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Lenox Hill Hospital, USA
Michelis has been Director of the Division of Nephrology at Lenox Hill Hospital for more than three decades. He is Clinical Professor of Medicine at the New York University School of Medicine. Dr. Michelis received a B.A. at Columbia College, Columbia University in New York City, and his M.D. degree at George Washington School of Medicine in Washington, D.C. He received his nephrology training at the University of Pittsburgh School of Medicine. Dr. Michelis has been selected for inclusion in the listing of top doctors in New York for the past several years. He is the co-Editor of several medical textbooks, and he has published dozens of articles in the area of general nephrology, electrolyte disorders, hypertension, and geriatric renal disease. He has lectured extensively throughout the United States, Hawaii, Japan, and in various European cities. He has served on the editorial board of several medical journals, and he also reviews articles for established journals in nephrology. He has received many awards and lectureships for his work in nephrology.
A variety of therapeutic interventions are available to alter the abnormalities seen in patients with chronic kidney disease (CKD). Programs can now be developed to slow the progression of CKD. This delay can be achieved by using accepted recommendations for optimal diabetes therapy (HbA1c target 7%), goals for blood pressure levels, reduction of proteinuria and the proper use of ACE/ARB therapies. For example, limits on dietary sodium and protein intake and reduction of body weight will be decrease proteinuria. Proper treatment for elevated serum phosphorus and parathyroid hormone levels as well as therapy for dyslipidemias and anemia can mitigate renal loss. Other less widely appreciated measurable abnormalities such as elevated FGF-23 levels, hyperuricemia and metabolic acidosis have more recently been recognized to be associated with progressive renal insufficiency. Efforts aimed at correction of these disorders may have an important role in altering the course of renal dysfunction. Data will be presented to support this strategy.
Washington University School of Medicine, USA
Zinselmeyer’s scientific education is broad and interdisciplinary. Earning his PhD in pharmaceutical science (University of Strathclyde 2006) has inspired him to focus on translational science, with an emphasis on research that has relevance to clinical medicine. The main focus of his work over the past 10 years has been intravital-multi-photon-imaging of cells of the immune system and the CNS. He was part in the team using these technique for the first time observing leucocyte dynamics in transplanted lungs in living mice and the beating heart. Dr. Zinselmeyer authored over 40 peer-reviewed articles cited over 2000 times
The combination of murine transplantation models, fluorescent reporter mice and intravital 2-photon microscopy enables an unprecedented view on the initiation of transplant rejection. In murine allogeneic models of lung transplantation we could observe the innate arm of the immune-system of the host. Minutes after transplantation neutrophils of the host regularly aggregated in dynamic clusters that formed and dispersed in the allogeneic transplant. These clusters were associated with CD115+ F4/80+ Ly6C+ host cells that had immediately entered the lung. Observing the adaptive arm of the immune system we could explain why allogenic lungs can be rejected in the absence of secondary lymphoid organs. Two-photon microscopy revealed that recipient T-cells are activated predominantly around lung-resident, donor-derived CD11c+ cells. These findings might be singular for the lung; however they demonstrate the value of intravital multiphoton imaging in the study of transplant rejection. Very recently we started using two-photon microscopy to study the three-dimensional structure of mouse podocytes in high temporal resolution in the present absence of inflammation. We found that healthy podocytes remained non-motile and maintained a canopy-shaped structure over time. On expression of constitutively active Rac1 or after induction of nephrotoxic nephritis podocytes changed shape by retracting processes and clearly exhibited domains of increased membrane activity. Furthermore, drastic activation of Rac1 also led to podocyte detachment from the glomerular basement membrane, and we observed detached podocytes crawling on the surface of the tubular epithelium and occasionally, in contact with peritubular capillaries. These findings potentially explaining the extinction of foot-process in a wide range of severe kidney-disease.