Scientific Program

Conference Series Ltd invites all the participants across the globe to attend 4th International Conference on Nephrology & Therapeutics Baltimore, USA.

Day 2 :

Keynote Forum

Paulo Roberto Santos

Federal University of Ceara, Brazil

Keynote: Spirituality, quality of life and depression among hemodialysis patients

Time : 09:00-09:30

Conference Series Nephrology-2015 International Conference Keynote Speaker Paulo Roberto Santos photo
Biography:

Paulo Roberto Santos is Associate Professor at Federal University of Ceará, Brazil, and coordinates the Graduate Program in Health Sciences of the Sobral Faculty of Medicine. His main research interests are self-perceived outcomes (quality of life, depression, coping strategies and sexuality) among end-stage renal disease patients.

Abstract:

Low quality of life and high prevalence of depression are universally found among end-stage renal disease patients undergoing hemodialysis. In the past decade, technical advances of dialysis therapy have not been sufficient to improve the quality of life or decrease the prevalence of depression. Many variables associated with poor quality of life and depressive symptoms are not modifiable, like gender, age, and comorbidity. The relationship of spirituality and well-being is well documented in the literature. In the nephrology area, there are reports of better quality of life and less depression among dialysis patients with a greater perception of spirituality and religiosity. Nevertheless, more studies on spirituality are necessary among hemodialysis patients, especially because to some extent spirituality can be modified, and strategies aiming at engaging patients in discussions about their spiritual concerns can be implemented by the care team. We conducted an observational study comprising 161 end-stage renal disease patients undergoing hemodialysis in the only dialysis center in the northern Ceará state, northeast Brazil. Spirituality was assessed by the Religious Coping Activity Scales (RCOPE). Depression was screened by the 20-item version of the Center for Epidemiologic Studies Depression Scale (CES-D). Quality of life was evaluated through the Brazilian version of the Medical Outcomes Study 36-Item Short Form Health Questionnaire (SF-36). We found depression rates of 27.3%. Positive religious coping was negatively correlated with depression score (r=-0.200; p=0.012), meaning the more positive religious coping was, the lower the depression score tended to be. In addition, positive religious coping was an independent protective factor for depression (OR=0.132; CI 95%=0.021-0.910; p=0.039). Regarding quality of life, positive religious coping was able to independently predict better quality of life scores related to the following dimensions: bodily pain (b=14.401; p=0.048) and vitality (b=12.580; p=0.022). On the other hand, negative religious coping independently predicted worste score of the dimension social functioning (b=-21.158; p=0.017). Our results add further evidence that spirituality is a powerful mediator of quality of life and depression. Clinical implications for the care team are:Patients using religious resources should be encouraged, while psycho-spiritual interventions should be tried targeting religious struggle (negative religious coping) among hemodialysis patients.

Keynote Forum

Lois J Arend

Johns Hopkins University, USA

Keynote: Novel roles for PKD genes in the reproductive tract and in stromal cells of the kidney

Time : 09:30-10:00

Conference Series Nephrology-2015 International Conference Keynote Speaker Lois J Arend photo
Biography:

Lois Arend is Associate Professor of Renal Pathology at Johns Hopkins University School of Medicine. Dr. Arend received a PhD in Physiology and her MD atrnMichigan State University, then completed residency and a fellowship in renal pathology at The University of Michigan. Dr. Arend has studied renal function andrndisease in areas such as the role of adenosine in normal kidney function, development of the kidney, and cystic kidney disease, and the pathology of vascular access and transplantation for 30 years, publishing over 65 peer-reviewed articles, reviews, and chapters in major textbooks such as Heptinstall’s Pathology of the Kidney. She is Director of Clinical Fellowship training for the Department of Pathology at Johns Hopkins University.

Abstract:

Autosomal dominant polycystic disease (ADPKD) is a very common genetic disease, affecting up to 1 in 500 people. Many affected individuals progress to end-stage renal disease (ESRD) by the fifth to sixth decade of life. Mutations in the Pkd1 gene account for over 85% of ADPKD cases, while the Pkd2 gene is believed responsible for the remainder. Despite this wellestablishedrngenetic basis, current mouse models do not adequately explain the clinical progress or reveal underlying pathogenic mechanisms in human ADPKD. Many of these models have been used as the basis for developing therapeutic strategies that have failed to produce results in subsequent clinical trials.rnWe have used novel approaches to investigate the renal and reproductive tract abnormalities in mice, opening new avenuesrnfor understanding PKD and its associated morbidities. Infertility and reproductive tract abnormalities in male ADPKD patientsrnare very common and have higher incidence than in the general population. In mouse models we developed, we identify novelrndefects in the reproductive tract that could form the basis for some of these issues. In addition, a mouse model targeting Pkd1rngene deletion in the stromal cells of the kidney offers a more faithful reproduction of human ADPKD than currently availablernmodels. In particular, these mice are being used to investigate the hypothesis that a “third hit” occurs during childhood or earlyrnadulthood leading to faster, more vigorous, or larger cyst development and greater risk of progression to ESRD.The study of ADPKD has stagnated due to a lack of models that reproduce the human condition for understanding pathogenesis, progression, and targeting therapies. These models may provide new mechanistic understanding of ADPKD and hold promise as a foundation for new therapeutic strategies.

  • Track 4: Renal Transplantation and Immunology
    Track 5: Nephritis, Onconephrology and Diabetic Nephropathy
    Track 6: Metabolic,Fluid and Electrolyte Disorders
Speaker

Chair

Dmytro D Ivanov

Shupky National Medical Academy, Ukraine

Speaker

Co-Chair

Rouchon-Isnard Myriam,

AURA Auvergne, France

Speaker
Biography:

Myriam Isnard-Rouchon has completed her MD in Clermont-Ferrand Auvergne University, her Master in Nutrition in Clermont II University. She works in a Non-Profit Association for Dialysis Patients in France. She is involved in clinical research, teaching at the University of Science and Technical for Physical and Sportive Activity, member of the Liaison Committee for Food and Nutrition in Auvergne. She has a good experience in physical activity for dialysis patients with 150 patients involved in her program among 400 dialysis patients (HD & PD), and begins an educational program for kidney transplant patients. The results are beginning to be published, and have been presented in the ASN Kidney Week in 2013 and 2014 (Posters).

