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Samir M. Parikh, MD

Instructor of Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School

330 Brookline Avenue, RN-280C
Boston, MA 02215

Office: 617-667-5813
Fax: 617-667-2646
Email: sparikh1@bidmc.harvard.edu

Parikh Lab >>

Education/Training/Appointments

Samir Parikh graduated magna cum laude from Harvard in 1997 with a degree in chemistry and received the valedictory award from Vanderbilt University School of Medicine in 2001. He completed post-graduate medical training at Beth Israel Deaconess Medical Center and Harvard Medical School, including a research fellowship with Vikas Sukhatme. Dr. Parikh joined the faculty of both institutions in 2006. He serves as a staff physician in the Division of Nephrology at Beth Israel Deaconess Medical Center and as a principal investigator with joint affiliations in the Division of Nephrology and the Center for Vascular Biology Research.

Research Interests

Vascular Dysfunction in Sepsis

Basic Research

The first major area of study is the dysregulation of circulation during sepsis. Sepsis is a common, deadly syndrome that arises from disseminated infection. Derangements in the circulatory system during sepsis lead to shock and multi-organ dysfunction, the most common causes of death from sepsis. Through work from our group and others, the endothelium has become increasingly recognized as a target cell that mediates several of the circulatory changes in sepsis. The angiopoietin/Tie-2 system appears to play a major role in the regulation of vascular permeability, acute lung injury, endothelial inflammation, and regulation vascular tone, making it a prime candidate for the development of new diagnostic and therapeutic tools for sepsis.

The second area of focus is sepsis-induced acute kidney injury. Among its other tasks, the kidney is responsible for the filtration of waste products from the blood; rapid shutdown of this filtration function affects up to one-third of individuals with sepsis. The combination of sepsis and acute kidney injury is associated with a mortality of 50-80%. Despite this, its pathogenesis is poorly understood. We are interested in determining the ischemic and inflammatory factors that render the kidney uniquely vulnerable during sepsis.

Translational Research

Dr. Parikh's laboratory investigates molecular mechanisms in the biology of critical illness. Individuals admitted to intensive care units develop poorly understood complications that affect the circulatory system, lungs, kidneys, and other organs, often with devastating consequences. We are using an array of complementary approaches to advances our understanding of these disorders.

Clinical Research

Our laboratory is performing human subject-based studies to evaluate the diagnostic and prognostic value of measuring soluble proteins that signal the endothelium in sepsis. We are also interested in discovering novel biomarkers of acute kidney injury.

New and Noteworthy Publications

View all publications via PubMed >>

  1. Parikh SM, Mammoto T, Schultz A, Yuan HT, Christiani D, Karumanchi SA, Sukhatme VP (2006). Excess circulating angiopoietin-2 may contribute to pulmonary vascular leak in sepsis in humans. PLoS Med, 3(3):e46-60. This study was the first to describe elevations of circulating angiopoietin-2 in septic human subjects; it was the first to correlate angiopoietin-2 levels with degree of lung injury in sepsis; and it was the first to demonstrate that systemic angiopoietin-2 excess is sufficient to cause pulmonary vascular leak in rodents.

  2. Mammoto T, Parikh SM, Mammoto A, Gallagher D, Chan B, Mostoslavsky G, Ingber DE, Sukhatme VP (2007). Angiopoietin-1 requires p190 RhoGAP to protect against vascular leakage in vivo. J Biol Chem, 282(33):23910-8. This study was the first to demonstrate that the protection against endotoxemic vascular leak conferred by angiopoietin-1 relies on the intra-endothelial cytoskeleton-regulatory protein p190RhoGAP. As such, it was also the first to link the microcirculatory barrier defense actions of angiopoietin-1 to its regulation of the endothelial cytoskeleton.

  3. Giuliano JS, Lahni PM, Harmon K, Wong HR, Doughty LA, Carcillo JA, Zingarelli B, Sukhatme VP, Parikh SM, Wheeler DS (2007). Admission angiopoietin levels in children with septic shock. Shock, 28(6):650-654. Pediatric septic shock is less well-studied than its adult counterpart. This study, for the first time, revealed that early elevations in circulating angiopoietin-2 correlated strongly with future survival in children admitted to ICUs.

  4. Gallagher DC, Bhatt RS, Parikh SM, Patel P, Seery V, McDermott DF, Atkins MB, Sukhatme VP (2007). Angiopoietin 2 is a potential mediator of high-dose interleukin 2-induced vascular leak. Clin Cancer Res. 2007;13(7):2115-20. High-dose interleukin-2 is administered to patients as a form of immunotherapy to treat metastatic melanoma or renal cell carcinoma. Its dose-limiting toxicity, however, is vascular leak that had been linked to endothelial inflammation. This paper was the first to suggest that circulating angiopoietin-2, but not VEGF, may underlie the vascular leak syndrome that invariably arises in IL-2 recipients.

Contact Information

Nicole Magner, Administrative Assistant
Center for Vascular Biology Research
Beth Israel Deaconess Medical Center
Research North
99 Brookline Avenue
Boston, MA 02215
617-667-0654
info.cvbr@bidmc.harvard.edu