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NDT Advance Access originally published online on December 5, 2005
Nephrology Dialysis Transplantation 2006 21(2):257-260; doi:10.1093/ndt/gfi325
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

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Genetic factors in progressive renal disease: the good ones, the bad ones and the ugly ducklings

Michael Eikmans, Joris A. Aben, Klaas Koop, Hans J. Baelde, Emile de Heer and Jan A. Bruijn

Leiden University Medical Center, Department of Pathology, Leiden, The Netherlands

Correspondence and offprint requests to: Dr Michael Eikmans, Leiden University Medical Center, Department of Pathology, Leiden, The Netherlands. Email: m.eikmans@lumc.nl

Keywords: animal models; gene expression profiling; genetic predisposition; kidney diseases; polymorphisms; repair capacity

The first 150 words of the full text of this article appear below.



   Introduction
 
Worldwide, >1 million people have developed end-stage renal disease (ESRD) and need renal replacement therapy. ESRD is secondary to a broad range of diseases that include diabetic nephropathy and focal and segmental glomerulosclerosis. The rate of progression to ESRD varies among patients suffering from kidney diseases, and is to a large extent determined by genetic factors. We will discuss studies that have provided evidence for a genetic component underlying susceptibility to progressive renal disease. On the one hand, gene mutations may result in a disturbed function of the corresponding protein, which will lead directly to kidney disease. On the other hand, genetic factors may become manifest only in the presence of systemic diseases, such as hypertension and diabetes mellitus, and thus modify the outcome of the kidney disease. For instance, polymorphisms in genes encoding proteins that are able to protect the renal tissue against permanent damage may be the basis . . . [Full Text of this Article]



   Genetic factors in kidney diseases
 


   Genetic predisposition to renal disease in animal models
 


   Regeneration capacity of the kidney
 


   Conclusion
 

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