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Paul W. Sanders, MD

Paul W. Sanders, MD
Department of Medicine
Division of Nephrology
LHRB 642 Zip 0007
Phone: 205-934-3589

I began my career as a physician, but was given a wonderful opportunity to develop a bench research program during my nephrology fellowship. For more than 30 years, I have been studying the pathophysiology of kidney disease and hypertension and mechanisms that lead to progressive loss of kidney function. I am also an active clinician who manages patients at all stages of their kidney disease, and my patients inspire and motivate me to continue my research. As a productive physician-scientist in Renal Medicine, I specifically study 1) the pathogenesis of kidney diseases associated with immunoglobulin light chains, 2) the endothelial cell responses to dietary salt and potassium intake, 3) mechanisms of salt sensitivity and salt-sensitive hypertension, and 4) acute and chronic kidney injury. I have expertise in fundamental and clinical research in cardiovascular and renal diseases.

Research/Clinical Interest

Mechanisms of Disease Progression in the Kidney
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

  1. Ying WZ, Aaron KJ, Sanders PW: Effect of aging and dietary salt and potassium intake on endothelial PTEN (Phosphatase and tensin homolog on chromosome 10) function. PLoS ONE 7:e41785, 2012. 23144940 
  2. Ying W-Z, CE Allen, LM Curtis, KJ Aaron, PW Sanders: Mechanism and prevention of acute kidney injury from cast nephropathy in a rodent model. J. Clin. Invest. 122:1777-1785, 2012 22484815 
  3. 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 
  4. 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 
  5. 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 
  6. 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 
  7. 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 
  8. Wang, P-X, and PW Sanders: Immunoglobulin light chains generate hydrogen peroxide. J. Am. Soc. Nephrol. 18:1239-1245, 2007. 17360948
  9. Wang, P-X, and PW Sanders: Immunoglobulin light chains generate hydrogen peroxide. J. Am. Soc. Nephrol. 18:1239-1245, 2007 17360948 
  10. 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 
  11. 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 
  12. 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 
  13. Ying, W-Z, and PW Sanders: Increased dietary salt activates rat aortic endothelium in vivo. Hypertension 39:239-244, 2002. 11847191 
  14. Ying, W-Z, H Xia and PW Sanders: A nitric oxide synthase (NOS2) mutation in Dahl/Rapp rats decreases enzyme stability. Circ. Res. 89:317-322, 2001. 11509447 
  15. Ying, W-Z, and PW Sanders: Mapping the binding domain of immunoglobulin light chains for Tamm-Horsfall protein. Am. J. Pathol. 158:1859-1866, 2001. 11337384 
  16. Ying, W-Z, and PW Sanders: Dietary salt modulates renal production of transforming growth factor-ß in rats. Am. J. Physiol. 274 (Renal Physiol. 43):F635-F641, 1998. 9575885 
  17. Huang, Z-Q, and PW Sanders: Localization of a single binding site for immunoglobulin light chains on human Tamm-Horsfall glycoprotein. J. Clin. Invest. 99: 732-736, 1997. 9045877 
  18. Huang, ZQ, KA Kirk, KG Connelly, and PW Sanders: Bence Jones proteins bind to a common peptide segment on Tamm-Horsfall glycoprotein to promote heterotypic aggregation. J. Clin. Invest. 92:2975-2983, 1993. 8254051 
  19. Sanders, PW, and BB Booker: Pathobiology of cast nephropathy from human Bence Jones proteins. J. Clin. Invest. 89:630-639, 1992. 1737851