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BIDMC scientist David J. Friedman, M.D., receives award from Doris Duke Charitable Foundation

BOSTON David J. Friedman, MD, a clinician and scientific investigator in the Division of Nephrology and Center for Vascular Biology Research at Beth Israel Deaconess Medical Center (BIDMC) has been selected to receive a Clinical Scientist Development Award (CSDA) from the Doris Duke Charitable Foundation. The three-year award, which totals $486,000, will support Friedman's research into the genetic and environmental factors that lead to kidney disease in African Americans, in particular the role of a gene called APOL1.

"As investigators, physician-scientists face a particularly large challenge: meeting both the demands of seeing patients and conducting research," said Betsy Myers, Director of the Medical Research Program for the Doris Duke Charitable Foundation. "Supporting the work of promising investigators while they're still early in their careers remains critical to keeping the clinical research workforce strong."

A graduate of Harvard College, Friedman received his medical degree from the Yale School of Medicine and went on to complete his residency at BIDMC. From 2003 to 2005 he was a Clinical Fellow in BIDMC's Division of Nephrology and from 2004 to 2007 was a Research Fellow in the Division of Nephrology. An Assistant Professor of Medicine at Harvard Medical School (HMS), Friedman is the recipient of numerous HMS teaching awards.

"Dr. Friedman's important work may one day translate into new diagnostic tools and therapeutic strategies to help prevent end-stage renal disease," explains BIDMC Chief of Nephrology Martin Pollak, MD. Last year Pollak and Friedman co-authored a paper in the journal Science that identified two common coding variants in the APOL1 gene on chromosome 22 which greatly increase the risk of end-stage renal disease in African Americans. "This devastating and costly condition affects nearly 500,000 people in the United States, and is four to five times more common in African Americans compared to Caucasian Americans. Clearly, new diagnostic and treatment options are needed," adds Pollak.

Furthermore, says Friedman, as many as 3.5 million African Americans likely have the high risk APOL1 genotype.

"This gene increases a person's risk of developing kidney failure approximately 10-fold," he explains. "Investigating this gene is particularly challenging because only humans and a few primate species have the APOL1 gene in their genomes. Studies in patients with the disease are essential, and with this support from the Doris Duke Charitable Foundation, we hope to develop a better understanding of the genetic and environmental influences that modify the major APOL1 risk alleles."


Contact: Bonnie Prescott
Beth Israel Deaconess Medical Center

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