Abstract:

Cardiovascular diseases are the main cause of morbidity and mortality in haemodialysis patients. Chronic Kidney Disease is a Cardiovascular Risk Factor (CVRF) associated with Hypertension (HTA), Dyslipidemia (low HDL), and Haemoglobin (Hb) variation. Oxidant stress also plays a central role in the development of cardiovascular diseases. Physical activity is well known in cardiology to allow a control of the CRF and a better survival. The impact of physical exercise on blood pressure levels, Dyslipidemia and Hb variation has been investigated intervention studies of cycling exercise program during haemodialysis. We already showed that intradialytic aerobic cycling training protocol exerts beneficial effects in CKD patients by reducing the most sensitive and reliable marker of OS (IsoP). The aim of this study was to determine if PA may allow a better control of the CVRF and decrease cardiovascular hospitalization.

Ana Laura Pimentel

Federal University of Rio Grande do Sul, Brazil

Title: Glycated hemoglobin in the screening and diagnosis of renal post-transplantation diabetes

Time : 10:25-10:50

Biography:

Ana Laura Pimentel is a PhD Candidate in Medical Sciences (Endocrinology) at Federal University of Rio Grande do Sul State (UFRGS, Brazil). She earned her MS in Medical Sciences (Endocrinology) from UFRGS. She is a pharmacist and has been working in the fields of diagnostic test accuracy, diabetes mellitus and renal transplantation.

Abstract:

Post-transplantation diabetes mellitus (PTDM) is a glucose metabolism alteration with high incidence during the first year after renal transplantation. It is associated with adverse outcomes, as graft rejection and cardiovascular disease. Available data in the literature show that, in renal transplant patients, the oral glucose tolerance test (OGTT) presents the highest diagnostic sensitivity for PTDM, although fasting plasma glucose (FPG) is the most requested test. Glycated hemoglobin (HbA1c) has been used in clinical practice for the monitoring of diabetes for more than 20 years. Since 2010, it has also been applied as a diagnostic test, with cut-off point of 6.5%. However, there are still controversies about the applicability of HbA1c results to detect PTDM. For now, OGTT should remain the reference test for PTDM once there is still no consensus on what HbA1c threshold to be applied for the screening and diagnosis of PTDM. The use of an algorithm with HbA1c test in combination with FPG and/or 2 h-plasma glucose after an OGTT seems to be an efficient strategy to diagnose or rule out PTDM in the early period after renal transplantation. The use of HbA1c cutoff points of ≥6.2% to rule in and ≤5.8% to rule out PTDM would reduce the number of OGTT in 85%.

Nasir Yunus Fulara

Grant Medical College & Sir Jamshedjee Jeejeebhoy Group of Hospitals, India

Title: Dyslipidemia in diabetic nephropathy

Time : 10:50-11:15

Speaker
Biography:

Nasir Yunus Fulara is a Professor of Medicine at Delhi National Board and Medical Research Centre. He is also serving as a Senior Physician, Cardiologist & Diabetologist at Jaslok Hospital & Medical Research Centre Mumbai, Saifee Hospital Mumbai and Breach Candy Hospital & Medical Research Centre Since last 34 years till date. He is also attached to Wockhardt Hospital- Mumbai South, an association with Partners Medical International (PMI) Boston, USA. He has also served as a Professor of Advanced Medicine at Tibbia Medical College in Mumbai. He has published Nephrology Journals and papers in Indian Journals of Nephrology. He is a respected Member of American Diabetic Association (ADA), European Association for Study of Diabetes (EASD) and Opinion Leader from India in International Diabetic Forum (IDF), Association of Physician of India (API) and Research Society for the Study of Diabetes in India (RSSDI). He was conferred the fellowship of the Texas Institute of Heart-Houston, The German Diabetes Center-Germany, AMI Group of Hospital-London. He has been awarded with prestigious Best Physician, Rajiv Gandhi Gold Medal Award in 1992

Abstract:

Diabetic nephropathy is the leading cause of kidney disease in patients starting renal replacement therapy and affects about 40% of type 1 and type 2 diabetic patients. It increases the risk of death mainly from cardiovascular causes and is defined by increased urinary albumin excretion in the absence of other renal diseases. Hyperglycemia, increased blood pressure levels and genetic predisposition are the main risk factors for the development of diabetic nephropathy. Recent epidemiological research revealed that dyslipidemia is also a risk factor for development and progression of diabetic nephropathy. The effect of Dyslipidemia on renal function can be explained by ‘lipid nephrotoxicity’ hypothesis. Under this hypothesis, mesangial proliferation caused by accumulation of lipoprotein into mesangial cells induces glomerulosclerosis. This theory has been updated recently including the concept of inflammation stress modifying lipid homeostasis and tissue lipid accumulation. Evidence from recent studies has suggested that dyslipidemia is one of the risk factors for progression and regression of diabetic nephropathy. But, there have been few studies reporting the association with end-stage renal disease or renal replacement therapy. Long-term follow-up studies are needed to demonstrate the causal relationships between dyslipidemia and end-stage renal disease from diabetic nephropathy. With regard to the treatment of dyslipidemia in patients with diabetes, there were some interventional trials of antihypercholesterolemic agents including fibrates and statins suggesting that these drugs are effective in lowering the decline of the estimated Glomerular Filtration Rate (eGFR) and reducing the progression of albuminuria.

Break: Networking & Refreshments 11:15-11:35 @ Foyer
Speaker
Biography:

 

Shuk-Man Ka has completed her PhD from National Defense Medical Center, Taipei, Taiwan and postdoctoral studies from the Department of Pathology, Tri-Service General Hospital, Taipei, Taiwan and the Initiative of Gene Therapy, Harvard Medical School. She is working as an associate professor at the Academy of Medicine, National Defense Medical Center, Taipei, Taiwan. She has published more than 45 papers in reputed journals.

