Conference Series


  • Improving Global Kidney Health: The ISN initiatives and Global Kidney Health Atlas

    Pr. A. Levin - Professor of Medicine, University of British Columbia

    Head Division of nephrology Executive director BC Provincial Renal Agency Immediate Past President International Society of Nephrology (2015-2017) Dr Levin’s interests in early CKD, co-morbidities, and biological systems, health systems, organizational structure, and clinical research have led her to have a diverse career in nephrology. She has mentored numerous students, residents and junior faculty, locally, nationally and internationally, and has co-lead a number of unique initiatives including early pan Canadian cohort studies in CKD, a curriculum targeted at cultivating translational kidney scientists, and most recently, is co Principal investigator of a $40million grant, for CAN SOLVE CKD, a pan Canadian network grant focused on Patient Oriented Research initiatives. She has received numerous awards for teaching and research over the years, including the Kidney Foundation Medal for Research Excellence in 2014, and the Martin Hoffman Research Excellence at UBC, in 2017. She was recognized for the totality of her efforts in improving the lives of people living with kidney disease in Canada, in 2015, with the Order of Canada (CM). Improving Global Kidney Health: The ISN initiatives and Global Kidney Health Atlas The ISN is committed to improving the health of people living with and at risk for kidney disease around the world. There are multiple activities, initiatives and programs to support the vision and mission of ISN. The importance of a robust measurement tool, which helps the renal community and the health community at large, appreciate the impact of all activities, cannot be overstated. The first ever attempt to capture the current state of Global Kidney Health, in accordance with the 6 components of Universal Health Care coverage, culminated in the Global Kidney Health Atlas (GKHA) published in April 2017. This document and the work it represents, serves as an excellent roadmap for countries and regions to address issues relating to access to care, gaps in participation in and application of research findings and ensures that data is available to facilitate advocacy campaigns. The talk will focus on the issues facing the global community, key findings in the Atlas, and stimulate discussion.
    Kidney Stones
  • UDP-glucose as a diagnostic for Acute Kidney Injury: how basic research led us into the clinic

    Pr. D. Brown - Professor of Medicine at Harvard Medical School

    Director of Program in Membrane Biology at the Massachusetts General Hospital (MGH). He received his Ph. D. from the University of East Anglia, Norwich, UK, and then spent 10 years working at the University of Geneva Medical School in Switzerland, before moving to MGH in 1986. Dennis Brown is an internationally recognized authority on membrane protein trafficking in epithelial cells, with special focus on water channels (aquaporins). His work is aimed at understanding basic cell physiology in order to develop novel therapeutic strategies for kidney disease. He has published over 370 articles in peer reviewed journals. He was Editor-in-Chief of the American Journal of Physiology (Cell Physiology) until July 2008, and is currently the Editor-in-Chief of Physiological Reviews, which has an impact factor of 30, and is one of the World’s most highly cited scientific journals. After serving on its National Council for three years, he is now the President of the American Physiological Society (APS), since April 2017. He has received numerous awards including the Carl Gottschalk Award for excellence in nephrology research from the APS Renal Section in 1999, the Robert Schrier endowed lectureship at the 2008 American Society of Nephrology meeting, the Hugh Davson Award for excellence in cell biology research from the APS Cell Section in 2011, and the prestigious Robert Pitts Lecture in Renal Physiology at the 2013 meeting of the International Union of Physiological Sciences in Birmingham, UK. In July 2013 he was awarded an honorary Doctor of Sciences degree by his alma mater, the University of East Anglia (UK) for his outstanding contributions to cell biology and physiology. He is the Director of the MGH Office for Research Career Development (ORCD) and has a long track record of developing young scientists, both basic researchers and clinical investigators. He was awarded the prestigious A. Clifford Barger “Excellence in Mentoring” award from Harvard University in 2005 and received the HMS Dean’s Award for the Advancement of Women in Science in 2012. He has obtained continuous support from the NIH since arriving in the USA in 1986, and one of his current grants received rare «MERIT» Award status (10 years of support) in 2008. Finally, Dr. Brown has served on numerous NIH study sections and was the chair of the NIH KMBD (Kidney Molecular Biology and Development) grant reviewing Study Section for 3 years from June 2010 until June 2013. UDP-glucose as a diagnostic for acute kidney injury (AKI): how basic research led us to the clinic This is the story of how basic research on kidney function led to an unexpected discovery that has the potential to not only diagnose, but also lead to a potential therapy for acute kidney injury (AKI). One third of intensive care unit (ICU) patients will develop AKI – around 300,000 die each year in the USA alone, more than from diabetes, breast cancer, prostate cancer and heart failure combined. AKI is also a causal factor in longer term chronic kidney disease (CKD), often requiring dialysis or transplantation. Among the major causes of AKI are cardiac surgery, sepsis, reduction of renal blood flow (ischemia), and dehydration – which is of special importance to this audience. Remarkably, AKI causes no symptoms during its early stages, and more than 50% of kidney function has already been lost before it can be diagnosed using current tests. Consequently, AKI is often referred to as “the silent killer”. We have recently identified a marker that detects AKI within a few hours of onset, rather than 2-3 days later when it may be too late to intervene to prevent the inexorable loss of kidney function. How did we find this marker? We are interested in defining the role of different cell types in the kidney. Some of these cells (intercalated cells) are involved in acid/base balance in the body. While examining these acid-regulating cells, we noticed that they express large amounts of a membrane protein called P2Y14, a member of the family of the purinergic receptor family. We could not ignore this protein (it was so abundant), and we learned that it is a receptor for a molecule called UDP-glucose (UDP-G). It turns out that damaged cells, in the kidney or elsewhere in the body including the heart, release UDP-G, which builds up in the kidney, where it interacts with P2Y14 on intercalated cells. This interaction causes these cells to release cytokines, molecules which attract inflammatory cells, thus provoking an inflammatory response. This is an early and important step in the onset of AKI. Thus, our finding provides a link between remote tissue damage (e.g., during surgery) and subsequent kidney injury, caused by UDP-G release and its interaction with the P2Y14 receptor in kidney intercalated cells. Based on this, we suspected that because UDP-G is released into the blood by damaged tissues and is filtered into the urine, it might be a sensitive marker for AKI. By following ICU patients, we demonstrated in a pilot study that UDP-G in patient urine reliably predicts AKI up to 48 hours before the standard test (serum creatinine). It outperforms other AKI biomarkers in its ability to selectively and specifically detect AKI. This would give physicians around 48 h advanced warning of AKI, allowing them to take early steps to prevent further damage. Importantly, we also have a compound in hand called PPTN, which blocks the interaction between UDP-G and its P2Y14 receptor. This represents a new potential therapeutic avenue for AKI. Thus, we believe that UDP-G is an actionable marker, and that targeting the UDP-G/P2Y14 pathway represents a very promising therapeutic approach for the prevention/mitigation of AKI in critically ill patients.
    Kidney Stones
  • Hydration For Kidney Health Initiative update

