In CRIC, says Dr. Parsa, we found that, indeed, the gene variants account for a very significant portion of the faster progression in blacks versus whites. If a person had two copies of the APOL1 risk variant, their kidney disease worsened faster and their chance of developing end-stage kidney disease nearly doubled. The researchers also found that APOL1 variants equally affected progression rates in patients with diabetes, a finding that had not been fully realized in previous studies. These results suggest that APOL1 gene variants affect the progression of established renal disease, regardless of the primary cause, adds Dr. Parsa.
Beyond that, however, the analysis showed that black patients without the APOL1 high-risk variants still had a slightly increased chance for end-stage renal disease. For this reason, the researchers conclude there may be some remaining unaccounted factors contributing to increased progression of kidney disease in blacks.
Further research will focus on the specific activity of the APOL1 variants. These gene variants can modify the genes function. However, we have not yet been able to delineate how they affect renal disease progression. Our next line of research is to find out what pathways are triggered by these gene variants and how they could cause worsening of renal disease, says Dr. Parsa.
This study underscores the importance of research examining genetic and racial disparities as part of the effort to improve outcomes by personalizing medicine, says E. Albert Reece, M.D., Ph.D., M.B.A., vice president for medical affairs at the University of Maryland and
|Contact: Bill Seiler|
University of Maryland Medical Center