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Meryl A. Waldman, M.D.

Photo of Meryl Waldman
Senior Research Physician: Kidney Disease Section, Kidney Diseases Branch
Scientific Focus Areas: Immunology, Clinical Research

Professional Experience

  • Senior Research Physician NIDDK, NIH, 2020-present
  • Chief, Clinical Nephrology Consult Service, 2020-present
  • Director, Dialysis, 2020-present
  • NIDDK Clinical Director's Award, 2020
  • Associate Research Physician, NIDDK, NIH, 2018-2020
  • Staff Clinician, NIDDK, NIH, 2006-present
  • Clinical Instructor, Columbia University, New York Presbyterian Hospital, Glomerular Disease Institute, 2005-2006
  • Nephrology Fellowship, Hospital of the University of Pennsylvania, 2001-2005
  • Internal medicine-Pediatrics Combined Residency, Baystate Medical Center, 1997-2001
  • M.D., Tufts University School of Medicine, 1997

Current Research

The focus of my research is the natural history, pathogenesis, and treatment of immunologically mediated glomerular diseases particularly  membranous nephropathy. The goal of my research is to find novel ways to suppress autoimmune responses that lead to kidney disease as well as to find more sensitive methods to monitor disease activity.

Select Publications

Lupus-like autoimmunity and increased interferon response in patients with STAT3-deficient hyper-IgE syndrome.
Goel RR, Nakabo S, Dizon BLP, Urban A, Waldman M, Howard L, Darnell D, Buhaya M, Carmona-Rivera C, Hasni S, Kaplan MJ, Freeman AF, Gupta S.
J Allergy Clin Immunol (2020 Aug 5) Abstract/Full Text
Type I interferon signature predicts response to JAK inhibition in haploinsufficiency of A20.
Schwartz DM, Blackstone SA, Sampaio-Moura N, Rosenzweig S, Burma AM, Stone D, Hoffmann P, Jones A, Romeo T, Barron KS, Waldman MA, Aksentijevich I, Kastner DL, Milner JD, Ombrello AK.
Ann Rheum Dis (2020 Mar) 79:429-431. Abstract/Full Text
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Research in Plain Language

I study new combinations of agents that reduce the activity of the immune system to treat individuals with immune-mediated kidney disease in which  kidney cells are damaged by immune responses or inflammation.