Day 1 :
Medical Society Gailezers Ltd., Latvia
Time : 10:00-10:40
Vladimirs Strazdins graduated from Riga Medical Institute in 1977 (now called Riga Stradins University). He served for two years as an Army Medical Officer and started to work in University Hospital for Children in Riga in 1983. In 1992, he was appointed as Head of Nephrology at the same hospital and held this position till 2009. He is a member of European Pediatric Dialysis Working Group under ESPN from 2004 till 2012, with published European Guidelines on Pediatric Dialysis. He is recently retired, but still working part-time in Hemodialysis Unit at MS Gailezers and provides second-opinion to the consulting patients. He currently focuses on antimicrobial resistence issues and its implications on urinary tract infections.
Antimicrobial resistance is a growing problem worldwide. Urinary tract infection (UTI) is not an exception. Therefore, it is crucial to regularly update the bacterial flora spectrum data and the efficacy of the recommended empiric treatment to make timely and appropriate amendments wherever necessary. This observational study was conducted during July-November 2014, when family physicians across Latvia submitted the anonymous patient data on recurrent UTI treatment in their practice. Anonymous patients’ electronic data files were received, 113 of those met the inclusion criteria and were further analyzed. Bacterial flora spectrum in Latvian adult recurrent UTI population was fairly consistent with data from other European countries, with Escherichia coli identified in 66 (58.41%) cultures, of those as monoculture in 55 (58,51%) and as combined culture in 11 (11.70%) cases. Combined cultures without Escherichia coli were obtained in 28 (29.79%) cases. Sensitivity against nitrofuran derivates (NFDs) was present in 88 cases (91.49% of total cultures), Escherichia coli resistance against NFDs was found in only 4 cases (6.06% of Escherichia coli cultures). The current first-choice empiric treatment of recurrent UTI by NFDs may stay unchanged. Particular NFD used in Latvia (Furamags®) is safe, well-tolerated and effective first-line UTI treatment choice.
Charité - Universitätsmedizin Berlin, Germany
Time : 10:40-11:20
Petra Reinke is Nephrologist and Clinical Scientist. Her scientific topics are: Transplantation medicine, development of new diagnostic and therapeutic approaches in transplantation. She is Project Coordinator for the EU founded FP7 consortium “BIO-DrIM”, was Steering Committee Member/Work-package Leader of the EU founded FP7 consortium “ONE- Study”, Steering Committee Member/Work-package Leader of the EU founded FP6 consortium “RISET”, Co-PI for a project founded by the Immune Tolerance Network, Co-Investigator ROTF grant. She is Head of the “Kidney Transplant Outpatient Clinic”; Head of research area “Immune System”, Head of the GMP-Facility, Steering Committee Member of the Berlin-Brandenburg Center for Regenerative Therapies, of the DFG-sponsored Berlin-Brandenburg School for Regenerative Therapies, of the Berlin Institute of Health (BIH) Stem Cell Center. She published more than 300 articles.
The intensity and long-term requirement for immunosuppression to prevent allograft rejection pre-disposes solid organ transplant (SOT) recipients to a wide range of viral complications, particularly within the first year of transplant. The agents administered post-transplant to prevent organ rejection compromise the host immune system leaving patients vulnerable to an array of latent and lytic viruses including cytomegalovirus (CMV), adenovirus (AdV), Epstein-Barr virus (EBV), human herpes virus 6 (HHV6) and BK virus. Many of the viruses account for a spectrum of clinical diseases in SOT recipients including allograft dysfunction. As a result, viral infection or reactivation is a frequent cause of morbidity and mortality in immunocompromised SOT recipients. Adoptive T-cell therapy using virus-specific T-cells (VST) has emerged as an effective treatment option in viral diseases after SOT and hematopoietic stem cell transplantation (HSCT). Despite vast success of anti-viral T-cell therapeutic approaches following HSCT, T-cell engraftment and longevity of the efficacy is incidentally limited in chronically immunocompromised SOT patients due to insufficient persistence of T-cells after infusion and reduced proliferation. Successful anti-viral T-cell immunotherapy depends on a range of cell and patient-dependent factors. In my presentation, I will describe challenges and limitations for VST production in the SOT setting, the innovations that allowed the production of anti-viral T-cell products, including an optimized T-cell subset composition of the VST infused, genetically modified VST, third-party VST and multi-virus-specific T-cell products, and I will discuss the potential and first clinical data for this approach.
New York Institute of Technology, USA
Time : 11:40-12:20
Alex Vasilyev received his PhD and MD degrees from Rosalind Franklin University of Medicine and Science. He then completed his residency training in Anatimic Pathology at the Massachusetts General Hospital and a Research Fellowship in Renal Pathology. He became an Instructor in Pathology at the Massachusetts General Hospital/Harvard Medical School, and later, he started as an Assistant Professor in Biomedical Sciences at the New York Institute of Technology, College of Osteopathic Medicine. He studies kidney development, regeneration and pathophysiology using zebrafish as a model.
Studies of kidney development and repair after injury are difficult in mammals due to complex architecture of metanephric kidney and the inherent difficulty of in vivo imaging in mammals. Transparent zebrafish larvae have simple pronephric kidneys that closely resembles mammalian nephron in segment identity and arrangement. This vertebrate model allows direct in vivo visualization of kidney development and repair after injury. We developed a novel assay of Acute Kidney Injury (AKI) in GFP transgenic zebrafish larvae using violet laser ablation. This technique allows us to directly visualize the sub-cellular, cellular and organ-level interactions driving kidney injury and repair. For example, by using this technique, we showed that collective cell migration is the primary repair mechanism after AKI. It had been recently proposed that rapid cyst induction in conditional mouse models of ADPKD requires a “third hit”, and that AKI serves this role. The suggested interpretation of the interaction between AKI and cyst formation is that injury induces proliferative response in kidney epithelia, thus promoting cyst progression. By utilizing our novel zebrafish model of AKI we show that kidney obstruction and not increased cell proliferation is the driving force leading to rapid cyst initiation after injury. We also show that PKD2 mutant zebrafish demonstrate slower resolutuon of transient cysts after acute injury when compared to control siblings. This findings shed new light on the nature of the “third hit” suggested by inducible mouse models of ADPKD.