Terry J. Watnick, M.D.

Assistant Professor of Medicine
Division of Nephrology 

Since 1996, Dr. Watnick has headed the Johns Hopkins Hereditary Renal Disease Clinic.  She follows over 150 patients with a variety of inherited kidney diseases including a large cohort with polycystic kidney disease. Based on her clinical and scientific expertise she is frequently consulted by clinicians at Johns Hopkins and across the country with respect to genetic testing for adult polycystic kidney disease (ADPKD).  She is also the Principal Investigator for a Phase II intervention trial which will look at the safety and efficacy of a V2 receptor antagonist in ADPKD.

Johns Hopkins PKD CORE CENTER

Research Interests:

Dr. Watnick has a track record of notable accomplishments in the field polycystic kidney disease. mention.  She was instrumental in developing the methods that now form the basis for the only commercially available DNA test for PKD1 (one of the two genes that cause autosomal dominant polycystic kidney disease or ADPKD). In addition she applied these methods to analyzing DNA that was extracted from individual renal cysts. This work led to our current understanding of the molecular basis for autosomal dominant polycystic kidney disease which depends on a "two hit" mechanism. Dr. Watnick was one of the first investigators to apply newly developed gene targeting techniques in Drosophila melanogaster in order to determine the role of polycystin-2 in the fruit fly. She is now using her extensive experience in genetics to study modifiers of polycystin signaling using murine models of ADPKD.

Dr. Watnick's research is currently focused on examining the role of polycystins in modulating TGF-b signaling pathways. The hypotheses are based on the novel observation made by Dr. Watnick and her collaborators demonstrating that loss of polycystin-1 can modulate the severity of aortic wall pathology in Fbn1 (the gene responsible for the Marfan syndrome) mutant mice.  Since several pathologic manifestations of Marfan's are thought to be due to up-regulation of TGFb signaling, Dr. Watnick hypothesizes that loss of polycystins may independently up regulate TGFb. She is using novel murine models as well as cell culture systems to confirm her observations. These studies are likely to provide important insights in to the pathogenesis of vascular disease in ADPKD.