5^th Global Nephrologists Annual Meeting April 01-02, 2016 Valencia, Spain

Biography:

Dr. Milliner is a member of the Divisions of Nephrology and Pediatric Nephrology, Departments of Internal Medicine and Pediatrics at the Mayo Clinic College of Medicine. She conducts research in pediatric stone disease, oxalate, and inherited forms of nephrolithiasis. She chaired the Seventh International Workshop on Primary Hyperoxaluria, served as chair of the Scientific Advisory Board of the Oxalosis and Hyperoxaluria Foundation and is past president of the Research on Calculus Kinetics Society. Dr. Milliner is medical director for the Mayo Clinic Hyperoxaluria Center and is principal investigator for the Rare Kidney Stone Consortium, funded by the NIH.

Abstract:

The prevalence of kidney stones is high and stone formation is associated with CKD and end stage kidney disease. High concentrations of oxalate in the urine pose risk not only for calcium oxalate urolithiasis, but also for kidney disease caused by deposition of calcium oxalate crystals in kidney tubules and interstitium. Crystal induced inflammation and subsequent fibrosis can cause chronic progressive, or acute, loss of kidney function. Gut flora play a role in bioavailability of oxalate in the intestinal lumen and a number of disease states increase oxalate absorption from the gut. Any intestinal disease that impairs fat absorption, such as Crohn’s disase, pancreatic insufficiency, or short bowel syndrome can lead to enteric hyperoxaluria. Management of the epidemic of obesity is increasing the frequency of enteric hyperoxaluria through use of medications such as orlistat and increasing numbers of gastric bypass procedures performed in many parts of the world. Malabsorbtive procedures, more effective for weight loss, are associated with hyperoxaluria and stones. Inherited forms of primary hyperoxaluria result in the highest urine oxalate observed in human disease. The hyperoxaluria is lifelong and kidney failure is frequent. Three types of primary hyperoxaluria have been recognized. They differ in the severity of hyperoxaluria and stone disease, and in the frequency of end stage kidney disease. Kidney stones and kidney failure related to hyperoxaluria are increasingly recognized. Mechanisms of kidney injury, treatments available and under investigation, and clinical management of patients with advanced oxalate related kidney disease will be discussed.

Biography:

Dr. Ahmed Zeidan, BSc.(Hons), MB ChB, is currently pursuing a Doctorate in Medical Science under the supervision of Professor Sunil Bhandari. He received his first degree in Medical Microbiology & Immunology from Newcastle University and obtained his Medical degree from the University of Sheffield in 2010. Following his undergraduate studies he worked as a junior doctor in Manchester and completed his training in General/Internal Medicine at Hull and East Yorkshire Hospitals Trust. As a research fellow in Cardiology and Nephrology he was offered a scholarship for his current PhD at York University. Beside his clinical and research work, he is also actively involved in hospital-based teaching, tutoring medical students and lecturing at Hull-York Medical School. He is also a final year undergraduate examiner at Manchester Medical School.

Abstract:

The heart is subject to a number of adaptive and subsequently maladaptive changes in patients with chronic kidney disease (CKD). There are structural changes with both concentric and eccentric hypertrophy in part linked to FGF-23; changes in energetics, with a switch from fatty acids to glucose metabolism; ischaemic vulnerability from both iron and erythropoietin deficiency; oxidative stress and changes in calcium cycling within the mitochondria. However, the key components in the process are the adjustments in mitochondrial function which serve as the powerhouse for all tissues.Iron plays a pivotal role in oxygen uptake, transport, storage and metabolism in both skeletal and cardiac muscle. In models of stressed hearts with CKD, there is an increase in stage 4 respiration in addition to an increase in uncoupling proteins leading to mitochondrial dysfunction and an increase in transition pore formation leading to impaired contractile function of cardiomyocytes. Therefore a deficiency of iron may lead to impaired mitochondrial function via effects on transition pore opening and subsequent inhibition of the pro-survival pathway and activation of apoptotic pathways. Also chronic iron deficiency may cause structural abnormalities in cardiac myocytes leading to reduced exercise capacity and performance. However, both in vitro and in vivo data suggest that there may be an increase in oxidative stress with intravenous iron administration whilst clinical data suggest improved functional capacity. Few studies have examined the effects of intravenous iron in patients with heart failure, anaemia, iron deficiency, and renal dysfunction and none have examined whether a single large dose of iron may lead to improvements in functional capacity without adverse effects. Therefore we have been examining the effect of iron and whether it leads to improvement in mitochondrial function and hence symptom improvement and cardiac function independent of haemoglobin in patients with CKD. In addition we are assessing if intravenous iron therapy affect markers of kidney injury and oxidative stress via generation of labile or catalytic iron. The results of these studies will provide an insight into the mechanisms underlying the conundrum with the benefits of iron related to incorporation into the iron sulphur clusters as part of the electron transport chain and TCA cycle, the changes in mitochondrial function and the potential iron related increase in oxidative stress and subsequent adverse effects.

