Leon Fine, MD

Vice Dean of Research and Research Graduate Education

Chair, Biomedical Sciences

Email:leon.fine@cshs.org
Phone:(310) 423-4691
Fax:(310) 423-0225

Academic Appointments

Professor, Biomedical Sciences
Professor, Medicine

Awards and Activities

Director (non-excutive), National Insitute of Clinical Excellence2002
Founding Fellow, Academy of Medical Sciences, UK1999
President, Association of Physicians of Great Britain and Ireland1993
Editor-in-Chief: Nephron JournalsCurrent
Editor-in-Chief: Experimental Nehrology1993 - 2002
American Society for Clinical Investigation1982
Association of American Physicians1998
Academy of Medical Sciences, UK1999

Research Focus

Principal research interest is in the biology of chronic renal disease and has made important contributions to the understanding of adaptations of ion transport in the diseased nephron, renal hypertrophy, and the cell biology of fibrogenesis and scarring of the kidney.

Contributions to the history of medicine and renal diseases

Research Contributions

Defined intrinsic transport adaptations in tubular function in the chronically-diseased kidney.
Defined molecular events in renal tubular cell hypertrophy
Proposed and demonstrated that chronic hypoxia is a mechanism of progression in chronic renal diseases

Current investigations include:

Analysis of hypoxia-mediated organ fibrosis

Selected Publications

  1. Norman JT, Fine LG: Intrarenal oxygenation in chronic renal failure. Clin. Exp. Pharmacol. Physiol., 33(10): 989-96, 2006
  2. Fine LG, Orphanides C, Norman JT: Progressive renal disease: the chronic hypoxia hypothesis. Kidney Int. Suppl., 65: S74-8, 1998
  3. Kitamura M, Taylor S, Unwin R, Burton S, Shimizu F, Fine LG: Gene transfer into the rat renal glomerulus via a mesangial cell vector: site-specific delivery, in situ amplification, and sustained expression of an exogenous gene in vivo. J. Clin. Invest., 94(2): 497-505, 1994
  4. Fine LG, Badie-Dezfooly B, Lowe AG, Hamzeh A, Wells J, Salehmoghaddam S: Stimulation of Na+/H+ antiport is an early event in hypertrophy of renal proximal tubular cells. Proc. Natl. Acad. Sci. U.S.A., 82(6): 1736-40, 1985
  5. Fine LG, Holley RW, Nasri H, Badie-Dezfooly B: BSC-1 growth inhibitor transforms a mitogenic stimulus into a hypertrophic stimulus for renal proximal tubular cells: relationship to Na+/H+ antiport activity. Proc. Natl. Acad. Sci. U.S.A., 82(18): 6163-6, 1985
  6. Fine LG, Schlondorff D, Trizna W, Gilbert RM, Bricker NS: Functional profile of the isolated uremic nephron. Impaired water permeability and adenylate cyclase responsiveness of the cortical collecting tubule to vasopressin. J. Clin. Invest., 61(6): 1519-27, 1978
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