Our primary goal at the Glomerular Disease Therapeutics Laboratory (GDTL)  is to develop novel mechanism based therapy for glomerular diseases and nephrotic syndrome. We use existing animal models, and develop new mechanistically relevant rat models of glomerular disease to study genes and proteins that have potential in future glomerular therapeutics. We also conduct a variety of cell biology, proteomic, molecular biology and imaging studies to rigorously test our hypothesis and develop new agents for treatment of human glomerular disease. Novel therapeutic strategies in advanced stages of development include the use of compounds that alter sialylation  in vivo, and various forms of recombinant Angiopoietin-like-4 in the treatment of some forms of nephrotic syndrome (see patents below).  We are actively engaged in identifying a circulating glomerulophilic proteome (CGP) that modulates human glomerular disease.

Location: We are physically located on the 6^th floor of Tinsley Harrison Tower (rooms 612, 611A, 611B and 611N) in the Division of Nephrology at the University of Alabama at Birmingham.

Patented therapeutic strategies in accelerated development

1)    The use of sialic acid precursors in the treatment of glomerular disease and nephrotic syndrome. U. S. patent and PCT have been filed. We welcome communication from parties interested in the licensing or commercialization of this patent.

2)    The use of recombinant Angiopoietin-like-4 and its mutants in the treatment of proteinuria, glomerular disease and nephrotic syndrome. A PCT have been filed. We welcome communication from parties interested in the licensing or commercialization of this patent.

Key recent publications

1. Chugh SS and Clement LC. Telomerase at the center of collapsing glomerulopathy. Nat Med 2012:18:26-27.
2. Chugh SS, Clement LC, Macé C. New insights into human minimal change disease: Lessons from animal models. Am J Kid Dis 2012;59:284-292. Published online October 4, 2011.
3. Avila-Casado C, Fortoul TI, Chugh SS. HIV-associated nephropathy: experimental models. Contrib Nephrol 2011;169:270-285.
4. Clement LC, Avila-Casado C, Macé C, Soria E, Bakker WW, Kersten S and Chugh SS. Podocyte – secreted Angiopoietin-like-4 mediates proteinuria in glucocorticoid-sensitive nephrotic syndrome. Nat Med. 2011;17: 117-122. published online Dec 12 2010. PMID: 21151138
5. Clement L, Liu G, Perez-Torres I, Kanwar YS, Avila-Casado C and Chugh SS. Early changes in gene expression that influence the course of primary glomerular disease.Kidney Int. 2007;72:337-347. PMID: 17457373
6. Liu G, Clement L, Kanwar YS, Avila-Casado C and Chugh SS. ZHX proteins regulate podocyte gene expression during the development of nephrotic syndrome. J Biol Chem 2006, 281;39681-39692. PMID: 17056598
7. Liu G, Kaw B, Kurfis J, Rahmanuddin S, Kanwar YS and Chugh SS. Neph1 and nephrin interaction in the slit diaphragm is an important determinant of glomerular permeability. J Clin Invest 2003;112:209-221. PMID: 12865409

Funding: NIH / NIDDK

Contact information: Sumant S. Chugh MD, Principal Investigator, Glomerular Disease Therapeutics Laboratory, UAB Division of Nephrology, THT 611L, 1900 University Blvd, Birmingham AL 35294. Email  This email address is being protected from spambots. You need JavaScript enabled to view it. . Phone (205)996-9641. Fax (205)996-9675.

Members

• Sumant S. Chugh MD, Professor of Medicine, Principal Investigator
• Lionel C. Clément PhD, Assistant Professor of Medicine, Investigator
• Camille E. A. Macé PhD, Postdoctoral Fellow
• Caroline Marshall MD, Assistant Professor of Medicine, Investigator
• Mariá Del Nogal Avila, Ph.D., Postdoctoral Fellow