Biography:

Barbara Schraml has completed her PhD at Washington University in St. Louis and her postdoctoral studies in the laboratory of Caetano Reis e Sousa at the London Research Institute. She has been and independent Emmy-Noether Research group leader since 2014. Her group at the Walter-Brendel-Centre for Experimental Medicine of the Ludwig Maximilians University Munich focuses on understanding tissue specific immune responses.

Abstract:

Mononuclear phagocytes sample the environment for signs of damage or infection. The classification of these cells as macrophages or dendritic cells (DC) has traditionally been done on the basis of differences in cell morphology, expression of specific markers or of select functional attributes. However, these attributes are not absolute and often overlap, leading to difficulties in cell type identification. To circumvent these issues, we have generated a model to define DC based on their ontogenetic descendence from a committed precursor. We show that in mice precursors of conventional DC but not other leukocytes are marked by expression of DNGR-1/CLEC9A. We generated a mouse model to genetically label Clec9a-expressing conventional DC precursors and their progeny with yellow fluorescent protein (YFP). Genetic labeling of these cells and their progeny specifically traces cells traditionally ascribed to the DC lineage and the restriction is maintained after infection. Notably, in some tissues cells previously thought monocytes/macrophages are in fact descendants from DC precursors. These studies provide the first in vivo model for lineage tracing of DC and allow the definition of DC based on ontogenetic rather than phenotypic, morphological or functional criteria. These studies establish DC as an independent immune lineage and distinguish them from other leukocytes, thus paving the way to unraveling the functional complexity of the mononuclear phagocyte system.

Biography:

Levent Yucetin is the director of Antalya Medicalpark Transplant Center Coordination. He studied and trained in Oxford, Cambridge, Harefield transplant centers, Barcelona University and TPM organisation between 1999-2001. He was the president of Turkish Transplant Coordinator's Society between 2005-2009, National Key Member of ETCO between 2002-2012. Turkey's leader at European Union projects ETPOD,ELIPSY,LIDOPS and ODEQUS. Member of Turkish Health Ministery's Transplant Coordinators and Organ Donation board. Trainer of Transplant coordinators at Helath Ministery Certification organisation. He has published more than 29 papers in reputed journals and 10 chapters at 4 repute books.

Abstract:

More than 1 million patients are estimated to have undergone transplantation in the past years. In recent years, living-donor kidney transplantation accounted for more than 50% of all transplantations. Kidney transplantation from living donors is regarded as a contradictory case to the “do no harm” principle as a major surgical intervention is performed on a normal and healthy person at the expense of recovery of the organ recipient. The purpose of this study was to investigate positive psychological experiences, specifically posttraumatic growth (PTG), among living kidney donors. The sample consisted of a total of 184 kidney donors. The age of donors ranged between 21-76 (mean, 50.76; SD, 10.93). In this study 67.9% of donors were female. The recipients on dialysis group had higher scores than the recipients who did not have dialysis; the mean difference was significant on the subscales of change in life philosophy, change in relationships, change in self-perception, and in the PTGI score. The donors with higher education levels received higher scores on the subscale of change in relationships in comparison with donors with low education. The donors who were married and older than 51 years had higher scores than donors who were not married or younger on the subscale of change in self-perception. This is a singlecenter study; this center performs more than 500 kidney transplantations per year. There is a good system and experience at each step before and after transplantation for donor and recipient and relatives. It is a really big potential trauma to donate a kidney to your relative; you can change this negative effect to a positive effect with a good system. The present study also showed that when compared with the scale’s absolute midpoint, kidney donors in the study sample experienced moderate-to-high levels of PTG.

Biography:

Donald Silverberg Graduated from Medical School University of Manitoba in 1962. He did his Residency in Internal Medicine and Nephrology at the Mayo Clinic Rochester Minnesota in 1962-1966 and Residency in Nephrology, University of Lund, Sweden in 1966-1967. He worked as Nephrologist University Hospital, Edmonton Canada during l968-1976. Has been living in Israel and practicing nephrology since 1976 in Tel Hashomer and Beilinson and Tel Aviv Medical Center. National Director of Hypertension Control Division, Kupat Holim Sick Fund 1978-1986 (Organizing the detection and treatment of hypertension for the Israeli population).

