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Stefanovic V.,Institute of Nephrology | Polenakovic M.,Macedonian Academy of Science and Arts | Toncheva D.,Medical University-Sofia
Pathologie Biologie | Year: 2011

Balkan endemic nephropathy (BEN), a familial chronic tubulo-interstitial disease with a slow progression to terminal renal failure, affects people living in the alluvial plains along the tributaries of the Danube River. One of its most peculiar characteristics is a strong association with upper urothelial cancer. An increased incidence of upper urinary tract (UUT) transitional cell cancer (TCC) was discovered among the inhabitants of endemic settlements and in families affected by BEN. In areas where BEN is endemic, the incidence of upper tract TCC is significantly higher, even 100 times, than in non-endemic regions. A high incidence of urothelial cancer in end-stage BEN patients strongly suggests preventive nephro-ureterectomy in all end-stage patients with BEN treated with either transplantation or dialysis. Better understanding of the molecular mechanisms involved in carcinogenesis and tumor progression, has provided a large number of molecular markers of TCC, with a potential diagnostic and prognostic value. Markers that distinguish among TCC, normal urothelium, and benign urothelial conditions are potentially diagnostic, prognostic, and therapeutic targets. The geographic correlation and presence of AA-DNA adducts in both BEN and associated urothelial cancer, support the speculation that these diseases share a common etiology. Dietary exposure to AA is a significant risk factor for BEN and its attendant transitional cell cancer. These are cases of well-known AA induced urothelial carcinoma, and could be detected worldwide. The presence of more than one risk factors is possible and it is important to test etiological hypotheses in different endemic foci, preferably as a multicentric research. © 2009 Elsevier Masson SAS.


Pletinck A.,Ghent University | Consoli C.,Institute of Nephrology | Van Landschoot M.,Ghent University | Steppan S.,Fresenius Medical Care Germany | And 4 more authors.
Nephrology Dialysis Transplantation | Year: 2010

Background. Dietary salt intake has been linked to hypertension and cardiovascular disease through volume-mediated effects. Accumulating evidence points to direct negative influence of salt intake independent of volume overload, such as cardiac and renal fibrosis, mediated through transforming growth factor beta (TGF-β). Epithelial-to-mesenchymal transition (EMT) has been implicated as a key process in chronic fibrotic diseases, such as chronic kidney disease or heart failure. The potential role of dietary salt intake on cell transdifferentiation has never been investigated. This study analysed the effect of dietary salt intake on EMT and fibrosis in the peritoneal membrane (PM) in a rat model.Methods. Twenty-eight Wistar rats were randomized to a normal salt (NS) or a high salt (HS) intake. NS and HS rats had free access to tap water or NaCl 2% as drinking water, respectively. After 2 weeks, samples of peritoneum were taken, and TGF-β1, Interleukin 6 (IL-6) and vascular endothelial growth factor (VEGF) mRNA expression were quantified with qRT-PCR. Fibrosis and submesothelial PM thickness were scored. EMT was evaluated using fluorescence staining with cytokeratin and alpha smooth muscle actin (α-SMA).Results. Dietary salt intake caused peritoneal fibrosis and thickening of the submesothelial layer and induced EMT as identified by colocalization of cytokeratin and α-SMA in cells present in the submesothelial layer. Peritoneal TGF-β1 and IL-6 mRNA expression were upregulated in the HS group.Conclusion. High dietary salt intake induces EMT and peritoneal fibrosis, a process coinciding with upregulation of TGF-β1. © The Author 2009. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.


PubMed | Tel Aviv University, Institute of Nephrology and Pediatric Infectious Disease Unit
Type: | Journal: Acta paediatrica (Oslo, Norway : 1992) | Year: 2017

This study investigated the under-researched area of annual influenza vaccination rates in children with chronic kidney disease and identified reasons for non-immunisation.A prospective cross-sectional study was conducted in the nephrology clinic and dialysis unit of a tertiary paediatric medical centre from August to October 2011 and September to October 2012. Parents were asked to complete a questionnaire on their childs immunisation against influenza.Of the 217 children studied, 45.6% were vaccinated against influenza. The major reason for non-immunisation was because the parents had not received the necessary information from the primary physician or treating nephrologist. The non-vaccinated children were significantly more likely to be less than two years old and female and to have parents who did not believe in the benefits of vaccination (p<0.05). Of the parents who did not vaccinate their child, 38% claimed they would have done so if the vaccine had been offered in the nephrology clinic.Children with kidney disease had a higher annual influenza vaccination rate than the general population, but it was still suboptimal. Nephrologists should be alerted to the need to provide parents with information on influenza vaccinations and they should be available in nephrology clinics. This article is protected by copyright. All rights reserved.


Kaidar M.,Schneider Children Medical Center | Kaidar M.,Institute of Nephrology | Berant M.,Schneider Children Medical Center | Krauze I.,Schneider Children Medical Center | And 4 more authors.
Pediatric Transplantation | Year: 2014

Cardiovascular-related mortality is 100-fold higher in pediatric renal transplant recipients than in the age-matched general population. Seventy-seven post-renal transplant children's charts were reviewed for cardiovascular risk factors at two and six months after transplantation (short term) and at two yr after transplantation and the last follow-up visit (mean 7.14 ± 3.5 yr) (long term). Significant reduction was seen in cardiovascular risk factors prevalence from two months after transplantation to last follow-up respectively: Hypertension from 52.1% to 14%, hypercholesterolemia from 48.7% to 33%, hypertriglyceridemia from 50% to 12.5%, anemia from 29.6% to 18.3%, hyperparathyroidism from 32% to 18.3% and hyperglycemia from 11.7% to 10%, and left ventricular hypertrophy from 25.8% at short term to 15%. There was an increase in the prevalence of obesity from 1.5% to 3.9% and of CKD 3-5 from 4.75% to 24%. The need for antihypertensive treatment decreased from 54% to 42%, and the percentage of patients controlled by one medication rose from 26% to 34%, whereas the percentage controlled by 2, 3, and 4 medications decreased from 21.9%, 5.5%, and 1.4% to 6%, 2%, and 0. Children after renal transplantation appear to have high rates of cardiovascular risk factors, mainly on short-term follow-up. © 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.