Abstract:

Lupus nephritis (LN) is a major complication of systemic lupus erythematosus (SLE). NLRP3 inflammasome activation, reactive oxygen species (ROS) and interstitial mononuclear leukocyte infiltration in the kidney have been shown to provoke the acceleration and deterioration of LN, although the exact pathogenic mechanism remains unclear. Development of a novel molecular pathogenesis-oriented therapeutic remedy preventing progression is clinically warranted. In the present study, Citral (3,7-dimethyl-2,6-octadienal), a major active compound in a Chinese herbal medicine Litsea cubeba, was used to test its renoprotective effects in an accelerated and severe LN (ASLN) model induced by repeated injections of lipopolysaccharide (LPS) to SLE-prone NZB/Wf1 mice. The results showed that Citral significantly ameliorated proteinuria, renal function, and renal lesions, including glomerular neutrophil infiltration, intrinsic cell proliferation, cellular crescents, fibrinoid necrosis, peri-glomerular infiltration of mononuclear leukocytes, and focal tubular atrophy in ASLN mice. In the kidney, Citral inhibited NLRP3 inflammasome activation and levels of ROS, NAD(P)H oxidase subunit p47phox, or COX-2, and it enhanced the activation of Nrf2. In LPS-primed macrophages, Citral reduced ATP-induced IL-1β secretion and caspase-1 activation, but did not affect LPS-induced NLRP3 protein expression. Our data suggest that Citral alleviate the mouse ASLN model by inhibiting the activation signal of NLRP3 inflammasome and increasing Nrf2 antioxidant signaling. Therefore, this type of treatment is predicted to be useful for therapy in human ASLN.

Amna Wahab

Karachi Medical & Dental College, Pakistan

Title: Chronic kidney disease and psoriasis in gestation

Time : 12:00-12:25

Speaker
Biography:

Dr Musleh Uddin Kalar graduated as a Medical Doctor from University of Karachi in 1997 and completed his MPH in 2008 from University of Northern Colorado. He is a medical researcher and has published more than 10 papers in international medical journals.

Abstract:

Chronic kidney disease (CKD) and psoriasis are an emergent health care dilemma lately recognized in their complete aspect. According to Kidney Disease Outcomes Quality Initiative (KDOQI) g uidelines on diagnsis and staging of CKD they focus on earlier stages of kidney disease when constant signs of renal damage are present but renal function may still be in normal ranges. It has been estimated that 3% of women of childbearing age are affected by CKD. Psoriasis is a chronic relapsing skin disease that affects 50% of women and majority have onset of disease before 40 years corresponding with the reproductive years.To compare the outcome of CKD with early kidney disease (normal renal function) in gestation. To determine the frequency of low birth weight having psoriasis in gestation.

Hongdong Huang

Capital Medical University, China

Title: CD4+CD25+ Treg cells may be useful for the treatment of IgAN

Time : 12:25-12:50

Biography:

Hongdong Huang, Medicine Doctor (PhD in Medicine), at present is an Associate Chief Physician and Vice Director at Department of Nephrology in Beijing Shijitan Hospital. In 2007, he received a Doctoral degree from Xiangya School of Medicine. He completed his Post-doctoral fellowship at Harvard Medical School/Massachusetts General Hospital from 2011 to 2013. Currently he is in charge of 5 research projects. Recently, He as published more than 10 papers in reputed journals and has been serving as Editorial Board Member of repute

Abstract:

Immunoglobulin A (IgA) nephropathy (IgAN) is the most common glomerulonephritis in the world. Although this disease was once considered to have a good prognosis, it has more recently been observed that 30-40% of IgAN patients’ progress to end-stage renal disease (ESRD) within 20 years. Recent studies have shown that CD4+CD25+ Treg cells are of critical importance to the maintenance of tolerance by inhibiting the activation and proliferation of auto reactive T cells. CD4+CD25+ Treg cells are regulators in nearly all of the animal models of human organ-specific diseases, transplant rejection and allergic diseases. A numerical and or functional deficit of CD4+CD25+ Treg cells might trigger the development of disease. Depletion of the minor (about 10%) CD4+CD25+ Treg cells results in the development of organ-specific autoimmunity. Autoimmune diseases can be prevented by reconstitution of the animals with CD4+CD25+ Treg cells. Powrie and colleagues demonstrated that transfer of CD4+CD25+ Treg cells protected mice from the development of inflammatory bowel disease and even reversed established gastrointestinal inflammation. The most notable immunomodulatory property of CD4+CD25+ Treg cells is their ability to limit the development of a pro-inflammatory CD4+ Th2 phenotype; this inhibition is characterized by reduced cytokine production. Abnormality of peripheral T cell and increased IgA can result from an inappropriate balance between allergen activation of CD4+CD25+ Treg cells and effector Th2 cells. This imbalance could result from a deficiency in suppression by CD4+CD25+ Treg cells or strong activation signals that overcome such regulation. Much evidence has shown that the tonsils are closely related to IgAN. Tonsillitis may induce nephritis or make nephritis. Tonsillectomy can improve the urinary findings, keep stable renal function and have a favorable effect on long term renal survival in some IgAN patients. Our experiments have shown that the number of CD4+CD25+Treg cells was significantly lower in tonsils and peripheral blood in IgAN; tonsillar CD4+CD25+Treg cells from IgA nephropathy patients have decreased imunosuppressive activity in experimental IgA nephropathy rats. Tonsillectomy may improve immune function, increase CD4+CD25+ Treg cells leading to attenuation of the severity of IgAN. Transfer of CD4+CD25+ Treg cells protected rats from the development of IgAN. Altering CD4+CD25+ Treg cell numbers and or enhancing CD4+CD25+ Treg responses may be useful in the treatment of IgAN.