Abstract:

Anemia (Hb <13g% in men and <12g% in women) is present in about 40% of Heart Failure (HF) patients. Iron deficiency (ID), if defined as either a serum ferritin of <100ug/l or a serum ferritin of 100-300 ug/l along with % Transferrin Saturation of <20%, is present in about 60% of the patients with anemia (about 24% of all HF patients) and in about 40% of patients without anemia (about 24% of all HF patients). Thus ID is present in about half the patients with HF. The ID in HF is associated with reduced iron stores in the bone marrow and the heart. ID is an independent risk factor for severity and worsening of the HF. Correction of ID with intravenous (IV) iron usually corrects both the anemia and the ID. Currently used IV iron preparations are very safe and effective in treating the ID in HF whereas little information is available on the effectiveness of oral iron. In metanalysis IV iron correction of ID in HF is associated with improvement in NYHA functional status, exercise capacity, C Reactive Protein, quality of life, rate of hospitalization for HF, cardiac dilation and hypertrophy, cardiac function, and renal function. Correction of the ID is also highly cost effective. The improvement seem to be related more to the correction of the iron deficiency than to correction of the anemia. The large placebo- controlled studies have only been done with Ferric sucrose and Ferric carboxymaltose. The incidence of adverse effects of these agents is similar to placebo. However large long-term adequately-controlled mortality-driven intervention studies are still needed to clarify the effect of IV iron in HF. Several Heart Associations, including the European, Australian and New Zealand Heart Associations, suggest that ID should now be routinely sought for in all HF patients and corrected if present.

Biography:

LAIDOUDI Aicha has completed her PhD at the age of 25 years from Ferhat Abbas University and she is in the postdoctoral studies, Mohamed Maherzi University School of Medicine. She is a doctor in the department of internal medicine, Mohamed Lamine Debaghine Hospital. She is in 5th and latest year of post-doctoral studies.

Abstract:

Introduction:The NITU syndrome is a rare combination characterized by the occurrence of tubulointerstitial nephritis (TIN) and uveitis (U), it is a rare disease of the adolescent and the young woman, its pathogenesis is unknown, autoimmune origin has recently been proposed including humoral and cellular immunity. In general, renal and eye damage tended to resolve with corticosteroid therapy. We report two cases of TINU syndrome occurring in adults in which the recovery of renal function was incomplete despite corticotherapy in the first observation, and immunological disorders which can create differential diagnostic difficulties. Case reports: Observation 1: A 25 year old woman, nurse, admitted to explore asthenia and weight loss of 6 Kg, associated with severe hypertension and acute unilateral anterior uveitis. She was taking no medications. Clinical examination revealed: a blood pressure (BP) of 170/130 mmHg, class II dyspnea (NYHA), a holosystolic heart murmur in the mitral area without heart failure signs, a mucocutaneous pallor but no signs of vasculitis, urine dipstick test finds traces of protein and hematuria; ocular fundus exam found grade I hypertensive retinopathy, the rest of the examination was normal. Biological studies showed kidney failure with GFR of 18.71 ml/mn/1.73m2 , proteinuria was 540 mg / 24h. Erythrocyte sedimentation rate between 37 and 76 mm (3-12) mm/hour. Kidney biopsy with histological examination showed a non caseating granuloma in the interstitial tissue with presence of rare hyaline casts in the kidney tubules, and tubulointerstitial nephritis with granulomatous lesions in the medullary parenchyma. Further exploration was done mainly oriented to sarcoidosis and tuberculosis and the other differential diagnosis was all negative but Quantiferon was 10 times normal with negativity of all other examinations to KB (koch’s bacillus). No other sites of granulomas. The patient responded to corticoid treatment (pulse IV followed by high-dose daily glucocorticoids then gradually tapered off but without normalization. The patient untimely stopped corticosteroids after 4 months of treatment that caused a decreased renal function that required a 2nd pulse then high-dose daily glucocorticoids. Glucocorticoid-sparing was provided by mycophenolate mofetil (MMF). The patient remained well without recurrence of uveitis 2 years later but without complete recovery of renal function which improved gradually with immunosuppressive treatment. Observation 2: A 46 year old patient, without specific personal history, but a mother who died of chronic kidney failure, presented a recurrent anterior uveitis, associated with an increase in serum creatinine; The clinical examination is unremarkable, the urine dipstick showed proteinuria (+), glycosuria: traces; Biological studies showed kidney failure with a GFR of 14 mL / min/1.73m2, inflammatory syndrome, proteinuria of 650 mg /day, research of infectious agents or auto-immunity origin was negative. Renal biopsy showed tubulointerstitial nephritis lesions in subacute stage; biopsy of the salivary glands showed stage III chronic lymphocytic sialadenitis (the Chisholm and Mason classification) without xerostomia, AntiSSA, antiSSB negative. Gallium scintigraphy did not find any signs suggesting a type of sarcoidosis inflammatory. The diagnosis of TINU syndrome was retained after exclusion of other differential diagnosis. The patient received corticosteroid treatment. Serum creatinine improved quickly with normalization 2 months later. The patient remained well without recurrence of the disease 6 years later. Discussion: TINU syndrome diagnosis is based on a combination of the bipolar impairment: renal and eye; and excluding other causes (infectious, drug and autoimmune). The treatment protocol is not yet codified, but corticosteroids at high-dose are first-line treatment of renal disease. In our patients, the presence of TIN in the renal biopsy, recurrent anterior uveitis, no notion of drug intake, the response to corticosteroids and exclusion of other diagnoses, so the diagnostic of TINU syndrome was retained. In the first observation, positivity of Quantiferon is explained by the fact that the TINU syndrome is associated with elevation of serological markers in the absence of their corresponding diseases, in the 2nd observation, the presence of stage III chronic lymphocytic sialadenitis can be explained by these immunological disorders in the absence of Sjogren syndrome. Conclusion: TINU syndrome is a rare entity, the pathogenesis is unknown, and its association with autoimmune diseases suggests its autoimmune origin. TINU syndrome is secondary to immunological disorders as evidenced interstitial infiltrate of the renal parenchyma, the inflammatory disease of the uvea and good response to corticosteroid therapy.

