Back to Main

Faculty Detail     Name PAUL W SANDERS   Campus Address LHRB 642 Zip 0007 Phone 205-934-3589 E-mail psanders@uab.edu Other websites

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Medicine  Med - Nephrology Professor Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor Center  Pathology   Cell Adhesion & Matrix Research Center Professor Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor Center  Medicine  Comprehensive Diabetes Ctr Professor Center  Medicine  Ctr Cardiovasc Bio Professor Center  Medicine  Nephrology Res & Trng Ctr Professor

Graduate Biomedical Sciences Affiliations Integrative Biomedical Sciences  Medical Scientist Training Program  Pathobiology and Molecular Medicine  Waiting to be Seated

Biographical Sketch  Dr. Sanders was born in Tampa, Florida, and has lived in Alabama most of his life. He received his degree in Medicine in 1979 from the University of South Alabama College of Medicine. After completing a residency in Medicine and fellowship in Nephrology at UAB, Dr. Sanders has remained on faculty at UAB, where he has risen in the ranks to Professor. Dr. Sanders has served as Chief of the Renal Section at the Birmingham Veterans Affairs Medical Center since 1989. He became Director of the Nephrology Research and Training Center in October 2009.

Society Memberships Organization Name Position Held Org Link American College of Physicians      American Heart Association      American Physiological Society      American Society For Clinical Investigation      American Society of Nephrology

Research/Clinical Interest Title Mechanisms of Disease Progression in the Kidney Description The laboratory of Paul W. Sanders, M.D., is funded through the National Institutes of Health to study the pathogenesis of salt-sensitive hypertension and hypertensive nephrosclerosis. More than 43 million Americans have high blood pressure and almost half are salt-sensitive. The frequency of occurrence of clinically important end-organ kidney damage is about 1 in 2,500 hypertensive patients, making hypertensive nephrosclerosis the second most common cause of end-stage renal disease. Salt-sensitive hypertension and hypertensive renal disease are enormously significant problems, but the pathogenetic mechanisms remain incompletely defined. Dr. Sanders uses a genetic model of salt-sensitive hypertension to understand how this problem develops and further how hypertensive renal disease occurs and may be prevented. Dr. Sanders' laboratory is also funded by Merit Awards through the Department of Veterans Affairs to study the mechanism of kidney damage from immunoglobulin proteins. Work in this area has most recently focused on understanding the molecular mechanisms of tubulo-interstitial kidney damage related to immunoglobulin light chains as well as glomerular lesions that result from the interactions between these proteins and mesangial cells to produce amyloid deposition and the syndrome known as monoclonal light chain deposition disease.

Selected Publications  Publication PUBMEDID Basnayake, K, W-Z Ying, P-X Wang, and PW Sanders: Immunoglobulin Light Chains Activate Tubular Epithelial Cells Through Redox Signaling. J. Am. Soc. Nephrol. 21:1165-1173, 2010.  20558542  Ying, W-Z, K Aaron, P-X Wang and PW Sanders: Potassium inhibits dietary salt-induced TGF-ß production. Hypertension 54:1159-1163, 2009.  19738156  Ying, W-Z, K Aaron, and PW Sanders: Dietary salt activates an endothelial Pyk2/c-Src/phosphatidylinositol 3-kinase complex to promote endothelial NO synthase phosphorylation. Hypertension 52:1134-1141, 2008.  18981321  Ying, W-Z, K Aaron, and PW Sanders: Mechanism of dietary salt-mediated increase in intravascular production of TGF-ß1. Am. J. Physiol. Renal Physiol. 295:F406-F414, 2008.  18562633  Curtis, LM, S Chen, B Chen, A Agarwal, CA Klug, and PW Sanders: Contribution of intra-renal cells to cellular repair after acute kidney injury: subcapsular implantation technique. Am. J. Physiol. Renal Physiol. 295:F310-F314, 2008.  18448588  Wang, P-X, and PW Sanders: Immunoglobulin light chains generate hydrogen peroxide. J. Am. Soc. Nephrol. 18:1239-1245, 2007.  17360948  Wang, P-X, and PW Sanders: Immunoglobulin light chains generate hydrogen peroxide. J. Am. Soc. Nephrol. 18:1239-1245, 2007  17360948  Ying, W-Z, H-G Zhang, and PW Sanders: EGF receptor activity modulates apoptosis induced by inhibition of the proteasome of vascular smooth muscle cells. J. Am. Soc. Nephrol. 18:131-143, 2007.  17151333  Ying, W-Z, and PW Sanders: Accelerated ubiquitination and proteasome degradation of a genetic variant of the inducible nitric-oxide synthase. Biochem. J. 376:789-794, 2003.  12959638  Ying, W-Z and PW Sanders: The inter-relationship between TGF-ß1 and nitric oxide is altered in salt-sensitive hypertension. Am. J. Physiol. Renal Physiol. 285:F902-F908, 2003.  12865256  First Prev   1 2 of  2  Next Last

Keywords salt-sensitive hypertension, transforming growth factor-ß, nitric oxide, hypertensive nephrosclerosis, monoclonal immunoglobulin light-chain-related renal diseases

© 2008 University of Alabama at Birmingham. All rights reserved. DisclaimerAbout this SiteGraphic Design Created by UAB Web Communications.
Calendar Designed by Medical Education Information Services. To report problems with the site, email us at meis@uab.edu. Last Revision: February 15, 2012.
The UAB School of Medicine Mailing Address: 1530 3rd Avenue South, FOT 1203, Birmingham AL 35294-3412