Break: Lunch Break 12:50-13:50 @ Eden’s Landing Restaurant

Punit Gupta

Pt. J N M Medical College & GBG Kidney Care Hospital, India

Title: Workshop onMAKE-D i.e Mobile Artificial Kidney Extended Dialysis

Time : 13:50-14:25

Biography:

Punit Gupta, was Profossser in Government medical college hospital (consider to be the tribal of india), raipur, India. He have done bachelor degree in 2000 I.e MBBS, than master degree in General Medicine in 2003 I.e MD, than Superspeciality in Nephrology I.e DM , With PHD DEGREE . He also awarded the prestigious ISPD SCHOLARSHIP and ASN fellowship. He have awarded with APCN developmental award in Malaysia. And also awarded with many oral n poster presentation National and International. He have presented highest number of papers I.e 31 abstract in single conference under his name till date around 175 paper and abstract is presented by him in different conferences.

Abstract:

The Mobile Artificial Kidney Extended Devices, also known as the MAKE-D, is a miniaturized dialysis device that can be worn like a jacket bag. It connects to a patient via a catheter. Like more sizable dialysis machines, it is designed to filter the blood of people whose kidneys are no longer working. Unlike current portable or stationary dialysis machines, it runs continuously on batteries and is not plugged into an electrical outlet or attached to a large water pipeline.

Speaker
Biography:

Chia-Wen Kuo is pursuing PhD at Department of Life Science and Agricultural Biotechnology of the National Chung Hsing University. He completed his MD at National Defence Medical Center in 1998 and is a specialist in Nephrology at Kaohsiung Veteran General Hospital in 2005. He has worked at Renal Units of Taichung Armed Forces General Hospital. He has published 8 papers.

Abstract:

Diabetic nephropathy is the leading cause of end stage renal disease in developed countries throughout the world. The imbalance between the production of reactive oxygen species (ROS) and the antioxidant defense system is the main problem that is responsible for the progression of diabetic kidney disease. In this study, we investigated whether human extracellular superoxide dismutase (hEC-SOD) can prevent diabetic nephropathy in the rat model. Diabetic nephropathy symptoms were induced by intraperitoneal injection with 60 mg/kg streptozotocin (STZ) in male Sprague-Dawley (SD) rats. After daily supplement of rhECSOD (3,200 U/kg/day) for 4 weeks, the serum or urine biochemical markers (glucose, creatinine, blood urea nitrogen, triglyceride, hemoglobin A1c, and microalbuminuria), histological changes, gene expressions (phox47, opn, and gapdh), and protein levels (TGF-β, AT1-R, phospho-p42/p44 MAPK, and p42/p44 MAPK) were determined Results showed that rhEC-SOD administration could reverse SOD activity measured in kidney and diabetic-associated changes, including the fibrosis change, expression of collagen I, transforming growth factor-beta (TGF-β) and angiotensin II receptor 1 (AT1-R), as well as the activation of the intracellular mitogen-activated protein kinase (MAPK) signaling pathway, associating with its inhibition of p42MAPK/p44MAPK (ERK1/2) phosphorylation. Additionally, diabetic nephropathy up-regulated the expression of the phox47 and opn genes, and these changes could also be suppressed. Though the proteinuria did not significantly reduce, treatment with rhEC-SOD ameliorates STZ-induced diabetic nephropathy, leading to reduced death rates, kidney weight/body weight ratio, fibrosis change and. TGF-β1 expression through the down-regulation of ROS/ERK1/2 signaling pathway. We conclude that rhEC-SOD can act as a therapeutic agent to protect the progression of diabetic nephropathy.

Speaker
Biography:

Ayman Aly Seddik was born in 1972,Graduated from in Shams University school of medicine 1996 very good with honour ,interenship and residency programm in Internal medicine and Nephrology 1997-2001 Assistant lecturere and Nephrology specialist in ain Shams University hospital , Nasser institute for research 2001-2006 , after obtaining md degree in Internal Medicine & Nephrology 2006 ain Shams University , work as consultant Nephrologist and lecturer Nephrologist in Ain Shams University hospitals ,senior specialist Nephrologist king fahd armed force hospital jeddah saudia arabia 2006-2008,consultant Nephrologist Northeren area armed force hospital 2009-2011 , programme director of Internal medicine residency programme in northeren area armed force hospital ,degree of assistant profeessor of Internal Medicine and Nephrology Ain Shams University, cairo, egypt 2012.Currently working as Nephrologist , Dubai hospital - Dubai health authority 2011-present .

Abstract:

Chronic kidney disease is associated with accumulation of uremic toxins that increases insulin resistance which will lead to blunted ability to suppress hepatic gluconeogenesis and reduce peripheral utilization of insulin. (1) CKD patients fail to increase insulin secretion in response to insulin resistance because of acidosis, 1,25 vitamin D deficiency, and secondary hyperparathyroidism. (2-4) Hemodialysis causes further fluctuations in glycemic control due to alterations in insulin secretion, clearance and resistance. DKA is uncommon in hemodialysis patients because of the abscense of glycosuria and osmotic diuresis which accounts for most of the fluid and electrolyte losses seen in DKA, anuric patients may be somewhat protected from dehydration and shock, although still subject to hyperkalemia and metabolic acidosis. (5) However substantial volume loss can still occur due to a prolonged decrease in oral intake or increased insensible water losses related to tachypnea and fever(2) there is no current guidelines for the management of diabetic ketoacidosis in anuric haemodialysis patients considering their differences than general population , we review of the literature for management protocols and expertise opinions in view of which we suggest to consider the following recommendations While managing DKA in haemodialysis patients : Recommendation 1: diagnosis of DKA should be suspected if there is persistent profound acidosis that does not respond to hemodialysis, or patients with marked symptoms of nausea and vomiting. Recommendation 2: Patients on dialysis have high total body stores of potassium and should not be started on potassium replacement until acidosis is corrected, and hypokalemia is documented. All HD patients should be monitored and if there is evidence of hyperkalemia (clinically or on ECG) immediate treatment with potassium lowering agents or dialysis should be initiated. (1,6) Recommendation 3: Dialysis patients might be fluid overloaded and are unable to excrete fluid load used routinely for management of DKA in non-CKD patients, therefore if fluids are required, small boluses should be used, with continuous monitoring and frequent re- evaluation of hydration status. If the patient is fluid overloaded then consider hemodialysis. (1,7) Recommendation 4: Patients with CKD fail to excrete acid load and are already fluid overloaded. Ketogenisis associated with ketoacidosis further adds to acidosis. This should be corrected with hemodialysis. There is no place for sodium bicarbonate infusion in management of DKA, and the associated sodium, volume and osmotic overload might be problematic in those patients. (1,7) Recommendation 5: Patients with CKD are immune compromised. They are also at high risk of cardiovascular events. These are very common precipitating factors that should be sought when managing any patient with DKA. (1 ) Recommendation 6: Increasing the frequency of dialysis might be helpful as it clears the overload, improves electrolyte imbalance and corrects acidosis .

