Scientific Program

Conference Series LLC Ltd invites all the participants across the globe to attend 3rd Annual Kidney Congress New York City, New York, USA.

Day 1 :

Keynote Forum

Michael F Michelis

Lenox Hill Hospital, USA

Keynote: Kidney: Nephrology and therapeutics

Time : 09:15-09:55

Kidney 2018 International Conference Keynote Speaker Michael F Michelis photo
Biography:

Michael F Michelis has been the Director of the Division of Nephrology at Lenox Hill Hospital for more than three decades. He is Professor of Medicine at the Zucker School of Medicine at Hofstra/Northwell. He received a BA at Columbia College, Columbia University in New York City, and his MD at George Washington School of Medicine in Washington, DC. He received his Nephrology Training at the University of Pittsburg, School of Medicine. He 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 diseases. 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.

Abstract:

Patients with the advanced renal disease have become more complicated and factors such as complex associated conditions, aging, increasing numbers of available pharmacologic agents and improvement in renal replacement therapies have made decision making more challenging. Subjects evaluated include proper approaches to blood pressure therapy in patients with pre, inter or intra dialysis blood pressure abnormalities. Medication characteristics outlined and the effects of various drugs as they relate to the dialysis procedure have been described. Also, metabolic issues such as approaches to hyperuricemia and metabolic acidosis have been reviewed and discussed. New agents and their benefits and limitations noted and present goals of therapy reviewed. Furthermore, the effects of increased body mass and glucose intolerance on survival, as well as possible corrective measures, elucidated. New approaches to glucose control and current blood pressure goals will be discussed. Finally, current approaches to renal replacement therapy will be reviewed and the importance of the timing of interventions and the choice of access and modality will receive consideration. These issues apply particularly to patients of advanced age. Factors influencing such decisions will be presented and critically evaluated.

Kidney 2018 International Conference Keynote Speaker John K Maesaka photo
Biography:

John K Maesaka was born in Hawaii, received degrees from Harvard College and Boston University School of Medicine, did his medical residencies at Barnes-Jewish Hospital at Washington University In St. Louis and Mount Sinai Hospital in New York and renal fellowship at Mount Sinai Hospital. His interest-driven decision to spend 5 years exclusively in the renal physiology laboratory at Mount Sinai Hospital as a renal fellow and member of the faculty proved to be the best investment he made to pursue an academic career in medicine. He was involved in developing colorimetric methods for the determination of uric acid and phosphorus in blood and urine that were applied to studying the transport characteristics of both electrolytes by renal micropuncture techniques in rat kidney. He developed several bioassays to demonstrate the presence of a natriuretic factor in the blood of patients with renal salt wasting and Alzheimer’s disease and more recently identified the elusive natriuretic factor after more than a 25-year pursuit.

 

Abstract:

Hyponatremia is the most common electrolyte abnormality that is undergoing dramatic changes in terms of its diagnostic approach and clinical outcomes. The approach for more than 50 years has been dominated mainly by the assessment of the volume status of the patient and determinations of urine sodium concentrations (UNa) that exceed 30 to 40mEq/L. This approach has been hampered by a universally agreed inability to accurately assess the volume status of patients by usual clinical criteria and perceived rarity of cerebral/renal salt wasting (C/RSW) among internists. Differentiating SIADH from C/RSW has been difficult because of identical clinical parameters that characterize both syndromes. We have accumulated enough data to identify the various causes of hyponatremia by determining fractional excretion of urate (FEurate) to propose an algorithm to approach hyponatremic conditions. In this algorithm, conditions with low FEurate <4% include extrarenal salt losses with normal kidney function, Addison’s disease, and edematous states such as heart failure, cirrhosis, and nephrosis.  Normal FEurate of 4-11% include psychogenic polydipsia and reset osmostat (RO), and increased FEurate > 11% SIADH/hydrochlorothiazide and C/RSW. SIADH can be differentiated from C/RSW by correcting the hyponatremia by any possible means and observing normalization of FEurate in SIADH as compared to being persistently increased in C/RSW. This algorithm greatly simplifies the diagnosis of patients with Addison’s disease and RO. Our report of C/RSW occurring in patients without cerebral disease has led to our proposal to change cerebral to renal salt wasting (RSW). We utilized this algorithm and differences in physiologic response to isotonic saline infusions between SIADH and RSW to evaluate hyponatremic patients from the general medical wards of the hospital.  Isotonic saline does not induce excretion of dilute urines or correct the hyponatremia in SIADH as compared to inducing excretion of dilute urines and correction of the hyponatremia in RSW. In 62 hyponatremic patients, 17 (27%) had SIADH, 19 (31%) had RO, 24 (38%) had RSW, 1 due to HCTZ and 1 Addison’s disease.  Interestingly, 21 of 24 with RSW had no evidence of cerebral disease and 10 of 24 with RSW had UNa <20mEqL. We conclude that 1. RSW is much more common than is perceived, 2. The term cerebral salt wasting should be changed to RSW 3. RO should be considered a separate entity from SIADH and 4. SIADH needs to be redefined. This new approach proves the ineffectiveness of the volume approach and the limited value of determining UNa, plasma renin, aldosterone or BNP. Lastly, we discuss the evolving identity of a natriuretic factor in RSW and its therapeutic applications.

 

Break: Networking and Refreshment Break 10:35-10:55

Keynote Forum

Moro O Salifu

SUNY Downstate Medical Center, USA

Keynote: The role of F11R antagonists in neointimal hyperplasia in dialysis vascular accesses

Time : 10:55-11:25

Kidney 2018 International Conference Keynote Speaker Moro O Salifu photo
Biography:

Moro O Salifu is Chair of the Department of Medicine, Chief of the Division of Nephrology and Director of the Kidney Transplant Program at SUNY Downstate. He is board certified in internal medicine, nephrology and certified in transplant nephrology and interventional nephrology. While in residency and Fellowship training, he won annual awards in the basic science category in the Department of Medicine for six consecutive years as well as four consecutive awards from the American College of Physicians. After fellowship training, he was retained by SUNY Downstate as Assistant Professor in 2001. He has directed the nephrology fellowship training program since 2001 and in 2008 assumed the roles of Chief of Nephrology and Director of the Transplant Program, roles that were crucial to the restructuring of the kidney dialysis and transplant programs at Downstate. He is also a fellow of the American College of Physicians. His research interests are CKD disease progression, vascular biology, and kidney transplant outcomes. His work on vascular biology contributed to the discovery, cloning, and sequencing of the human F11 receptor (F11R) gene. The human F11R is located on platelets and on endothelial cells and involved in platelet adhesion to endothelial cells under inflammatory conditions.

Abstract:

Neointimal hyperplasia (NIH) is the proliferation and migration of smooth muscle cells from the media into the intima in response to vessel injury resulting in luminal narrowing. It is initiated by arterial wall damage induced mechanically or by shear stress resulting from high flow, pressure, and turbulence. The damaged endothelium exposures ligands that attract platelets and recruitment of inflammatory cells and release of cytokines (PDGF, TNF, IL1b, FGF, TGFb, etc.), that facilitate vascular smooth muscle cell proliferation and migration. Clinically, NIH may be the primary underlying lesion in vasooclusive diseases such as stenosis observed in artero-venous fistulas, artero-venous grafts and arterial bypass grafts or secondarily associated with the development of atherosclerosis. Although many advances have been made in the primary and secondary prevention of atherosclerosis, including the use of statins and antiplatelet agents, the approach to NIH using several pharmacologic agents have failed largely because none of the agents address the pathophysiology of NIH, which is an entirely different entity from atherosclerosis. Our group was the first to demonstrate the important role of the F11 receptor (F11R)/JAM-A), in human smooth muscle cell (HSMC) proliferation and migration in vitro. We demonstrated that HSMC exposed to three cytokines TNF, INF , and IL expressed F11R resulting in proliferation and migration. When F11R was partially knocked down using F11R siRNA, HSMC proliferation and migration was abrogated suggesting that inflammation-induced release of cytokines in blood vessels may induce the expression of F11R, which in turn, would cause the migration and proliferation of activated human HSMC into the intimal layer. Utilization of F11R inhibitors, therefore, represents a logical intervention for pharmacologic prevention and regression of NIH. In this presentation, we will explore the role of F11R in the pathogenesis of NIH and F11R inhibitors as potential therapeutic agents.

