Handwriting Paul

Biography

Associate Professor of Nephrology Director, Chair and School of Specialization in Nephrology University Health Care San Raffaele Director, Strategic Research Program in the Area of ​​Nephrology San Raffale Scientific Institute Curriculum of studies: 1985 Degree in Medicine and Surgery (cum laude), University of Sassari 1989 Specialization in Cardiology, University of Sassari 1993 Ph.D. Physiology Hypertension (cum laude), University of Marland 2000 Specialization in Nephrology (cum laude ), University of Milan Academic curriculum and principal assignments 1990-1993 "Post Doctoral Research Fellow" Department of Physiology, School of Medicine, University of Maryland, Baltimore, Maryland, USA 1995-2007 Hospital Assistant at the Division of Nephrology, Dialysis and Hypertension Hospital San Raffaele Milano Outpatient Center Coordinator of HSR Venture Center Ready for service for dialysis service HSR dialysis 2002 Associate Professor of Nephrology 2003 to present Professor of Nephrology Specialization Schools of the State University of Milan and the University of Vita-Salute (Anesthesia and Resuscitation, Hematology, Endocrinology, Immunology, Medical Oncology and Urology). 2007 to date: Director of Strategic Research Project in Nephrology and Dialysis, University of San Raffaele Foundation, Milan 2007 to date: Director of the School of Specialization in Nephrology, Vita-Salute University San Raffaele Milano

Research Interest

I started my research activity at the University of Sassari by studying, with Prof. Nicola Glorioso, the role of ionic transporters (Na / K ATPase, Na / K transporter, Na / Li counterpart) in human arterial hypertension. In the early 1990s, a Na pump pump inhibitor, long considered a key factor in hypertension, Ouabaina Endogena (EO), in the laboratory coordinated by Prof. John Hamlyn of the University of Maryland in colluding with Upjohn Company. I started the Post Doctoral fellow at the laboratory of Prof. J. Hamlyn in 1990 working on the research field currently called "Ouabainomics" for the study of the EO. The results obtained have clarified both the role of ouabain in hypertension, both as taking Na has an effect on the circulating levels of EO in humans. After the Baltimore experience, I returned to the University of Sassari for a year and later I was invited to join the research team of Prof. Bianchi (1994) at San Raffaele Hospital in Milan. The group of Prof. Bianchi identified the Adducina gene (ADD1), which causes hypertension in 25-30% of all hypertensives. Studying the transition from hypertension to normotension, both in the animal model and in hypertensive patients, several hypertensive phases have been identified. In addition, much of my work has continued to focus on the relationship between EO circulating levels and kidney and cardiac complications. The results obtained have led us to be considered as an international benchmark in the study of the role of the EC in kidney and cardiovascular diseases. Our field of research is particularly aimed at studying the key factors of early phases of essential hypertension. For example, from one third to half of hypertensive patients there is an increase in circulating endogenous oubain. Numerous experimental and clinical evidence suggests that ADD1 and EO trigger activation of renal Na / K ATPase with increased Na resorption leading to hypertension, while in vascular cells causes vasoconstriction. On the contrary, In the late phases of hypertension, the genetic determinants that lead to progression of chronic kidney disease (CKD) to terminal endothelial insufficiency (ESRD) or ventricular hypertrophy and cardiovascular complications have been studied. Again, in extensive clinical trials, in collaboration with Prof. Jan Staessen, ADD1 and EO were among the major causes of hypertension cardiovascular complications such as CKD, ESRD and LVH. Our translactic medicine approach to pharmacogenomics has allowed us to identify genetic profiles that predict the antihypertensive response. For example, a specific inhibitor of the ADD1-EO mechanism causes a reduction in blood pressure in those patients carrying the specific genetic profile. This is the first example of personalized medicine in a complex illness such as hypertension. In the challenge of understanding genetic and humoral factors and the study of the genes networks involved in the development of organ damage we have embarked on new challenges involving acute renal failure, human tissue gene expression, always starting from our scientific background. Acknowledgments & Awards 1992 American Heart Association (Council of Hypertension). 1996 Italian-American Nephrology Society 2000 SIN Italian Society of Nephrology (top poster presentation) 2004 SIN Italian Society of Nephrology (5 top oral presentations). 2004 European Hypertension Specialist of the European Hypertension Society 2005 SIN Italian Society of Nephrology (top poster presentation) 2008 ERA / EDTA Congress (top oral presentation) 2008 13th International SHR Meeting (Invited Speaker) 2008 University of Maryland (Baltimore, USA), invited speaker at the Seminar "Link between salt and hypertension: role of Na + / CA ++ exchanger gene and endogenous ouabain in hypertensive patients" 2010 The Hebrew University of Jerusalem "Interactions of cardiac steroids and the Na +, K + -ATPase: molecular, physiological and pharmacological implications" Participation in scientific societies : Italian Society of Arterial Hypertension Italian Society of Experimental Biology Italian Society of Nephrology European Society of Hypertension (ESH) Member of the Editorial Board of the Italian Journal of Nephrology Member of the "Scientific Committee" of the ASL City of Milan (2001-2003). ERA-EDTA (European Dialysis and Transplant Association) Clinical Hypertension Specialist of European Society of Hypertension (Nomination 2004) American Society of Nephrology (ASN) International Hypertension Society (ISH)