Biography:

Jun-ya Kaimori has completed his PhD from Osaka University and Postdoctoral studies from Johns Hopkins University School of Medicine. He is the Associate Professor of Department of Advanced Technology for Transplantation, Osaka University Graduate School of Medicine. He has published more than 25 papers in reputed journals of the broad fields including Nephlorogy, Genetics, immunology, and Radiology.

Abstract:

Background: The incidence of malignancies in kidney transplant recipients is increasing. Breast cancer is a common malignancy after kidney transplantation and can be more aggressive in kidney transplant recipients than in the general population. In this study, we evaluated the incidence and prognosis of breast cancer in kidney transplant recipients. Findings: Between 1993 and 2013, 750 kidney transplant patients were followed-up at our center. Since 1999, annual physical examination, mammography, and breast ultrasonography have been performed for such patients. Diagnostic studies, including core needle or mammotome biopsy, were performed for suspected malignancies. Patients with malignant neoplasm were administered the appropriate treatment and followed-up to assess tumor response and symptoms. Nine patients were diagnosed with breast cancer during the follow-up period. The mean age at the initial detection of the breast cancer was 47.7±8.4 years. The mean interval from transplantation to diagnosis was 148.7 ± 37.1 months. Of the 9 patients, 8 were detected through the screening test; 7 were treated with breast conservative surgery and 1 was treated with modified radical mastectomy. The cancer stages were 0 (n=2), I (n=6), and II (n=1). The incidence of breast cancer tended to be unchanged with time between transplantation and diagnosis, inconsistent with the increase in the duration of immunosuppression. Conclusion: Annual screening tests are crucial in the early diagnosis of breast cancer. Early treatment of breast cancer can result in an excellent prognosis in kidney transplant recipients

Speaker
Biography:

Nasim Musa is serving as Medical Director and Chief Consultant, NIPRO JMI Dialysis Center Limited, Bangladesh. He is board certified in MBBS at Dhaka university, and M. MED Science in Nephrology at university of Sheffield, UK.

Abstract:

Patients with Insulin Dependent Diabetes Mellitus (IDDM) patients posses high risk of developing diabetic nephropathy. The goals of treatment of diabetic nephropathy are to slow the progression of kidney damage and control related complications. Studies have shown that Angiotensin Converting Enzymes Inhibitor (ACEI) and Angiotensin Receptor Blockers (ARB) are beneficial in reducing the progression of microalbuminuria in normotensive patients with type 1 diabetes. Current effort to perform a systematic review of available published evidence regarding role of ACEI and ARB in type I diabetic nephropathy and to assess whether these drugs are helpful in improving renal function, slowing progression of chronic renal failure in patients IDDM with nephropathy.

Break: Networking & Refreshments 16:05-16:25 @ Foyer

Elena Rampanelli

Academic Medical Center, University of Amsterdam, The Netherlands

Title: Renal dysfunction and metabolic syndrome: the chicken or the egg?

Time : 16:25-16:50

Speaker
Biography:

Elena Rampanelli has completed her Medical Biotechnology studies at the University of Bologna (Italy). Before starting her PhD, she carried out scientific research at the Rizzoli Orthopedic Institute in Bologna (Italy) and at the Queensland Institute of Medical Research in Brisbane (Australia). Between 2008 and 2013, she worked as a PhD student at the Academic Medical Hospital of Amsterdam (The Netherlands). She then carried out her first post-doc at the Institute of Clinical Chemistry and Laboratory Medicine of the University Hospital of Regensburg (Germany). She is currently conducting postdoctoral research at the Academic Medical Hospital in Amsterdam (The Netherlands).

Abstract:

The impact of diet-induced obesity, dyslipidemia and hypertension (metabolic syndrome, MetS) on kidney health and function is now emerging . Despite epidemiologic analyses show that MetS/dyslipidemia puts patients at higher risk for chronic kidney diseases (CKD), a causal relationship between dyslipidemia and renal dysfunction has not been completely elucidated. In our latest work, we aim to unravel the effects of high-fat diet (HFD) on renal physiology and the direct impact of LDL (low density lipoproteins) on cultured renal tubular epithelial cells (TEC). Our data show that LDL overload leads to TEC damage, by inducing phospholipidosis, mitochondrial damage and apoptosis, and causes alterations in the plasmatic membrane composition. These effects associate with impaired absorptive functions, decreased ATP levels, and defective cellular responses to growth factors in terms of signaling and proliferation. Low-grade inflammation is a hallmark of MetS. Soon after LDL exposure, TEC start secreting TNF-α and IL-1β and display increased intracellular levels of active caspase-1, which is required for the cleavage of pro-IL-1β. The maturation of both caspase-1 and IL-1β indicates the activation of the NLRP3 inflammasome, which is a multimeric danger-sensing complex implicated in the onset of obesity-induced inflammation and MetS. Interestingly, absence of a fully active NLRP3 inflammasome (shRNA/sgRNA) reduces the rate of LDL-induced phospholipidosis in cultured TEC. Accordingly, lack of NLRP3 attenuates the HFD-induced cholesterol and phospholipid accumulation in proximal tubules in mice. In conclusion, our research offers insight into the molecular processes at play in renal tubular cells during metabolic overloading and shed light on the role of NLRP3 in renal lipid metabolism.