Keynote Forum

Aruna V Vanikar

GR Doshi and KM Mehta Institute of Kidney Diseases & Research Centre, Dr HL Trivedi Institute of Transplantation Sciences, India

Keynote: Calcineurin inhibitor toxicity in renal transplantation: The good, bad and ugly

Time : 11:25-11:55

Kidney 2018 International Conference Keynote Speaker Aruna V Vanikar photo
Biography:

Aruna Vanikar a Professor and Head, Dept. of Pathology, Lab Medicine, Transfusion Services and Immunohematology, Stem Cell Therapy and Regenerative Medicine, IKDRC-ITS, Ahmedabad. Awards: 1st recognized teacher of Post-Doctorate Renal And Transplant Pathology Course by Indian Academy of Pathologists, pioneer lady scientist of India, etc; 2 patents: adipose-derived mesenchymal stem cells, and insulin-making SC (given away to IKDRC-ITS), >200 publications. Research: immune tolerance, history, and evolution of Indian renal diseases; generation of MSC, Insulin-secreting SC, Neuronal SC, Cardiomyocytes, Hepatocyte-like cells, regulatory cells etc. On editorial board+reviewer for several journals and TTS abstracts. Currently, President of ISRTP.

 

Abstract:

Calcineurin inhibitors (CNI) cyclosporine (CsA) and Tacrolimus have significantly improved the early outcome of renal transplantation (RT) by reducing the incidence of acute rejections. Toxicity in the form of diabetogenicity, tremors, gastrointestinal disturbances, hyperlipidemia, and hirsutism are known. Acute CNI nephrotoxicity in the form of acute arteriolopathy, tubulopathy with isometric vacuolization and glomerulopathy in the severest form of thrombotic microangiopathy has been recorded at normal blood levels and chronicity in the form of irreversible stripped interstitial fibrosis, tubular atrophy, and associated glomerular loss are known. Our experience with about 5000 RTs in Indian and African patients shows that these races require lower doses of CNI and yet graft function can be maintained. In a 9 year study of 2392 renal allograft biopsies, we have found CNI toxicity in 11.3% biopsies. In a subset of 157 RT patients, we found that with doses of 0.02-0.03 mg/KgBW Tacrolimus, trough levels were 3.6±3 ng /ml in age group <30 years and 6.3±3.9 ng /ml in patients >30 years. With doses of 0.04-0.05 mg/KgBW, trough levels were 4.3±2.1 ng /ml for patients <30 years and 8.4±5.5 ng /ml in patients > 30 years. Tissue toxicity was noted in the majority of the patients with normal trough levels. To conclude, CNI is essential to game winners in early RT however they prove to be losers when used for > 5 years.

  • Kidney
Speaker

Chair

Michael F Michelis

Lenox Hill Hospital, USA

Speaker

Co-Chair

John K Maesaka

NYU Winthrop Hospital, USA

Session Introduction

Grant T Fankhauser

University of Texas Medical Branch, USA

Title: Challenges and opportunities for vascular surgery in native and transplanted kidneys

Time : 11:55-12:25

Speaker
Biography:

Grant Fankhauser serves as a vascular surgeon on the faculty of the University of Texas Medical Branch. He completed general surgery and vascular surgery training at the Mayo Clinic. He practices all aspects of open vascular and endovascular surgery, including in the treatment of native and transplanted kidneys. He earned master’s degrees in business administration and health administration since joining the faculty. He serves as the director of quality for the surgery department and has research interests in quality, value, and cost-effectiveness. He serves on numerous editorial boards and committees. 