Biography:

Francesco Fontana, MD, is currently terminating his training in Nephrology at University of Modena and Reggio Emilia, Modena, Italy. In 2014 he attended an internship at the Instituto de Fisiologia Molecular, Instituto de Nutricion, Mexico City, Mexico. In 2015 he entered as a PhD student the Doctorate School of Clinical and Experimental Medicine at University of Modena and Reggio Emilia. His research interests focused on hemorheology in kidney transplantation and dialysis, acute kidney injury (AKI) models in rats and AKI – chronic kidney disease transition, biocompatibility and clinical aspects of miniaturized devices for chronic dialysis.

Abstract:

Although the burden of end stage renal disease is worldwide expanding, current dialytic options are unsatisfactory, mainly due to their intermittent character. Benefits of continuous treatments on rates of complications and mortality are clearly demonstrated, and a miniaturization of dialysis devices would allow delivery of continuous treatment without limiting patient’s freedom. Miniaturization poses several technical challenges, in terms of dialysis membranes, dialysate regeneration, vascular access, patient monitoring, power sources and pumping systems. First attempts in the creation of a portable/wearable artificial kidney (WAK) for hemodialysis (HD) date back to the seventies, but technology later needed to be refined with development of dialysate regeneration modules based on sorbents and enzymes. These advances paved the way to first, short-term validations in humans obtaining promising results in terms of safety and effectiveness but needing further confirmations. WAK have also been proposed to enhance the efficacy of peritoneal dialysis (PD), circumventing the problems of a direct access to blood system and continuous anticoagulation, main bottlenecks for a widespread use in HD. Dialysis market is presently offering some options for portable/home devices, but no WAK is marketed. Hot topics in recent researches on under development WAKs have been the selectivity and regenereability of sorbents and a reappraisal of electro-oxidation for urea elimination. Furthermore, promising, although preliminary, advances have been made in the development of implantable devices, most promising consisting in a combination of sorbents and a scaffold with renal epithelial cells.

Biography:

Alsayed Alnahal is currently working as Assistant Professor at Zagzaig University Hospital and is a previous Director of the dialysis unit. He is graduated in 1996 and obtained his Post-graduate in Zagazig University. He has published more than 12 publications in reputed journals

Abstract:

