Baltimore, MD November 9, 2013 New research provides direct evidence that genetic variations in some African Americans with chronic kidney disease contribute to a more rapid decline in kidney function compared with white Americans. The research, led by investigators from the University of Maryland School of Medicine and Johns Hopkins University, may help explain, in part, why even after accounting for differences in socioeconomic background, end-stage kidney disease is twice as prevalent among blacks as whites. Results are published online today in the New England Journal of Medicine.
What we found is pretty remarkable that variations in a single gene account for a large part of the racial disparity in kidney disease progression and risk for end-stage kidney disease, says co-lead author and nephrologist Afshin Parsa, M.D., M.P.H., assistant professor of medicine and member of the Program in Personalized and Genomic Medicine at the University of Maryland School of Medicine. If it were possible to reduce the effect of this gene, there could be a very meaningful decrease in progressive kidney and end-stage kidney disease within blacks.
Previous landmark discoveries revealed that two common variants within a gene called apolipoprotein L1 (APOL1) were strongly associated with non-diabetic end-stage renal disease in blacks. Having only one copy of the variant APOL1 gene variant is associated with a health benefit protection against African sleeping sickness, a potentially lethal parasitic infection transmitted by the tsetse fly, found only in sub-Saharan Africa. However, people with two copies of the variant are at a higher risk for kidney disease.
The current research expands on these prior findings and demonstrates the effect of these variants on the progression of established kidney disease and development of end-stage renal disease; analyzes their role in black-versus-white renal disease disparities; investig
|Contact: Bill Seiler|
University of Maryland Medical Center