Niharika Mehta

Brown university, USA

Title: Nephrolithiasis in pregnancy

Time : 16:50-17:15

Speaker
Biography:

Mehta is an assistant professor of Medicine at the Warren Alpert Medical School at Brown University. Having completed the Obstetric medicine fellowship through Brown University, she proceeded to join Women and Infants Hospital, department of OB medicine as a consulting attending. She is currently the Director of Ambulatory Services in the Division of Obstetric Medicine at Women and Infants’ hospital in Providence, RI.

Abstract:

Nephrolithiasis leading to renal colic is the most common nonobstetric cause of abdominal pain in pregnancy, necessitating hospitalization. There are several physiologic and anatomical changes in pregnancy that lead to increased propensity for stone formation. The proposed talk will include a review of these changes, the effect of disease on pregnancy, preferred imaging modalities in pregnancy and management considerations, with special reference to interventions in the light of pregnancy safety.

Speaker
Biography:

John K. Healy graduated MB. BS. (Hons), Sydney University and is a Fellow of the Royal Australasian College of Physicians. He has worked at Renal Units at Sydney Hospital and Georgetown University Hospital, Washington DC. He was LIONS Renal Research Fellow, Princess Alexandra Hospital, Brisbane, then a Visiting Consultant at Royal Brisbane Hospital Renal Unit until 2005. He is an Emeritus Fellow of Wesley Hospital, Brisbane and a former President of the Australian Society for Medical Research. He has published many papers in international peer reviewed literature.

Abstract:

Investigation of PHAII has led to a marked expansion of knowledge of distal renal tubular electrolyte handling, which controls critical final urinary composition. This disease, found from infancy to late adulthood, is characterized by hyperkalemia, with up to 9 mmol/l plasma K+, despite a normal glomerular filtration rate. The hyperkalemis leads to acidosis, sometimes severe enough to limit growth. Hypercalciuria and renal calculi may occur. Hypertension occurs in 75% of patients. Plasma renin is depressed and plasma aldosterone is low normal. Even if normotensive at presentation, hypertension generally develops over about 30 years. The hypertension is linked to increased Na+ and Cl- reabsorption through the Na+-Cl- co-transporter (NCC) in the distal convoluted tubule (DCT). Although frequently familial, 36% of cases of PHAII are de novo. The hyperkalemia has been ascribed in humans to (a) suppression of renal outer medullary K+ secretion (ROMK), or (b) increased chloride (Cl-) reabsorption (a Cl- shunt) depressing the degree of negativity at the site of K+ secretion in exchange for Na+ at the epithelial Na+ channels (ENaC), or (c) decreased Na+ delivery to the ENaC in the late distal nephron reducing K= secretion at that site. In 2000, geneticists discovered a serine-threonine kinase in rats they called WNK1, because it lacked lysine at the usual catalytic point (With No lysine (=K)),and soon WNK’s 2,3 and 4 were found. In man, mutations of WNK’s 1 and 4 (WNK’s 1 and 4) localised to the distal nephron in the critical site of electrolyte homeostasis, and were found to cause PHAII by failing to cause suppression of the NCC , which is the function of normal WNK’s. It was eventually found that mutations in WNK1 and WNK4 cause 13% of PHAII. Recently a further system regulating distal electrolyte handling called cullin 3 and kelch-like3 was found in an E3 ubiquitination ligase complex in the distal nephron, and mutations of these (CUL3 and KLHL3) cause 79% of PHAII. Clinical severity of PHAII is, in decreasing order, CUL3, recessive KLHL3, dominant KLHL3, WNK4, andWNK1. CUL3 and KLHL3 block ubiquitination (removal for degradation) of WNK4, accumulation of which causes suppression of ROMK and so can cause hyperkalemia as in mechanism (a) above. Mutant WNK4 also stimulates Cl- reabsorption by the paracellular pathway, supportive of (b) above. Although over-activity of the NCC may initially decrease Na+ delivery to the ENaC as in (c) above, in a stable state Na+ delivery to the ENaC would be normal, and sodium sulphate and sodium bicarbonate infusion studies, with ample delivery of Na+ to the ENaC, failed to provide even a quantitatively normal kaliuretic response, weakening the argument for (c) above. Thiazides are the most effective treatment of PHAII, as they inhibit the NCC. They produce mild hypovolemia in regular use, which may cause antidiuretic hormone release and this is a potent stimulator of K+ secretion. Thus, dDAVP rapidly reverses the hyperkalemia of PHAII, and this has been used successfully in treatment of this condition. Na+ restriction should be used with caution as it has been shown to increase plasma K+ in some studies, while in others it has reduced it or had no effect. If still needed, dietary K+ restriction may be effective.

Speaker
Biography:

Glenda Gobe is Director of the Translational Research Laboratory for the Centre for Kidney Disease Research at the Translational Research Institute, and professor of medicine at the School of Medicine, University of Queensland. She leads a multidisciplinary team of researchers that include cell & molecular biologists, clinician scientists and biological engineers. A/Prof Gobe has extensive expertise in research into chronic kidney disease (CKD) and is a member of the NHMRC Centre for Research Excellence for CKD–Queensland (CKD.QLD). She has published >200 original research and invited review articles on determinants of kidney regeneration, fibrosis, immunity and inflammation, and kidney cancer.