Introduction: Serum creatinine is unreliable early biomarker for diagnosis of acute kidney injury (AKI) after cardiac surgery requiring cardiopulmonary bypass, we need to search for rapid and dependable marker for detection of AKI. Aim of work: This study was designed to test urinary netrin-1as marker of early kidney injury post-cardiac surgery. Our study included 39 subjects with preoperative normal creatinine. All patients underwent full history and routine laboratory investigation. Both serum creatinine and urinary netrin-1 were measured at 0, 6 and 24 hours after cardiac surgery. Results: 14 patient developed AKI after cardiac surgery. A statistically significant elevation in urinary netrin-1 is found at 6 and 24 hours after CPB surgery in the AKI group; while serum creatinine failed to show any statistically significant elevation at 6 hours after CPB in the same group. No statistically significant change in level of creatinine or urinary netrin-1 at 6 and 24 hours after CPB surgery in the non AKI group. The sensitivity and specificity of urinary netrin-1 to detect AKI at 6 h after CPB surgery was 86.7% and 91.7% respectively at a cutoff value of 107.3 pg/ml. Combined urinary netrin-1 and serum creatinine have the same sensitivity and specificity. Conclusion: Urinary netrin-1 may be considered as early sensitive biomarker of acute kidney injury at 6 hours after cadio-pulmonary bypass surgery instead of serum creatinine that rise only 24 hours after CPB surgery in cardiac surgery associated- acute kidney injury patients.

Biography:

Francois Cachat has completed his MD from Lausanne Medical School in Switzerland in 1991. After training in pediatrics in Switzerland, he completed a fellowship in pediatric nephrology in Charlottesville, VA, USA, where he conducted research on experimental obstructive uropathy. His current research interests are the measurement of renal function in children, and the application of Evidence-Based Medicine in the field of pediatric Nephrology. He is currently chief of pediatric nephrology at the Inselspital Bern, Switzerland. He has authored more than 70 peer-reviewed papers, and serves in more than 20 Journals as reviewer or member of the Editorial board.

Abstract:

Background Microalbuminuria (MA) has been shown to be an early biomarker of renal damage. It is postulated that MA is the early result of hyperfiltration, which could evolve into glomerular sclerosis and renal failure if hyperfiltration is left untreated. We hypothesized that MA is a good indicator of hyperfiltration in children with kidney disorders, obviating the need to calculate the filtration fraction (FF). Methods 155 children or young adults were prospectively included [42 single kidney (SK), 61 vesicoureteral reflux, 23 obstructive uropathies, 29 other kidney diseases]. We measured inulin, para-aminohippuric acid clearances, FF and MA. Prediction of hyperfiltration was explored by studying the association between FF and other variables such as urinary albumin (Alb), urinary albumin–creatinine ratio (ACR), creatinine clearance. Results A significant but weak association between urinary Alb or ACR and FF was found in subjects with SK (Spearman correlation coefficients 0.32 and 0.19, respectively). Multivariate analysis also showed that urinary Alb and ACR significantly predict FF only in subjects with a SK (r2 = 0.17, P = 0.01 and r2 = 0.13, P = 0.02, respectively). This holds true only in subjects with a SK and inulin clearance >90 mL/min/1.73 m2 (r2 = 0.41, P < 0.001). There was no association between creatinine clearance and FF. Conclusions MA is not associated with FF in subjects with nephro-urological disorders, except in those with a SK, where the association is weak, indicating that MA is due to other mechanisms than high FF and cannot predict hyperfiltration in such groups.

Biography:

Jose Luis Gorriz is a doctor at the department of Nephrology in Doctor Peset university Hospital and department of Medicine in University of Valencia, Spain

Abstract:

Abstract: Renal insufficiency increases the risk of stroke and bleeding in atrial fibrillation patients. Although vitamin K antagonists reduce the risk of stroke in patients with moderate renal dysfunction, this observation is less clear in patients with renal impairment. Moreover, the risk of bleeding with vitamin K antagonists increases as renal function worsens. Maintaining international normalized ratio values within therapeutic targets is more difficult in patients with renal dysfunction, and those agents may cause warfarin-related nephropathy and vascular calcification. Rivaroxaban is the only nonvitamin K oral anticoagulant with a dose specifically tested in patients with moderate renal insufficiency. Rivaroxaban is effective for the prevention of stroke in atrial fibrillation patients with moderate renal dysfunction, with a lower risk of intracranial and fatal bleeding. Key words: Atrial fibrillation , chronic kidney disease , new oral anticoagulant, nonvitamin K oral anticoagulant , renal function , renal insufficiency , rivaroxaban, vitamin K antagonist.

