Salant is Professor of Medicine and Vice-Chair for Research. He received his medical degree from University of the Witwatersrand in South Africa and completed his clinical training at Johannesburg General Hospital. He received his research training at Boston University with Dr. William G. Couser and joined BU’s nephrology faculty in 1979. Dr. Salant is an internationally renowned physician-scientist and an acclaimed educator. His research primarily explores the immune basis for glomerular diseases and the mechanisms of podocyte injury. He was among the first to identify podocytes as the primary target of injury in antibody-mediated glomerular diseases. In a landmark New England Journal of Medicine paper in 2009, Drs. Salant, Beck and colleagues described their discovery of the target antigen in membranous nephropathy and showed that a high proportion of MN patients have circulating autoantibodies to the phospholipase A2 receptor on human podocytes. Dr. Salant is a past chairman of the ABIM Sub-specialty Board of Examiners in Nephrology, and recipient of several national and international awards for his scientific contributions, including election to the American Society of Clinical Investigation and the Association of American Physicians, an Established Investigator Award from the American Heart Association, the John P. Peters Award from the American Society of Nephrology, the Jean Hamburger Award from the International Society of Nephrology, the Donald W. Seldin Award from the National Kidney Foundation, the Marilyn Farquhar Award at the 11th Annual Podocyte Conference and the Edward N. Gibbs Award and Lectureship from the New York Academy Sciences.
Experimental models of immunological glomerular diseases and autoimmunity resembling those seen in man are used to obtain a fundamental understanding of the immunopathogenetic mechanisms of injury.
Antibody-mediated podocyte injury:
The primary focus of the Salant laboratory is on the immune basis of glomerular diseases with particular regard to the humoral mechanisms of glomerular cell injury. Current work will elucidate the mechanisms by which antibodies alter the function and morphology of glomerular visceral epithelial cells (podocytes).
1. We have identified the target antigen in human membranous nephropathy as the phospholipase A2 receptor (PLA2R) and shown that about 75% of patients have circulating ant-PLA2R autoantibodies. Current work is directed at defining the mechanisms of podocyte injury induced by anti-PLA2R using a combination of in vitro, in vivo and human genetic techniques. Additional studies will explore the role of anti-PLA2R in the development of recurrent membranous nephropathy post renal transplantation.
2. Ongoing interests include the role of podocyte-specific antibodies, and the effects of complement-mediated injury on podocyte structure, composition of the filtration slit diaphragm and its attachment to the cytoskeleton, and on cell-matrix adhesion using animal models, cell biological and immunochemical methodologies.
Mechanisms of post-inflammatory renal fibrogenesis:
We have also developed a murine model of antibody-dependent rapidly progressive glomerulonephritis in which necrotizing and crescentic glomerulonephritis is associated with the activation of chemokine and interstitial-type collagen genes, followed by the development of interstitial fibrosis and renal failure. Since interstitial fibrosis and tubular atrophy are common to all forms of chronic progressive renal diseases and are the most reliable pathological indicators of an adverse long-term prognosis in humans, this mouse model in which the onset of immune injury is rapidly followed (within 5 days) by the induction and proliferation of interstitial cells expressing high levels of mRNA for type I collagen affords a unique opportunity to study the mechanisms of post-inflammatory renal fibrogenesis
- Professor, Nephrology, Medicine, Boston University School of Medicine
- Vice Chair, Research Implementation, Medicine, Boston University School of Medicine
- Member, Evans Center for Interdisciplinary Biomedical Research, Boston University
- Graduate Faculty (Primary Mentor of Grad Students), Boston University School of Medicine, Graduate Medical Sciences
- University of the Witwatersrand, MBBCh
- Published on 4/1/2020
Skopelja-Gardner S, Colonna L, Hermanson P, Sun X, Tanaka L, Tai J, Nguyen Y, Snyder JM, Alpers CE, Hudkins KL, Salant DJ, Peng Y, Elkon KB. Complement Deficiencies Result in Surrogate Pathways of Complement Activation in Novel Polygenic Lupus-like Models of Kidney Injury. J Immunol. 2020 May 15; 204(10):2627-2640. PMID: 32238460.
- Published on 3/24/2020
Pisarek-Horowitz A, Fan X, Kumar S, Rasouly HM, Sharma R, Chen H, Coser K, Bluette CT, Hirenallur-Shanthappa D, Anderson SR, Yang H, Beck LH, Bonegio RG, Henderson JM, Berasi SP, Salant DJ, Lu W. Loss of Roundabout Guidance Receptor 2 (Robo2) in Podocytes Protects Adult Mice from Glomerular Injury by Maintaining Podocyte Foot Process Structure. Am J Pathol. 2020 04; 190(4):799-816. PMID: 32220420.
- Published on 12/16/2019
Beck LH, Salant DJ. Refining Our Understanding of the PLA2R-Antibody Response in Primary Membranous Nephropathy: Looking Forward, Looking Back. J Am Soc Nephrol. 2020 Jan; 31(1):8-11. PMID: 31871252.
- Published on 7/24/2019
Salant DJ. Does Epitope Spreading Influence Responsiveness to Rituximab in PLA2R-Associated Membranous Nephropathy? Clin J Am Soc Nephrol. 2019 Aug 07; 14(8):1122-1124. PMID: 31340980.
- Published on 5/9/2019
Belghasem ME, A'amar O, Roth D, Walker J, Arinze N, Richards SM, Francis JM, Salant DJ, Chitalia VC, Bigio IJ. Towards minimally-invasive, quantitative assessment of chronic kidney disease using optical spectroscopy. Sci Rep. 2019 05 09; 9(1):7168. PMID: 31073168.
- Published on 1/1/2019
Salant DJ. Unmet challenges in membranous nephropathy. Curr Opin Nephrol Hypertens. 2019 01; 28(1):70-76. PMID: 30451735.
- Published on 12/3/2018
Kasinath V, Yilmam OA, Uehara M, Jiang L, Ordikhani F, Li X, Salant DJ, Abdi R. Activation of fibroblastic reticular cells in kidney lymph node during crescentic glomerulonephritis. Kidney Int. 2019 02; 95(2):310-320. PMID: 30522766.
- Published on 11/1/2018
Beck LH, Salant DJ. Deep pockets are not necessarily a good thing in membranous nephropathy: evidence for a modifier allele. Kidney Int. 2018 11; 94(5):855-857. PMID: 30348302.
- Published on 6/21/2018
Estrada CC, Paladugu P, Guo Y, Pace J, Revelo MP, Salant DJ, Shankland SJ, D'Agati VD, Mehrotra A, Cardona S, Bialkowska AB, Yang VW, He JC, Mallipattu SK. Krüppel-like factor 4 is a negative regulator of STAT3-induced glomerular epithelial cell proliferation. JCI Insight. 2018 06 21; 3(12). PMID: 29925693.
- Published on 5/23/2018
Caster DJ, Korte EA, Tan M, Barati MT, Tandon S, Creed TM, Salant DJ, Hata JL, Epstein PN, Huang H, Powell DW, McLeish KR. Neutrophil exocytosis induces podocyte cytoskeletal reorganization and proteinuria in experimental glomerulonephritis. Am J Physiol Renal Physiol. 2018 09 01; 315(3):F595-F606. PMID: 29790391.
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