Abstract:

Oxidative stress is implicated in progression and development of chronic kidney disease (CKD). This study sought to investigate the effects of a 12-month (12-mo) exercise and lifestyle intervention program on changes in plasma biomarkers of oxidative stress in pre-dialysis CKD patients. 136 stage 3-4 CKD patients were randomized to receive standard nephrological care with or without a lifestyle intervention (multidisciplinary care clinic, a lifestyle program, and aerobic and resistance exercise training) for 12-mo. Plasma total F2-isoprostanes (IsoP), glutathione peroxidase (GPX) activity, total antioxidant capacity (TAC), anthropometric and biochemical data were collected at baseline and at 12-mo. We found there were no significant differences between groups (64 in standard care and 72 in lifestyle intervention) at baseline. There were no significant differences in changes for standard care and lifestyle intervention, respectively, in IsoP (35.2±117.8 pg/mL versus 26.9±146.6 pg/ml; p=0.88), GPX (5.0±4.1 U/L versus 5.3±6.0 U/L; p=0.87), or TAC (-0.03±0.1 versus -0.05±0.2; p=0.56). Patients identified as having high IsoP at baseline (>250 pg/mL) had a greater decrease in IsoP with lifestyle intervention (-106.2±157.8 pg/mL) compared to standard care (-38.1±81.6 pg/mL) (p=0.06). There was no difference in the change in eGFR between standard care (-0.2±7.8 mL/min/1.73m2) and lifestyle intervention (-1.6±6.7 mL/min/1.73m2) (p=0.33). In conclusion, exercise and lifestyle modification in stage 3-4 CKD did not produce changes in systemic biomarkers of oxidative stress over a 12-mo period. However patients with high IsoP may benefit most from the addition of intervention to standard care.

Speaker
Biography:

Peter Linz has completed his PhD in 2001 from the University Erlangen and specialized in electrophysiology and electrolyte metabolism. In 2008 he established sodium magnetic resonance imaging at the university clinic for an insight into human salt metabolism in nephrological and neurodegenerative diseases.

Abstract:

Sodium is stored in skin and muscle tissue. The amounts stored in hemodialysis (HD) patients are unknown. We hypothesized that 23Na magnetic resonance imaging (Na-MRI) could allow assessing tissue Na+ and its removal. We studied 24 HD patients, and 27 age-matched healthy controls. We also investigated 20 HD patients before and shortly after HD with a batch dialysis system, permitting direct measurements of Na+ in dialysate and ultrafiltrate. Age was associated with higher tissue Na+ content in controls and this increase was paralleled by an age-dependent decrease of circulating levels of vascular endothelial growth factor-C (VEGF-C). Older (>60 years) HD patients showed increased Na+ and water in skin and muscle. HD patients showed lower VEGF-C levels than age-matched controls. After HD treatment, patients with low VEGF-C levels had higher skin Na+ content than patients with high VEGF-C levels (low VEGF-C: 2.30.3 ng/ml and skin Na+: 24.38.2 mmol/L; high VEGF-C: 4.11.0 ng/ml and skin Na+: 18.25.8 mmol/L; P<0.05). We conclude that Na-MRI quantitatively detects Na+ stored in skin and muscle in humans and allows studying Na+ storage reduction in ESRD patients. Age and VEGF-C-related local tissue-specific clearance mechanisms may determine the efficacy of tissue Na+ removal with HD. Prospective trials on the relationship between tissue Na+ content and hard endpoints could provide new insights into Na+ homeostasis, and clarify whether increased Na+ storage is a cardiovascular risk factor.

Speaker
Biography:

Paulo Roberto Santos is Associate Professor at Federal University of Ceará, Brazil, and coordinates the Graduate Program in Health Sciences of the Sobral Faculty of Medicine. His main research interests are self-perceived outcomes (quality of life, depression, coping strategies and sexuality) among end-stage renal disease patients.

Abstract:

Low quality of life and high prevalence of depression are universally found among end-stage renal disease patients undergoing hemodialysis. In the past decade, technical advances of dialysis therapy have not been sufficient to improve the quality of life or decrease the prevalence of depression. Many variables associated with poor quality of life and depressive symptoms are not modifiable, like gender, age, and comorbidity. The relationship of spirituality and well-being is well documented in the literature. In the nephrology area, there are reports of better quality of life and less depression among dialysis patients with a greater perception of spirituality and religiosity. Nevertheless, more studies on spirituality are necessary among hemodialysis patients, especially because to some extent spirituality can be modified, and strategies aiming at engaging patients in discussions about their spiritual concerns can be implemented by the care team. We conducted an observational study comprising 161 end-stage renal disease patients undergoing hemodialysis in the only dialysis center in the northern Ceará state, northeast Brazil. Spirituality was assessed by the Religious Coping Activity Scales (RCOPE). Depression was screened by the 20-item version of the Center for Epidemiologic Studies Depression Scale (CES-D). Quality of life was evaluated through the Brazilian version of the Medical Outcomes Study 36-Item Short Form Health Questionnaire (SF-36). We found depression rates of 27.3%. Positive religious coping was negatively correlated with depression score (r=-0.200; p=0.012), meaning the more positive religious coping was, the lower the depression score tended to be. In addition, positive religious coping was an independent protective factor for depression (OR=0.132; CI 95%=0.021-0.910; p=0.039). Regarding quality of life, positive religious coping was able to independently predict better quality of life scores related to the following dimensions: bodily pain (b=14.401; p=0.048) and vitality (b=12.580; p=0.022). On the other hand, negative religious coping independently predicted worste score of the dimension social functioning (b=-21.158; p=0.017). Our results add further evidence that spirituality is a powerful mediator of quality of life and depression. Clinical implications for the care team are:Patients using religious resources should be encouraged, while psycho-spiritual interventions should be tried targeting religious struggle (negative religious coping) among hemodialysis patients.

Speaker
Biography:

Shahid is a Specialist Biomedical Scientist and a member of the Health Professions Council (HCPC), a member of the Institute of Biomedical Sciences (MIBMS) and also a Registered Biomedical Scientist under the Science Council (RSci). Shahid is also a member of the British Blood and Transfusion Society (BBTS). Shahid co-founded the RPSG in (2009) which is a social media platform - a ‘place’ where awareness and research meet. Shahid has a specialist interest in Paediatric Nephrology and Immunology. Shahid has presented and published research in various arenas and has been a panel member for a number of initiatives.

