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Am J Physiol Renal Physiol. 2014 Oct 01;307(7):F757-76. doi: 10.1152/ajprenal.00306.2014. Epub 2014 Jul 30.

Genetic and epigenetic factors influencing chronic kidney disease.

American journal of physiology. Renal physiology

L J Smyth, S Duffy, A P Maxwell, A J McKnight

Affiliations

  1. Nephrology Research, Centre for Public Health, Queen's University of Belfast, Belfast, Northern Ireland.
  2. Nephrology Research, Centre for Public Health, Queen's University of Belfast, Belfast, Northern Ireland [email protected].

PMID: 25080522 DOI: 10.1152/ajprenal.00306.2014

Abstract

Chronic kidney disease (CKD) has become a serious public health problem because of its associated morbidity, premature mortality, and attendant healthcare costs. The rising number of persons with CKD is linked with the aging population structure and an increased prevalence of diabetes, hypertension, and obesity. There is an inherited risk associated with developing CKD, as evidenced by familial clustering and differing prevalence rates across ethnic groups. Previous studies to determine the inherited risk factors for CKD rarely identified genetic variants that were robustly replicated. However, improvements in genotyping technologies and analytic methods are now helping to identify promising genetic loci aided by international collaboration and multiconsortia efforts. More recently, epigenetic modifications have been proposed to play a role in both the inherited susceptibility to CKD and, importantly, to explain how the environment dynamically interacts with the genome to alter an individual's disease risk. Genome-wide, epigenome-wide, and whole transcriptome studies have been performed, and optimal approaches for integrative analysis are being developed. This review summarizes recent research and the current status of genetic and epigenetic risk factors influencing CKD using population-based information.

Copyright © 2014 the American Physiological Society.

Keywords: chronic kidney disease; dna methylation; epigenetic association; genetic single-nucleotide polymorphisms; population-based epidemiology

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