Marc Abramowicz10, Daniel Abramowicz2 and Eric Alamartine1*

Author Affiliations

1 Nephrology-Renal Transplantation Department, CHU de Saint Etienne & EA3064, GIMAP, Université Jean Monnet, Saint Etienne 42055 Cedex 02, France

2 Nephrology-Renal Transplantation Department, Universitair Ziekenhuis Antwerp - Université Libre de Bruxelles (ULB), Brussels, Belgium

3 Department of Biostatistics, School of Public Health, ULB, Brussels, Belgium

4 Nephrology-Renal Transplantation Department, CHU Tours, Tours, France

5 Nephrology-Renal Transplantation Department, CHU Limoges, Limoges, France

6 Nephrology-Renal Transplantation Department, CHU Brest, Brest, France

7 Nephrology-Renal Transplantation Department, CHRU Lille, Lille, France

8 Nephrology-Renal Transplantation Department, CHU Poitiers, Poitiers, France

9 Nephrology-Renal Transplantation Department, CHU Bordeaux, Bordeaux, France

10 Medical Genetics Department and IRIBHM (Institut de Recherche Interdisciplinaire en Biologie Humaine et Moleculaire), ULB, Brussels, Belgium

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BMC Nephrology 2014, 15:138  doi:10.1186/1471-2369-15-138

Published: 28 August 2014

Abstract

Background

Genetic factors are suspected in the pathogenesis of IgA nephropathy, as well as in the course of IgA nephropathy progression towards end stage renal failure. UMOD polymorphism rs12917707 is known to associate with end stage renal failure of mixed aetiologies.

Methods

We tested a large cohort of Caucasian patients for association of rs12917707 with IgA nephropathy showing a benign, stable course and with IgA nephropathy that progressed toward end stage renal failure.

Results

No association was observed between either groups, and a non-significant trend was observed for more severe IgA nephropathy with the allele reported to protect against end stage renal failure of mixed aetiologies.

Conclusion

We conclude that UMOD is unlikely to play a role in IgA nephropathy pathogenesis nor progression to end stage renal failure, and suggest that UMOD effects are restricted to some causes of renal disease, e.g. diabetes or hypertension.