Biography:

Juan Pablo Preciado is a medical student currently enrolled in the 6th semester of medicine school from Universidad de Guadalajara, in the campus of Puerto Vallarta, Jalisco. Mexico. He has participated actively in numerous national conferences and actualization courses, nowadays want to attend to an international event, this, in order to gain experience on the international arena, that will be useful to practice in medical sciences and broaden his personal experience in medical investigation area. Currently my strongest engagement is with my career. Volunteering and getting involved in various scholar activities allow me to develop skills and attitude to effectively participate in multiple areas of medical sciences. The Knowledge and love to my career have given me the motivation to give the best of me every day and act responsibly

Abstract:

Background: End-Stage Kidney Disease is directly related to hypertension, diabetes and dyslipidemia, which is today diseases that have reached epidemic proportions in our country. Methods: We conducted an analytical, observational, cross-sectional, retrospective study based on individuals, involving 18 patients assigned to the ISSSTE Hospital located in Puerto Vallarta, Jalisco. México, diagnosed with End-Stage Kidney Disease, in which we seek to establish an approximate time frame for the diagnosis of End-Stage Kidney Disease in patients with a previous diagnosis of Systemic Hypertension, Diabetes Mellitus Type 2 and both associated. Statistical analysis was performed using the Excel Analysis ToolPak for Microsoft Office Excel 2013. Results: Data were collected from 18 patients diagnosed with End Stage Kidney Disease, of which only 15 patient's (83.33%) were analyzed, otherwise 3 patient's (16.66%) were excluded, 2 of them by presenting a diagnosis of ESKD simultaneously to Type 2 Diabetes or Systemic Hypertension, and the remaining patient did not present any comorbidity when establishing the diagnosis of ESKD. Of the selected patients it was found that the category who took a shorter time to have as diagnosed ESKD were patients with Hypertension as unique comorbidity, with an average of 5.6 years, while the category of type 2 diabetes mellitus and associated hypertension, had an average of 9 years, and finally patients with type 2 diabetes mellitus only, showed an average of 20 years of evolution before they make a diagnosis of ESRD. Conclusions/Discussion: The results show a direct causal link between type 2 diabetes mellitus and hypertension, with the onset of chronic kidney failure, this time depending on the evolution of the disease. Being patients with hypertension as the only comorbidity those with the shortest period to develop terminal chronic renal impairment compared to patients with diabetes mellitus as one comorbidity, who show a slow and progressive deterioration, perhaps associated with various factors, a major by inhibiting the renin-angiotensin system, which slows the progression of kidney disease.

Biography:

Agnieszka Pozdzik has completed her medical study from University School of Medicine (Lublin, Poland) and has completed a PhD from Université Libre de Bruxelles (Brussels, Belgique). She is a nephrologist and Associate Professor at the Department of Nephrology. Since October 2012, she is the manager of the "Biobank of chronic kidney disease and urinary tract" (MARENVU) and, since June 2012, of the multidisciplinary center of nephrolithiasis. She has published more than 20 research papers in reputed journals and has been serving as a reviewer of repute journals.

Abstract:

Tubulointerstitial nephritis (TIN) is a manifestation of IgG4-related diseases, which arecharacterized by infiltration of target organs by IgG4+ plasma cells and severe fibrosis. Cortico-sensitivity is one of the diagnostic criteria, but the treatment of steroid resistant and dependent forms is not well defined. We present a case of a 47-years-old patient with IgG4-related NTI followed for 72 months. He complained of fatigue and recurrent postprandial abdominal pain. With the exception of elevated levels of gamma-glutamyl transferase (GGT), transaminases and IgG4, kidney function remained normal (serum creatinine ≤ 0.9 mg/dL). After 2 cures of methylprednisolone (2010-11) azathioprine was associated in 2012. Due to the corticodependence and persistence of bilateral focal renal lesions detected by diffusion-weighted magnetic resonance imaging (DW-MRI), Rituximab (RTX) was given (2 × 376 mg/m²/15 days) in 2013. Before the first injection, positron emission tomography (PET) showed metabolic hyperactivity corresponding to axillary and abdominal aorta lymph nodes but not in the kidney. After 4 months of RTX, the patient became asymptomatic. All biological alterations disappeared. PET showed a decrease in metabolic activity at extrarenal lesions described above. A dramatic regression of bilateral renal lesions was noted by DW-MRI: the apparent diffusion coefficient had almost doubled (0.776 vs 1.111x10-3 mm²/sec) and the volume of renal lesions was reduced by 50%, which was never observed under other treatments. Our observations demonstrate: (1) the clinical, biological and radiological efficacy of rituximab in a steroid-dependent form of IgG4- related TIN and (2) the interest of DW-MRI as a non-nephrotoxic radiological and PET complementary approach not only in monitoring the effectiveness of immunosuppression but also in the early detection of renal involvement during IgG4 related disease. key words : chronic kidney diseases, renal fibrosis, membranous nephropathy, renal pathology, peritoneal dialysis, nephrolithiasis

Biography:

Aamir Jalal Al Mosawi, advisor doctor, Iraqi ministry of Health is currently the Head of Iraq Headquarter of Copernicus Scientists International Panel. He published more than 25 scientific papers in international journals and published many books and book chapters with international publishers. He joined the International Association of Pediatric Nephrology (IPNA) during the year 2000. He is the founding editor of an international peer-reviewed medical journal “The New Iraqi Journal of Medicine (2005-2013)”, and member of the World Association of Medical Editors (WAME). He also served as a member of the advisory council the International Association of Medical Colleges (IAMC).