Abstract:

Vascular disease is a well-known source of renal insufficiency. Diseases such as atherosclerosis, fibromuscular dysplasia, aneurysms, and polyarteritis nodosa can negatively affect kidney function. Vascular surgeons must be familiar with these diseases, their diagnosis, and treatment options. New diagnostic and treatment options are available but are underutilized in most centers. A review of these diagnostic and treatment options is presented. Vascular surgeons must also be aware of less common renal-vascular problems that may arise such as with transplanted kidneys, renal bypasses, and juxtarenal aortic aneurysms. Vascular surgeons should familiarize themselves with these surgeries, the possible complications, and the long-term renal repercussions. These renal-vascular challenges offer an opportunity to use open surgical and endovascular techniques to rescue threatened kidneys and help preserve long-term renal function. In the setting of end-stage renal disease, vascular surgeons must be aware of the effect of vascular disease on dialysis access in both the venous and arterial systems and have various techniques ready to address them. The diagnostic and therapeutic options of this disease are discussed and a preview of emerging technologies is presented.

 

Hua Zhou

The Shengjing Hospital of China Medical University, China

Title: The inhibition of renal miR-150 attenuated kidney injury in lupus nephritis by reducing inflammation and fibrosis

Time : 12:25-12:55

Speaker
Biography:

Hua Zhou completed her MD at China Medical University, PhD at Hamamatsu Medical University in Japan, and postdoctoral works at NIDDK. Prior to returning to China, she had conducted medical research at NIH for 9 years. Currently, she serves as the Vice Director of the Nephrology Department at Hospital of China Medical University, one of the top 20 medical universities in China. She has published 32 papers in prominent nephrology journals and has reached a citation number of 2300+. She also serves as an outstanding committee member of the Chinese Society of Renal Pharmacology and the Chinese Society of Renal Pathology.

 

Abstract:

We had previously reported that renal miR-150 correlates with chronicity in repeated kidney biopsies from lupus nephritis (LN) patients and that miR-150 agonist upregulates profibrotic and downregulates antifibrotic proteins in human podocyte, tubular, and mesangial cells. This suggests that miR-150 may be a target for treating renal fibrosis. We recently found that circular HLA-C might regulate miR-150 in LN patients with simple class IV. In this study, we subcutaneously injected locked nucleic acid (LNA)-anti-miR-150 (2mg/kg) in fcgr2b-/- mice, which is a spontaneous LN mouse model with different pathological classification. LNA-anti-miR-150 with FAM was seen in kidneys 6hr after injection. Renal miR-150 increased 2-fold in 40-week LN mice. LNA-anti-miR-150 (twice/week for 6-8 weeks) decreased renal miR-150 levels to around 30% of the diseased mice with scrambled LNA injection but did not show any other organ toxicity. Inhibition of renal miR-150 significantly attenuated proteinuria and kidney injury seen on PAS and MASSON. The levels of proinflammatory genes (Il6A, Ifn-γ, Tnf-α) and profibrotic genes (TGF-β, α-smooth muscle antibody, fibronectin) remarkably decrease and the expression of the anti-fibrotic gene (suppressor of cytokine signaling 1) increased. Lastly, we validated miR-150 in renal biopsies from new onset female LN patients with class III to class V (n=18) without treatment of steroid and immunosuppressant. We found renal miR-150 in LN patients increased compared with normal kidney tissue. We conclude that miR-150 inhibition protected LN from progression by downregulating proinflammatory and profibrotic genes and up-regulating anti-fibrotic genes. This suggested that LNA-anti-miR-150 may be a potential agent for treating renal fibrosis.

