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Glomerular Disease Workshop

Catherine M. Meyers^*, Mark Geanacopoulos^*, Lawrence B. Holzman and David J. Salant

^* Division of Kidney, Urologic and Hematologic Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, US Department of Health and Human Services, Bethesda, Maryland; Division of Nephrology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan; and Renal Section, Evans Biomedical Research Center, Boston University Medical Center, Boston, Massachusetts

Address correspondence to: Dr. Catherine M. Meyers, NIH/NIDDK, Two Democracy Plaza, 6707 Democracy Boulevard, Suite 641, Bethesda, MD 20892. Phone: 301-594-7717; Fax: 301-480-3510; E-mail: cm420i{at}nih.gov

Recent observations regarding intrinsic glomerular cell biology, particularly in the podocyte, have provided exciting new insights into potential pathogenic mechanisms of human glomerular disease. Although both immune and nonimmune mechanisms of glomerular injury have been studied previously, experimental models of disease and recent techniques that provide tools for molecular profiling show great promise for identifying glomerular disease biomarkers. Despite these recent advances, additional work in both basic and clinical studies of glomerular disease is needed to advance the field. Standardization of animal models of distinct forms of glomerular disease would likely facilitate the search for biomarkers. Several factors limit current efforts to implement clinical trials of glomerular disease. Identification of disease biomarkers, development of disease-specific end points, and organization of collaborative clinical groups are critical for ultimately designing and implementing appropriately powered trials of glomerular disease.

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673