Abstract:

The use of new dietary therapies to lower urea levels simulating dialysis procedures has been recently described and has been sometimes called intestinal or dietary dialysis. In the commonest form of this new dietary approach, the patient consumes relatively a large amount of soluble fiber. The most commonly used soluble fiber acacia gum is digested by colonic flora, thereby increasing the amount of nitrogen that is eliminated as fecal waste. When acacia fibers gum are added to a low protein diet in patients with advanced chronic kidney disease (CKD) who do not have access to dialysis, their serum BUN levels can be lowered and they experienced a decrease in uremic symptoms. In a series of 80 patients with chronic renal failure (CRF), 14 (16.5%) patients were treated with a new therapeutic dietary regimen. This new dietary regimen consists of using acacia gum as dietary supplement in addition to the traditional conservative measures used in the management of CRF. The use of this novel technology resulted in amelioration of the uremic symptoms and lowering of blood urea levels and delaying the need for dialysis. In this sample of 80 patients the longest survival of 5 years was achieved in 2 patients, both treated initially with IPD. One of them was transplanted and the other was treated with new dietary technology.

Biography:

Mustapha Bouatia is professor at department of medicine and pharmacy in Mohammed V University, Morocco

Abstract:

Biography:

Khalfaoui Mohamed Amine is a doctor at the department of Nephrology at University Hospital Ibn Rushd Casablanca, Morocco. His current speciality interests are the Nephrology-Hemodialysis and renal transplantation.

Abstract:

Introduction: The immunodeficiency, moderate in patients with chronic renal failure (IRC), explains a susceptibility greater to viral infections including viral hepatitis B, unfortunately these patients respond badly to vaccination against hepatitis B. In addition, their rate of Ac protectors decreases more rapidly than in the general population. We have studied the decay of the rate of Ac Hbs in renal failure chronic non-dialysis and vaccinated against hepatitis B. Patients and methods: We have measured the rate of Ac Hbs every 3 to 6 months in renal failure not on dialysis followed in consultation and having been vaccinated with success against hepatitis B (Ac Hbs>10 IU/ml). Result : Forty patients aged 48±11years, with creatinine clearance to 28±13ml/min which 57.5 per cent of men and 42.5 per cent of women have been followed on average 12 months (min 6 months/max 18 months). The initial nephropathy was a diabetic nephropathy in 18 patients (45 % ), the nephroangiosclerose 11 patients (27.5 % ), and finally of chronic glomerulonephrites in 7 patients (17.5 %) and 4 patients with an indeterminate nephropathy. The rate of Ac at the beginning of the follow-up was on average to 260 IU/ml . This rate declined by an average of 30 IU/ml per month. The threshold of 10 IU/ml below which patients are no longer protected was reached in 10 months on average. Among the factors studied (creatinine clearance, sex, weight, diabetes, baseline albumin, protidemie, type of nephropathy) none was predictive of the rate of reduction of the Ac. Discussion: The decrease in the rate of Ac HBS is fast among the IRC which makes necessary a serological monitoring regular all the more that nothing allows you to predict the speed of decay for a given patient. Our study allows giving an estimate of the rate of the monitoring and of the delay before a new vaccination in function of the initial rate of Ac. Conclusion: The renal disease loses their protection against hepatitis B in 12 months on average which makes the serological surveillance necessary.

Biography:

Mohamed Alqadhi is a doctor at the department of Nephrology and Urology in National Institute of Urology & Nephrology, Egypt

Abstract:

Objective: To review our 5 years’ experience with ureteroscopy treatment of distal ureteric calculi. Patients and methods: We reviewed the medical records of 136 patients who underwent ureteroscopic procedures for the treatment of distal ureteric calculi from February 2007 to October 2012. Patient and stone characteristics, treatment modality and outcome were assessed. Procedure’s duration, status “stone free” and hospital stay were also evaluated. The mean clinical and radiological follow-up period was 31.8 months for 74.2% of eligible patients. Results: The stone free rate following an initial ureteroscopy was 79.4. The ultimate success rate for stone removal after “second look” improved to 95.9%. The mean operative duration was 51 minutes. The intraoperative complication rate was 8.6%, the postoperative complication rate was 7.5%, and the mean hospital stay was 1.1 days. We could detect one ureteric stricture and one vesico-ureteric reflux (0.9% for each). A significant ureteric perforation was detected in 4.1% and ureteric perforation in 0.7% of the study group. We could find that the longer the operative duration, the greater the complications. Stone impaction and size were also found associated with higher morbidity. Conclusion: Growing skills and experience of ureteroscopy will lead to a significant increase in the success rate and also reducing serious complications.

