Two common gene variations are associated with the risk for developing chronic kidney disease, according to a study by researchers at the Johns Hopkins Bloomberg School of Public Health and other institutions. One variant increases risk and the other decreases risk with a similar effect in whites, African-Americans, diabetic and non-diabetic individuals. The study, published in the June 15 edition of JAMA, is the first large-scale investigation of the role Apolipoprotein E (APOE) alleles play in chronic kidney disease. APOE is known to be associated with risk of Alzheimer’s disease and heart disease but interestingly, the kidney disease association is in the opposite direction.
Results of the study found that a variant of the APOE gene, the e2 allele, was associated with a moderately increased risk for chronic kidney disease. The study also confirmed that the e4 variant offered protection against the development of chronic kidney disease. The e4 allele is also a known risk factor for Alzheimer’s disease and a weaker risk factor for coronary heart disease. The e2 allele is known to be associated with abnormalities in plasma triglycerides, a condition that is also common with kidney disease. Smaller previous studies have suggested that the e2 increased and e4 alleles decreased the risk of kidney disease, but those studies mostly focused on individuals with diabetes.
"Consistency of association across a number of previous studies is important in convincing us this effect is real. However, our large study suggests that the effect of the APOE gene is much weaker than previous smaller studies indicated," said Josef Coresh, MD, PhD, corresponding author and professor of epidemiology, medicine and biostatistics at the Bloomberg School of Public Health. "Our understanding of the biology and genetics of kidney disease is improved, which may point to directions for future improvements in therapy. However, population screening for kidney disease risk is still best focused on diabetes, hypertension and protein in the urine."
Tim Parsons | EurekAlert!
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