Abstract:

Chronic Kidney Disease (CKD) is on the rise in all ethnicities. Evidence also highlights that this disease negatively impacts quality of life and places an enormous financial implications on the health care system for the provision of care to patients. Thus, it is of utmost importance to devise strategies that prevent CKD and delay progressive loss of renal function in the wider population. This thesis aims to provide an overall perspective on Chronic Kidney Disease (CKD) as it currently stands within the United Kingdom (UK) and evaluate the utility of renal biomarkers to monitor nephrotoxicity and efficacy of immunosuppression therapy post renal transplantation. More emphasis is being placed on the prevention and early detection for CKD. Individuals who are at high risk of renal failure need better ‘preparation’ and prompt early referral to secondary care is a must in order to allow the best prognosis. In addition, the utility of biomarkers for monitoring post-transplant immunosuppression therapy (IST) has to become more specific in post-transplant IST monitoring. Neutrophil Gelatinase-Associated Lipocalin is becoming more apparent in this respect. Biomedical scientists now have a more active and larger role to play with respect to monitoring. Whilst there have been guidelines on the screening and monitoring of anticoagulation-based medication, there perhaps needs to be more collaborative guidelines to monitor mainstay IST post-transplant patients receive. Specialists from both clinical and laboratory practice need to come together to further inform which biomarkers would be specific for monitoring IST titres.

Speaker
Biography:

Itagores Hoffman II Coutinho has completed his PhD at the age of 36 years from São Paulo University Medical School. He is the director of Medical School – Federal University of Tocantins, Palmas, TO, Brazil. He was the founder and is coordinator of medical residency in Nephrology at Federal University of Tocantins.

Abstract:

Introduction: Screening for chronic kidney disease (CKD) has been advocated with increasing frequency. Population-based studies relating to the prevalence of CKD in the community are limited. We prospectively studied whether stratification by SCORED values could be useful in identifying subjects who are at high-risk for CKD in a general population-based sample. Methods: The frequency of individuals at high-risk for CKD was determined using a cross-sectional study of 873 adult households in Palmas, Brazil, that were randomly selected using a stratified, cluster method. Age, gender, and race of the study sample were similar to the population of Palmas. Results: An estimated GFR <60ml/min/1.73 m2 was present in 46(5.3%) of the participants studied, and the risk of CKD was greater in women than in men, and increased with age from 2.7% in the 18-44 age group to 19.0% in those ≥65 years. The frequencies of CKD Stage 3, 4 and 5 were 4.8%, 0.5%, and 0%, respectively. The SCORED values included 224 (25.7%) patients with high SCORED values (≥4), and 649(74.3%) subjects with low SCORED values. The subjects with higher SCORED values were at a significantly higher risk for CKD compared with those who had lower SCORED values (12.9% vs. 2.6%, χ2=35.58; p<0.001). Sensivity, specificity and negative predictive value for predicting CKD by the SCORED model was 63%, 76%, and 76%, respectively.
 Conclusion: High SCORED values were associated with a higher risk for CKD in a general population-based sampling. This simple screening tool was useful in identifying individuals at high-risk for CKD.

Cosmin Alecu

Antilles Guyane University, France

Title: Stroke and kidney disease, the dangerous connections
Speaker
Biography:

Cosmin ALECU, Neurologist, has completed his MD at the age of 25 years from Craiova University School of Medicine (Romania) and his PhD at the age of 42 years from Nancy University (Lorraine, France). He is head of the Stroke Unit of the University Hospital of Pointe à Pitre. He has published more than 25 papers in reputed journals concerning the Neurovascular, Neurophysiology and Vascular Physiology domains.

Abstract:

Caribbean stroke patients are younger and their risk factors are different from those of European and North American patients, particularly in young. The analysis of a prospective study of consecutive patients with a first hemispheric stroke admitted in Pointe-à-Pitre (Guadeloupe, French West Indies) between December 2010 and February 2011 revealed us that chronic kidney disease is very frequent, 23.6% of chronic renal failure. The study included 78 patients (33 women), 24.4% with haemorrhagic stroke. The mean age was 62.1 ±17.7 years, 70.5% of patients had hypertension, 29.4% a diabetes. A common origin of stroke and kidney disease by microangiopathy can be suggested by the high rate of hypertension and diabetes. Nevertheless, stroke aetiologies (TOAST classification), were cardio-embolism (19.3%), atherosclerosis (61.4%), lacunar stroke (1.8%), other known (3.5%) and unknown or indeterminate aetiologies (14%). Chronic renal failure has significant influence on functional state one year later (p=0.03) and probably influences the post stroke death (p=0.07 in our population). We discussed in this presentation, enclosing literature data and results of our study, the kidney disease and neurovascular disease association.

Speaker
Biography:

Laurent Metzinger has completed both PhD and Pharmaceutical studies from University of Strasbourg, France and was a postdoctoral fellow from University of Oxford (UK) in a leading lab on Duchenne muscular Dystrophy (Pr. Kay Davies). He leads a team in the INSERM U1088 unit of Amiens (dir. Pr. Ziad Massy). He has published some of the first papers showing a role for microRNAs in chronic kidney disease. He has published more than 30 papers in reputed journals, including Nature and Cell, and has been serving as an editorial board member for RNA & Diseases and Journal of Nephrology and Urology

Abstract:

Development of disease is often due to deregulation of gene expression. The gene program is controlled at the post-transcriptional level by the action of small non-coding RNAs known as microRNAs (miRNAs), short, single-stranded molecules that control mRNA stability or translational repression via base pairing with regions in the 3\' untranslated region of their target mRNAs. Over the last decade, considerable progress has been made to elucidate the roles of miRNAs in vascular pathogenesis and develop the use of miRNAs as innovative biomarkers in diagnostics, and as groundbreaking drugs in pharmacological treatments. We have recently shown that miR-223 is implicated in the course of chronic kidney disease (CKD) and is associated with vessel damage, such as vascular calcifications and atherosclerosis. This inflammatory miRNA is increased in vitro in vascular smooth muscle cells subjected to uremic toxins and is also increased in vivo in more advanced stages of CKD. Finally, miR-223 levels have been found to be deregulated in murine and human serum in the course of experimental CKD and in human diabetic patients. We are now in the process of evaluating its role in pre-clinical models of cardiovascular diseases, and are finding clues concerning its gene regulatory actions, using a combination of transcriptomics, proteomics and metabolomics. In conclusion, miR-223 could play a role in CKD vascular remodeling and may therefore represent an useful target to prevent or treat complications of CKD.