Scientific Advisory Board

Martin R. Pollak, M.D.
Harvard Institutes of Medicine
Department of Genetics
Chief, Division of Nephrology
Beth Israel Deaconess Medical Center
Associate Professor of Medicine
Harvard Medical School
185 Pilgrim Rd, Farr 819
Boston MA 02115
Business:  617-632-9845
Email: mpollak@bidmc.harvard.edu
URL: Click Here

Dr. Martin R. Pollak is the Chief of the Renal Division at Beth Israel Deaconess Medical Center in Boston, MA. Dr. Pollak is also a member of the Cancer Genetics Program at the Dana-Farber/Harvard Cancer Center.

Dr. Pollak attended medical school at New York University School of Medicine. He completed both his internship and residency at Columbia-Presbyterian Medical Center in the field of Internal Medicine. Dr. Pollak went on to accomplish his fellowship at Brigham and Women’s Hospital in the area of Nephrology. He was an associate professor in the Department of Medicine at Brigham and Women's Hospital of Harvard before being named to his current position. Dr. Pollak’s clinical interests include general nephrology and inherited kidney disease.

Dr. Pollak’s laboratory studies the genetic basis of kidney disease. His lab is particularly interested in kidney disease characterized by proteinuria and glomerulosclerosis. This phenotype is common and is often seen as a response to forms of injury such as hypertension, diabetes, and HIV infection. His lab also works to identify genes involved in the development of FSGS in minority populations.

Selected Publications:

Möller CC, Pollak MR, Reiser J. The genetic basis of human glomerular disease. Adv Chronic Kidney Dis 2006 Apr; 13(2):166-73

Reiser J, Polu KR, Moller CC, Kenlan P, Altintas MM, Wei C, Faul C, Herbert S, Villegas I, Avila-Casado C, McGee M, Sugimoto H, Brown D, Kalluri R, Mundel P, Smith PL, Clapham DE, Pollak MR. TRPC6 is a glomerular slit diaphragm-associated channel required for normal renal function. Nat Genet. 2005, 37(7):739-44.

Yao J, Le TC, Kos CH, Allen PG, Denker BM, Pollak MR. ?-actinin-4 mediated FSGS: an inherited kidney disease caused by an aggregated and rapidly degraded cytoskeletal protein. Public Library of Science Biology, 2004, 2(6):787-794.