Biography:

Bruce Hendry is President of the UK Renal Association and Emeritus Professor of Renal Medicine at King's College London. He graduated in medicine from the University of Oxford and received his PhD in Biophysics from the University of Cambridge. His major research interests are in the cell and molecular biology of progressive renalfibrosis and in the design of novel therapeutic approaches. His current work is focused on the study of new approaches to the problem of aberrant renal cell proliferation leading to fibrosis; this work includes the use of antisense and small molecule strategies. Recent work has examined the role of antisense as therapy in renal fibrosis and ADPKD and the targeting of T-type calcium channels in glomerular disease. He has clinical research interests in diabetic nephropathy, HIV and the kidney and in polycystickidney disease.

Abstract:

There is a lack of effective therapeutic options for patients with Chronic Kidney Disease (CKD) related to IgA nephropathy and proteinuric nephropathies. Treatment with inhibitors of the Renin Angiotensin System (RAS) is standard but residual risk of progression of CKD remains high. In this context this lecture will explore an innovative strategy for therapy in CKD targeting T-type calcium channels. T-Type Calcium Channels (TTCC) are closely related to the more familiar L-Type Calcium Channels (LTCC). We have extended work on the role of TTCC in smooth muscle proliferation by demonstrating that TTCC have a role in mesangial cell function. TTCC are also expression in the efferent arteriole and TTCC inhibition reduces glomerular capillary pressure. In vitro human and rat mesangial cell proliferation is dependent on TTCC and not LTCC. Moreover, in models of glomerular cell proliferation, inhibition of TTCC reduces glomerular damage, reduces cell proliferation and inhibits monocyte infiltration, with improved renal function. In parallel with this work a series of studies in Japan has demonstrated that TTCC inhibition reduces glomerular proteinuria in animal studies and in small clinical studies of diabetic nephropathy. Taken together these studies provide the basis for optimism about TTCC inhibition as a new therapy in renal diseases where mesangial cell proliferation is coupled with significant proteinuria. Such diseases include IgA Nephropathy, Diabetic Nephropathy and lupus nephritis

Biography:

Květa Bláhová is an Associate Professor in the Department of Pediatrics at Charles University and University Hospital Motol in Prague. She received many awards. She has membership in prestigious European societies. She has published numerous papers in reputed journals

Abstract:

Hemolytic-Uremic Syndrome (HUS) is the most common cause of acute renal failure in children below 3 years of age. It is defined by a triad of symptoms which associates hemolytic anemia with fragmented erythrocytes, thrombocytopenia and acute renal failure. Three types of HUS can be distinguished: typical HUS also called diarrhoea-associated (D+) HUS, atypical HUS (a-HUS/ D-HUS) and secondary HUS (drug induced, C+HUS, in patients receiving marrow transplantation, post partum etc.). The common event among these entities appears to be vascular endothelial cell injury, which induces mechanical destruction of erythrocytes, activation of platelet aggregation and local intravascular coagulation, especially in the renal microvasculature. D+ HUS represents nearly 90% of HUS in children. Evidence of exposure to Shiga toxin (STx 1, 2) producing Escherichia Coli (STEC) - also called Enterohemorrhagic Escherichia Coli (EHEC) - has been demonstrates in many countries in about 85% of cases. Recently serotypes O157:H7, O26 are the most frequent. Early and accurate supportive treatment and early start of dialysis is the major importance and allows a current mortality rate below 5%. Vital prognosis is compromised in cases with CNS or multi-visceral involvement. After 15 years or more of apparent recovery, 20% to 60% of patients have residual renal symptoms, with up to 20% having Chronic Renal Insufficiency (CRI) or End-Stage Renal Disease (ESRD). Atypical HUS represents less than 10% of HUS in children. Some of these cases (familial) are associated with low C3 levels, hereditary deficiency of factor H or with mutations in factor H gene. The deficiency of von Wille brand factor cleaving protease deficiency in D+HUS, as reported in adults with Thrombotic Thrombocytopenic Purpura (TTP), is not present.