Thangamani Muthukumar, MD
Photo: Thangamani Muthukumar

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Elected 2017

I am an Associate Professor of Nephrology and a Transplant Physician at the Weill Cornell Medical College - New York Presbyterian Hospital. I received my MBBS from the Madras Medical College, Chennai, India; MD (Internal Medicine) from the Stanley Medical College, Chennai, India; and DM (Nephrology) from the Post Graduate Institute of Medical Education and Research, Chandigarh, India. I was a research fellow in the laboratory of Dr. Suthanthiran, Chief of Nephrology and Transplantation at the Weill Cornell Medical College and completed my residency in Internal Medicine and Fellowship in Nephrology from the New York Presbyterian Hospital- Cornell.

My research is focused on allograft rejection and tubulointerstitial fibrosis in the kidney allografts. My research efforts at Cornell have identified the following for the first time: (1) acute rejection of human renal allografts is associated not only with overexpression of cytolytic molecule granzyme B but also with its natural antagonist proteinase inhibitor-9; (2) urinary cell levels of mRNA for FoxP3 are an independent predictor of renal allograft rejection reversal and graft loss following an episode of acute rejection; and (3) fibrosis of the kidney allograft can be accurately and noninvasively diagnosed by the expression profile of a select panel of genes in the urinary cells. In an on-going collaboration with the Tuschl laboratory at Rockefeller University, I have characterized for the first time the microRNA transcriptome of human kidney allografts with or without fibrosis. Recently, I have developed urinary cell mRNA profiles to accurately and noninvasively distinguish different causes of kidney allograft dysfunction. My translational studies have helped develop a prognostic index for allograft outcome in kidney recipients with transplant glomerulopathy, an important cause of late allograft failure. Currently, I am applying RNA sequencing to further resolve mechanisms of rejection including microvascular inflammation, tubulointerstitial fibrosis and kidney allograft functional decline.