 

Break: Lunch Break 12:55-13:55
Speaker
Biography:

Geraldo Silva Junior has completed his PhD at the age of 32 years from the Federal University of Ceara (Brazil) in the field of Medical Sciences and postdoctoral studies from the Federal University of Bahia (Brazil) in the field of Public Health and Epidemiology. He is Adjunct Professor at the Medicine School and Graduate Programs (Master and PhD) at the University of Fortaleza (Brazil) and member of the Department of Epidemiology and Prevention of Kidney Disease of the Brazilian Society of Nephrology. He has published more than 100 papers in reputed journals.

 

Abstract:

Kidney involvement is common in the course of many tropical diseases, which increases its morbidity and mortality. Acute kidney injury (AKI) is part of the classic severe forms of some diseases such as leptospirosis (Weil’s disease), malaria and viral hemorrhagic fevers. Different patterns of glomerular involvement have been described in many tropical diseases, including diffuse proliferative glomerulonephritis, membranoproliferative glomerulonephritis, mesangial proliferative glomerulonephritis, and focal/segmental glomerulosclerosis. Diseases with a chronic pattern, such as leprosy and visceral leishmaniasis, frequently cause glomerulonephritis, including those described above and even less frequent lesions such as amyloidosis and IgA nephropathy. Renal tubular dysfunction has also been described as a consequence of tropical infections. Renal tubular acidosis, for example, is one of the initial manifestations in visceral leishmaniasis, which is usually asymptomatic and can also be found in other infectious diseases. Another important public health problem faced in tropical areas of the globe is animal poisoning. The more common are spider and snakebites, which can complicate with AKI. Recently, new biomarkers for early detection of kidney injury in tropical diseases have been investigated, including neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), which seem to be promising tools to help Physicians to early detect kidney injury in the setting of tropical diseases and then adopt renal support measures as soon as possible and avoid severe complications such as end-stage renal disease and permanent dialysis need. In this plenary, we present important highlights from research in the field of Tropical Nephrology from Brazil.

 

Yasin Idweini Saed Matrouk

Al-Bashir Teaching Hospital-Ministry of Health , Jordan

Title: Vesicoureteral reflux endoscopic treatment by using electrocoagulation

Time : 14:25-14:55

Speaker
Biography:

Yasin Idweini, Senior consultant of Urology-Amman Jordan. He received a medical degree (1976) and specialty in Urology at Barcelona University-Spain (1980). He obtained Jordanian Board of Urology (1998). He obtained his PhD in Urology with graduating Magna Cum Laude (Barcelona University, 2003). He earned (FEBU) in Paris-France (2004). He published his book titled “Tratamiento del Reflujo Vesicoureteral por Electrocoagulation” (2011). He is an examiner in Jordanian and Arab BOARD of Urology. He obtained the World Academic Championship-2018 in Urology(Electrocoagulation)and in Endoscopic Treatment by the International Agency for Standards and Rating and Fellow Directorate of Urology IASR.

 

Abstract:

Purpose: We reviewed our experience with endoscopic treatment of (VUR) Vesicoureteric Reflux by electrocoagulation; as a simple technique to determine the efficacy and lack of morbidity of this procedure.

Material and methods: From January 1998 to December 2002, 150 patients with vesicoureteric reflux (210 refluxing ureters) underwent 291 endoscopic electrocoagulation in the hemitrigone in order to treat the reflux. The ratio of male to female was 2:8. Age ranged from 2 months to 47 years and median: 7 years. Localization was bilateral 39% Rt. Side 20%, Lt Side 41%. The grade of vesicoureteric reflux ranged from 2 to 5th grade. Secondary reflux was in 18% of the cases.

Results: Good results achieved in 85% of patients, 25% of the patients underwent repeated coagulation (2-3 times). 12% underwent surgical treatment because of the associated abnormalities (paraureteral vesical diverticulum, ectopic ureterocele, posterior urethral valves, ureteral duplication etc.).

Conclusions: Endoscopic treatment of VUR by electrocoagulation is a simple and safe procedure, with less morbidity, and it is cost effective.

