Keynote and Named Lectures

WCN 2007 Opening Lecture and Keynote and Named Lectures, to be given by distinguished colleagues on a broad range of timely and hot topics within the field, will be simultaneously translated into Portuguese and Spanish.

Welcome and Opening Lecture
Saturday April 21
17:00 - 19:00

Richard P. Lifton, M.D., Ph.D.
Howard Hughes Medical Institute Investigator, Yale University School of Medicine, New Haven (USA)

Genes, Genomes and the Future of Nephrology
Virtually all renal diseases have a genetic component. Tools emerging from the human genome project have enabled the identification of these susceptibility genes. Success with this endeavor has the capacity to define the genes and pathways that underlie both rare and common diseases. Knowledge of the inherited contributions to disease has the potential to illuminate the environmental factors that contribute to disease as well. This new knowledge permits identification of inherited susceptibility in the preclinical phase and has the potential to identify key targets for new therapeutic intervention that will improve health.

The first phase of the human genetic revolution has identified a large number genes responsible for Mendelian traits in which typically rare mutations impart large effects on disease risk. These have included genes for high and low blood pressure and electrolyte abnormalities, genes for polycystic kidney disease, glomerular disease, and abnormalities of renal development. The identification of genes that contribute to common, complex diseases has proved more challenging. Nonetheless, with the completion of the human genome sequence, the comprehensive identification of common variations in DNA sequence and copy number, and the ability to rapidly re-sequence large segments of the genome, the opportunity to identify the contribution of both rare and common variants to common diseases is at hand, and one can anticipate continued great progress in the field over the next decade. Barriers to progress include the paucity of large, well-characterized cohorts for investigation and
difficulties in scientific culture that fail to adequately reward interdisciplinary collaboration. Overcoming these obstacles will allow determination of the inherited contributions to renal disease, markedly advance our understanding of disease biology, and result in improved approaches to diagnosis and therapy.

Donald Seldin Lecture
Sunday April 22, 2007
11:50 – 12:30

Kevin Davies, Ph.D.
Editor-in-Chief, Bio·IT World, Boston (USA)
Author, Cracking the Genome

Systems Biology and the Promise of Personalized Medicine
The recent completion of the Human Genome Project was a historic accomplishment in the annals of biomedical research. But as one commentator put it, the landmark was simply “halftime for genetics.”Transposing the fruits of the genome sequence into rational therapies for common disease and a new era of personalized medicine will depend upon advances in gene discovery, systems biology, information technology, and social policy.

New high-throughput technologies such as systems biology are key to revealing the internal machinations of cells in health and disease. Advances in genome sequencing and cataloguing global genetic variation, spurred by the International HapMap project, will revolutionize molecular diagnostics and personalized medicine. The growing use of in silico biology promises a similar impact on the process of drug development.

Drawing on examples in renal and vascular diseases, Kevin Davies will explore the changing face of biomedical research in the post-genomic era and illustrate how new technologies are paving the way towards an exciting new era of personalized medicine.

ISN Brenner-Dirks COMGAN Lecture
Monday April 23, 2007
11:50 – 12:30

Organ Donation and Allocation: The Global Problem

Luc Noël, M.D.
World Health Organization, Geneva (Switzerland)

The Role of the WHO

Francis L. Delmonico, M.D.
Harvard Medical School, Boston (USA)

The Role of the Transplantation Society
The burden and opportunity for successful kidney transplantation is now regularly placed upon the willingness of a well human being to donate. The widespread acceptance of live organ transplantation is clearly counter to what historically had been a medical dictum to do no harm. The WHO and the Transplantation Society are aligned in their efforts to enhance the care of live kidney donors and kidney transplant recipients around the world.

The guiding principles on organ and tissue transplantation developed by the WHO will be presented. Guidelines pertaining to the medical suitability of the live kidney donor (hypertension, diabetes etc.) developed by The Transplantation Society will also be covered. Measures to improve the outcomes of kidney transplant recipients worldwide by the following basic medical issues will be discussed: cardiovascular disease; cancer and infection; anemia, bone disease, reproductive issues, growth and development; graft maintenance and the relevance of the GFR in the care of the transplant recipient.

