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Nephrol Dial Transplant (2002) 17: 542-545
© 2002 European Renal Association-European Dialysis and Transplant Association

Editorial Comment

Controversies concerning the importance of genetic polymorphism in IgA nephropathy

Luc Frimat and Michèle Kessler

Department of Nephrology, University Hospital Nancy, France

In a recent letter to Nature Genetics, Gharavi and colleagues reported a study of 30 multiplex kindreds, demonstrating the linkage of IgA nephropathy (IgAN) to 6q22-23 [1]. This finding is a considerable step towards a comprehensive explanation of this form of chronic glomerulonephritis. As previously suggested, genetic studies of familial IgAN provide the best way to identify IgAN genes [2]. Following this approach, the number of publications on genetic polymorphism underlying IgAN grew rapidly in the 1990s. For example, in 1996, in this journal, significant results of the first studies showing an association between a genetic polymorphism of the renin-angiotensin system (RAS) and IgAN were met with great enthusiasm [3]. A few years later, reports of negative findings with respect to this association tempered this initial impression [2,4,5]. Some authors were even unable to confirm their own . . . [Full Text of this Article]

IgAN as a complex, multifactorial disorder

Defining IgA nephropathy

Identifying genes that initiate IgAN or promote kidney failure

Correlations, interactions and causation

Notes

References


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