Kamal V Kanodia

Dr HL Trivedi Institute of Transplantation Sciences, India

Title: Antibody-mediated rejection in kidney transplantation

Time : 14:55-15:25

Speaker
Biography:

Kamal Kanodia completed his MD in 1995 from Saurashtra University, India and post-doctoral certificate course (PDCC) in Renal and Transplant Pathology by Indian College of Pathologists in 2003. Currently, he is Professor in Department of Pathology, Laboratory Medicine, Immunohematology, and Transfusion services in Institute of Kidney Diseases and Research Center (IKDRC)-Institute of Transplantation Sciences (ITS), Ahmedabad, India. He has a keen interest in renal and liver transplant pathology. He has 47 publications and serves on editorial board and reviewer in several journals. He has presented several oral and poster presentations at various national and international conferences.

Abstract:

Antibody-mediated rejection (ABMR) is the most common cause of allograft failure. Acute ABMR occurs in ~ 30% of renal allograft biopsies; ~60% of late allograft dysfunctions are due to chronic ABMR. In renal transplants, acute ABMR is characterized by graft dysfunction manifesting over days and results from pre-formed/de novo donor-specific antibodies (DSA). According to revised Banff ’15 classification all three features must be present for diagnosis of acute/active AMR; (1) histologic evidence of acute tissue injury which includes microvascular inflammation (g>0 and/or peritubular capillaritis ([PTC]>0), fibrinoid necrosis/transmural arteritis (v>0), acute thrombotic microangiopathy, or acute tubular injury; (2) linear C4d staining in PTCs (C4d2/C4d3 by immunofluorescence), or C4d>0 by immunohistochemistry [IHC]. For C4d negative lesions, at least moderate microvascular inflammation (g+PTC ≥ 2)/increased expression of endothelial-associated gene transcripts (ENDATs) (3) serologic evidence of DSAs (HLA/non-HLA). For chronic ABMR, the morphologic evidence is transplanted glomerulopathy (TG) (cg>0), PTC basement membrane multilayering (on electron microscopy) and arterial intimal fibrosis of new onset. The cellular and molecular pathways regulating ABMR are still under study. However, evidence suggests B-cell and plasma cell activation results in the generation of DSAs, which bind to human leukocyte antigen (HLA) or non-HLA molecules expressed on endothelial cells within the renal allograft. In our experience of 2316 allograft biopsies from 2008 to 2016, ABMR was seen in 23.6% of patients. Mean HLA was 2.11±1.44 and mean S.Cr. was 2.7±1.45mg/dL.

Khamisa Almokali

King Abdullah Children Specialized Hospital, Riyadh, Saudi Arabia

Title: Carnitine and its role in a patient with renal failure

Time : 15:25-15:55

Speaker
Biography:

Khamisa Almokali completed her MBBS degree from King Saud University, Saudi Arabia. Then she joined King Abdulaziz Medical City where she finished her pediatric residency program, she has Saudi Board and as well Arab board in Pediatric. In 2010 she joined Sick Kid Hospital, Toronto, Canda to do 3 years pediatric nephrology fellowship program. And currently working as pediatric nephrology consultant at King Abdullah Children Specialized Hospital, Riyadh, Saudi Arabia. As well she is the program director of the pediatric nephrology fellowship. She joined Harvard medical school training program for introduction of clinical research from December 2016 till May 2017.

 

Abstract:

Carnitine is an important intermediary in fat metabolism. Carnitine deficiency may be a significant problem in a patient with kidney disease, especially those who are requiring maintenance dialysis. In hemodialysis patient, total plasma carnitine level is elevated with reduced free carnitine concentration and the ratio of acyl to free carnitine is markedly increased compared to healthy controls, carnitine deficiency in dialysis patient might cause significant side effects such as cardiomyopathy, intradialytic hypotension, and muscle weakness. Supplementation in such cases is required with good response. The national kidney foundation-kidney disease outcomes quality initiative (NKF-KDOQI) working group developed guidelines for the nutrition in chronic kidney disease including carnitine supplementation.