Joint Keynote Lecture
Tuesday April 24, 2007
11:00 – 11:45

Giuseppe Remuzzi, M.D., FRCP
Mario Negri Institute for Pharmacological Research, Bergamo (Italy)

Preventing Disease Progression and Nephropathy of Diabetes: Feasible Strategies to Limit the Need of Dialysis
The number of patients with chronic renal disease is increasing worldwide. Most chronic nephropathies lack a specific treatment and progress relentlessly toward ESRD. In the last two decades an enormous wealth of information has been gathered from animal and human studies that have shed light on the mechanisms of progression and indicated the means of prevention.

The concept of renoprotection has emerged and is already growing into a combined approach to renal diseases. Pharmacological control of blood pressure and reduction of proteinuria have proven to be the most important measures to arrest progression. A multimodal protocol is emerging as the modern management for renal patients, which includes combination of several antihypertensive drugs lowering lipids, smoking cessation, tight glucose control for diabetics. A number of new compounds are under evaluation in animal studies, and will hopefully soon form part of the treatment strategy.

With the available therapies, delay of dialysis initiation is an achievable goal today for many patients with chronic nephropathies, but it is only a limited result given that less dialysis is what is really needed. Remission of renal diseases and regression of renal structural damage of the kidney are the pre-requisite for such an objective: there are initial experimental and clinical data that suggest that this is possible.

Less dialysis (and maybe no more for some patients) remains an optimistic but not unfounded perspective for future years to come.

Joint Keynote Lecture
Tuesday April 24, 2007
11:45 – 12:30

Eberhard Ritz, Ph.D., M.D.
Nierenzentrum, Heidelberg (Germany)

Kidney Dysfunction and Cardiological Risk
The high coronary mortality of hemodialysed patients was recognized by Belding Scribner more than 30 years ago, but only recently has the dramatic increase in cardiovascular events in patients with even minor renal dysfunction, albuminuria/proteinuria and reduced GFR been recognized. The risk is particularly increased in patients with an acute ischemic event.

Although accelerated atherosclerosis has been proven in experimental animals and humans with renal dysfunction, the major causes of death, in addition to myocardial infarction, are sudden death and heart failure – in part explained by inappropriate cardiac hypertrophy, fibrosis, microvessel disease and impaired ischemia tolerance.

Several lines of evidence point to endothelial cell dysfunction as the major pathomechanism linking renal dysfunction and cardiovascular risk. Deplorably renal patients receive on average less intense risk factor management and less acute cardiological treatment than nonrenal patients, although observational studies strongly point to the high efficacy of interventions in renal patients.

Claude Amiel Lecture
Wednesday April 25, 2007
11:20 – 12:30

Gregg L. Semenza, Ph.D., M.D.
Professor of Pediatrics, the Institute of Genetic Medicine, Johns Hopkins University School of Medicine
Baltimore, Maryland (USA)

The Role of Hypoxia-Inducible Factor 1 in Erythropoietin Production, Ischemic Protection, and Clear Cell Renal Carcinoma

Delivery of O2 to cells is regulated by multiple homeostatic mechanisms, which maintain a balance between O2 supply and demand. Hypoxia-inducible factor 1 (HIF-1) is a transcription factor that functions as a master regulator of O2 homeostasis. HIF-1 controls the expression of genes whose protein products promote O2 delivery through the control of erythropoiesis and vascularization. HIF-1 also controls the expression of genes that allow cells to survive O2 deprivation, either by inhibiting hypoxia-induced apoptosis or by mediating anaerobic ATP production via glycolysis.

In the clear cell type of renal cell carcinoma, loss of function of the von Hippel-Lindau tumor suppressor protein results in dysregulated HIF-1 activity that contributes to tumor angiogenesis, glycolysis, autocrine growth factor signaling, and invasion/metastasis. Strategies designed to inhibit or activate HIF-1 may lead to novel therapies for cancer and ischemic cardiovascular disease, respectively, which are the major causes of mortality in industrialized societies.

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