    Pr. L. Moist - Nephrologist, Professor of Medicine and Epidemiology and Biostatistics.

    Associate Chair of the Division of Nephrology and Scientist in the Program of Experimental Medicine at Western University, London, Canada. Her clinical and research interests are focused on: the prevention of chronic kidney disease, with a special interest in hydration; and dialysis, with expertise in the vascular access for hemodialysis. Dr. Moist has had a number of leadership roles including The Ontario Renal Network Physician Lead for Dialysis Access, the Internal Medicine Physician Lead for the SW Local Health Integrated Network, and Chair of the ISN-H4KH Research Initiative. Dr. Moist is a recognized educator, clinician and researcher with multiple achievement awards, research grants and over 130 peer reviewed academic papers. Hydration For Kidney Health Initiative update Danone Nutricia Research and the ISN have collaborated to create the HYDRATION for KIDNEY HEALTH (H4KH) Research Initiative to stimulate interest of both established and new researchers to explore the role of hydration in kidney health. This need for science and evidence is driven by the recognition of detrimental effects of dehydration, heat and environmental factors on kidney function. The objectives of the H4KH Research Initiative are to: enhance awareness and level of scientific evidence of the effects of hydration on kidney health; expand research capacity by supporting investigators focusing on prevention of chronic kidney disease; engage researchers in the development of trans-disciplinary research networks and to create sustainable momentum in supporting research in this field of study. Three research opportunities have been created to meet the above objectives. They include: The ISN-H4KH New Investigator Award, the H4KH Research Grant and the inaugural H4KH Fellowship Grant
    Kidney Stones
  • Plasma copeptin as predictor of Cardio-renal disease

    Dr. S. Enhörning - Post doc at the department of Clinical Sciences at Lund University

    Medical doctor at the department of Endocrinology at Skåne University Hospital in Lund, Sweden. Dr. Sofia Enhörning graduated from medical school at Lund University and obtained her Ph.D degree in Internal Medicine at Lund University. Her research has focused on genetical and epidemiological studies of the vasopressin system and its links to metabolic disease. She is currently focusing on experimental intervention studies, investigating the role of hydration on the vasopressin system and gluco-regulatory hormones, and on epidemiological studies, investigating the links between the vasopressin marker copeptin and renal disease. Furthermore, she is investigating genetic predisposition for altered copeptin levels and will use a Mendelian Randomization approach to study if elevated copeptin is causally related with renal and cardiometabolic disease. Dr. Enhörning has received the Scandinavian Society for the Study of Diabetes (SSSD) Young Investigation Award and the ”best clinical diabetes thesis of the year” award in 2012 from the Swedish Society for Diabetology. In 2016, she was awarded with the Hydration and Kidney Health Grant. Plasma copeptin as predictor of Cardio-renal disease Vasopressin (VP), also known as antidiuretic hormone, is a vasopressor and antidiuretic peptide commonly known as an important operator in the salt and water regulation of the body. We and other groups recently established a link between the VP system and several cardiometabolic risk factors. Elevated VP, measured as copeptin (the C-terminal cleavage product of the VP precursor), predicts development of type 2 diabetes and abdominal obesity, and is an independent risk factor for diabetic heart disease and premature mortality. We are currently investigating effects of increased hydration on copeptin, glycemia and gluco-regulatory hormones. Previous studies in humans and animals suggest a role for VP in renal function decline both in diabetes patients and in the general population. We are currently studying the link between copeptin and incident renal disease in large population based cohorts including the Malmö Diet and Cancer - Cardiovascular Cohort (n=5162) and the Malmö Preventive Project (n=5158). Copeptin is measured at baseline in the populations and disease is captured using nation-wide registers. Furthermore, we are planning a Mendelian Randomization study to test if VP (measured as copeptin) is causally related with renal and cardiometabolic disease. Susceptibility genes associated with altered copeptin levels will be identified using data from genome-wide association studies conducted in the Malmö Diet and Cancer - Cardiovascular Cohort, the Malmö Preventive Project, the FINRISK-97 cohort and the PREVEND cohort, followed by test of association with metabolic and cardiorenal disease in the DIAGRAM and CARDIOGRAM cohorts. Our previous and current data suggest that copeptin is an independent predictor of cardiometabolic and renal diseases which can be used to identify individuals that are at higher risk for developing diabetes, renal disease and its cardiovascular complications in order to offer early preventive strategies.
    Kidney Stones; Vasopressin


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