 

Break: Networking and Refreshment Break 15:55-16:15

Bogdan Dima

Cliniques de l’Europe – Hôpital “Sainte Elisabeth”, Belgium

Title: Vesico-Ureteral Reflux between the paediatric nephrologist and the surgeon

Time : 16:15-16:45

Speaker
Biography:

Bogdan Dima has completed his medical studies in Bucharest, Romania at “Carol Davila” University of Medicine and Pharmacy. He worked as a Medical Resident and as a Specialised Paediatrician in the Department of Paediatric Nephrology and Dialysis at Fundeni Clinical Institute (Bucharest, Romania) before moving to France in 2009. He attended the Inter-Universities Paediatric Nephrology Course in France (Paris, Nice, Lyon, and Montpellier). Since 2011 he is living and working in Belgium (from 2011 until 2016 in Charleroi University Hospital, and since 2016 in Cliniques de l’Europe in Brussels in the Paediatrics and Neonatology Department).

 

Abstract:

Throughout the last decades, there were different approaches to the management of the Vesico-Ureteral Reflux (VUR), varying from a conservative medical to an “aggressive”, surgical way. The use of different monitoring and therapeutical methods made the results difficult to compare. In the last years though, thanks to the statistical analysis of various studies results, a more integrated approach emerged. The author of this presentation is sharing his experience with the follow up of the children presenting congenital VUR, focusing on the role of the radiology investigations and of renal scintigraphy in determining the adequate management approach for each child. The conclusions drawn are seen as a base for a debate meant to harmonize the management of the children diagnosed at birth with VUR.

 

Umang G Thakkar

Dr HL Trivedi Institute of Transplantation Sciences, India

Title: Stem cell therapy for glomerular diseases

Time : 16:45-17:15

Speaker
Biography:

Umang G Thakkar got his DCH (Paediatrics) from India and has > 10-years’ experience in the field of regenerative medicine. Currently, he is working as an Associate Professor at IKDRC-ITS, Ahmedabad, India. His research interests are stem cell therapy for various disorders, pediatrics. He has >40 publications in various medical journals. He is included as an editorial board member in various journals and a reviewer also. He also received the Government Scholarship and distinguished Awards in the past. He was granted a Young Investigator Award in TTS 2016 at Hong Kong, for his research paper.

Abstract:

Stem cell therapy (SCT) has the potential to develop a novel therapeutic approach to glomerular diseases (GDs). The main goal of SCT is to achieve and sustain the recovery of altered renal functions. We present our preliminary experience of allogeneic SCT included adipose-derived mesenchymal stem cell (AD-MSC) and hematopoietic stem cells (HSC) for GDs. This was IRB approved non-randomized open-labeled prospective clinical study included 8-volunteer GDs’ patients with their informed consent subjected to allogeneic SCT from May,’13 to December,’17. Volunteer donors from blood-related family members were subjected to adipose tissue resection and BM aspiration for in vitro generation of AD-MSC and HSC respectively. Patients were diagnosed with GDs and confirmed by renal biopsy. Primary FSGS was noted in 4, LN in 2, and primary IgAN and MePGN in 1 patient each. In vitro generated SCs were infused via femoral catheterization under local anesthesia into bilateral renal arteries, portal circulation, and thymus (by IITV guidance), with the mean cell volume of 70ml, 30ml, and 3ml respectively, under conditioning of Bortezomib and subtotal lymphoid irradiation. Infused mean MSC count was 34.89x104 cells/KgBW and HSC count was 4.97x108 cells/KgBW with mean CD34+/CD90+/CD73+ of 0.82%, 38.9% and 21.1% respectively. SCT was safe and uneventful. Over mean follow-up of 31.38 months, there was sustained reduction in mean 24-hours proteinuria from 1.356 to 0.45gm/day, decreased SCr from 1.14 to 0.78mg/dL and increased S.alb to 3.68gm/dL with improvement in creatinine clearance and eGFR. Thus, Co-infusion of AD-MSC + HSC offers safe, viable approach to achieve remission in GDs.

Speaker
Biography:

Beishebaeva Nasira Adylbekovna completed her PhD of Medical Sciences in the year 2004; on the theme “Duration of children’s glomerulonephritis in combination with HBV-infection in Kyrgyzstan.” She did her post-graduation studies during 1998–2002 in pediatric nephrology. She is the Head of the nephrology department, NCMCHP of the Ministry of Healthcare of the Kyrgyz Republic, Kyrgyzstan.

Abstract:

Purpose: Assess the diastolic dysfunction (DD) of the heart with different forms of glomerulopathies (GP).

Materials and Methods: 55 patients with GP were examined (32 men, 23 women) aged from 17 to 58 years (on the average 32.76±10.3). All patients carried out kidney biopsy. IgA, IgG and IgM GP were diagnosed.

Results: The disease debuted at a young age of over 17 years in most patients (78.1%). Clinically, most often there was a nephrotic syndrome (in 65.4%), and in most cases - in men (72.2%). Systolic and diastolic blood pressure was 130.3±20.0 mm Hg. Art and 83.2±13.06 mm Hg. art., respectively. By the nature of the immune deposits with different morphological types of GP, we divided them into three subgroups. In the course of the analysis, the highest value of blood pressure was found in patients with IgG and IgM deposits (138.3±21.6 mm Hg and 136.0±21.0 mm Hg, respectively), so there is a reason to believe, that the formed immune complexes are a factor of endothelial damage. In the study of clinical data, statistically significant differences between groups of patients were revealed. DD was diagnosed in 36.4% of patients with heart failure in the early stages of the disease, before the development of renal failure. The main differences between cohorts were a significant elongation of the isovolumic relaxation time (IVRT) in the group with IgM nephropathy (P<0.005). However, a significant difference in late diastolic movement of the medial part of the mitral ring [A'] (P<0.04) was observed only in the group of patients with IgM nephropathy.

Conclusion: Left ventricular diastolic dysfunction was diagnosed in each third patient with GP in the onset of the disease, without renal failure. The most pronounced signs of diastolic filling identified in patients with IgM nephropathy, as evidenced by the significant differences between groups.

Speaker
Biography:

Jagdish Kanagaraj has completed him under graduation (MBBS) from Pondicherry Institute of Medical Sciences (in 2009). He has received medal of honor in Internal Medicine. He pursued his masters in internal medicine in Government Stanley Medical College in Chennai and completed his course in 2013 with medal of honor in internal medicine. His special area of interest includes glomerulonephritis, transplantation in all sensitized individuals and post-transplant infections. He completed his masters in Nephrology in 2017 in Christian medical college, Vellore and was awarded with JCM Shastry award for the year 2017. He has two publications and he is a reviewer in Indian journal of nephrology and international journal of nephrology and Endourology. He is currently working as consultant nephrologist and transplant physician in Meenakshi hospital in Tanjore, Tamil Nadu, India.

Abstract:

Plasmapheresis is a life-saving procedure that either is a treatment modality or a stop-gap procedure to buy time till immunosuppression acts. Unfortunately it removes necessary vital plasma components including immunoglobulins, albumin and coagulation factors. Various selective plasmapheresis options exist. One such is double filtration plasmapheresis which can selectively remove certain component of immunoglobulins. In our experience, with a small prospective observational cohort study, cumulative immunoglobulin removal in various renal indications was as follows-IgG is 72% which is suboptimal, whereas IgA and IgM cumulative removal were 89% and 96% respectively. We also observed effluent fluid albumin concentration will be more physiological way of replacement and serum fibrinogen values less than 50mg/dl resulted in spontaneous bleeding.

Break: Panel Discussion