Vasilescu C.,Fundeni Institute of Digestive Disease and Liver Transplantation | Tudor S.,Fundeni Institute of Digestive Disease and Liver Transplantation | Popa M.,Fundeni Institute of Digestive Disease and Liver Transplantation | Aldea B.,Bucharest Institute of Oncology | Gluck G.,Institute of Nephrology
Surgical Laparoscopy, Endoscopy and Percutaneous Techniques | Year: 2011

Objective: We present an entirely robotic total pelvic exenteration and extended lymphadenectomy with "barreled ureterocutaneostomy" and end colostomy for recurrent endometrial cancer. In 1948, Brunschwig first described a pelvic exenteration as treatment of advanced recurrent malignancy in the pelvis. Currently it represents the only potentially curative option for patients with recurrent endometrial cancer. Methods: A 69-year-old female with perineal recurrence invading urethral and vaginal walls, lower rectum and anal sphincter was the perfect candidate for total pelvic exenteration. Results: Total operative time was 250 minutes, with a console time of 175 minutes. The estimated blood loss was 365 mL. Conclusions: Good oncological results are expected after robotic total pelvic exenteration owing to the accurate, precise dissection and the extension of lymphadenectomy in the narrow space of the deep pelvis similar to robotic prostatectomy and total mesorectal excision. Copyright © 2011 by Lippincott Williams & Wilkins.


PubMed | Beilinson Hospital, Institute of Nephrology, Western Galilee Hospital, Tel Aviv University and 2 more.
Type: Journal Article | Journal: Clinical transplantation | Year: 2016

From 1982 to 2011, 53 kidney transplantations (KT) for pediatric focal segmental glomerulosclerosis (FSGS) were recorded in the National Israeli Kidney Transplant Registry (NIKTR): 22-primary (1) FSGS, 25-proved/suspected genetic-secondary (2) FSGS, six lost/incomplete files/other. Half (56%) of 23 patients with 2 FSGS were Israeli-Arabs vs 29% of 1 FSGS KT recipients. 1 FSGS recurrence occurred in 64% (14/22) of 22 KT in 17 patients aged (median) 14years vs 1/25 of 2 FSGS (P<.001). Early graft days/nonfunction occurred in 9/14 (64%), 2/8 (25%) and 2/25 (4%) of recurrent 1 FSGS (rFSGS), nonr1 FSGS and 2 FSGS, respectively. Twelve biopsies performed in nine of these grafts at (median) 8days (range 5-60days) post-KT showed: ATN-5, suspected rejection-4, rFSGS-2, normal kidney-1; rFSGS was diagnosed eventually in 8/9. Dialysis need during the first month post-KT was significantly associated with FSGS recurrence: 6/14 (43%) for rFSGS vs 2/8 (25%) for non-rFSGS. Plasmapheresis (PP) achieved complete and partial rFSGS remission in 5/9 and 2/9 grafts, respectively. Three grafts were excised during the first 60days post-KT for: nonfunction (1) and bleeding (2). Remaining grafts GFR was: 78, 42, and 91mL/min (median) at 5.3, 4.75, and 8years follow-up for non-rFSGS, rFSGS, and 2 FSGS grafts, respectively.Early PP implementation should be considered after KT for 1 FSGS patients with early graft dysfunction despite delayed proteinuria and nonspecific biopsy.


Alfandary H.,Institute of Nephrology | Davidovits M.,Institute of Nephrology | Davidovits M.,Tel Aviv University
Pediatric Nephrology | Year: 2015

Background: Idiopathic membranoproliferative glomerulonephritis (MPGN) is a rare disease, accounting for 3–5 % of all cases of primary nephritic syndrome. We report an uncommon case of familial MPGN type I associated with a new mutation in the complement factor H gene (CFH). Methods: Clinical data were collected on three siblings with known factor H deficiency who presented with MPGN. All underwent immunological and genetic assays. Their parents and ten healthy adults served as controls for the DNA analysis. Results: All three children presented with recurrent episodes of hematuria and proteinuria, the youngest starting at age 5 months. One child currently has nephrotic syndrome and end-stage renal disease. All of the children were found to be homozygous for a C.262C > A (p.Pro88Thr) mutation in exon 3 of CFH that is associated with a quantitative/functional deficiency of factor H. The parents of the three siblings were found to be heterozygous for the mutation. None of the controls carried this mutation. Conclusions: Different mutations in CFH may be responsible for different glomerular diseases, including MPGN type I. A modifier gene or an environmental trigger may contribute to this phenotype–genotype discrepancy. Understanding the role of the alternative complement pathway in this disease would allow us to offer these patients more targeted therapy, including a clinical trial of eculizumab. © 2015, IPNA.


Kolesnyk I.,Institute of Nephrology | Noordzij M.,University of Amsterdam | Kolesnyk M.,Institute of Nephrology | Kulyzky M.,Institute of Nephrology | Jager K.J.,University of Amsterdam
Clinical Kidney Journal | Year: 2014

BackgroundLittle is known about the status of renal replacement therapy (RRT) in the post-Soviet countries. We therefore investigated the epidemiology and treatment outcomes of RRT in Ukrainian patients and put the results into an international perspective.MethodsData from the Ukrainian National Renal Registry for patients on RRT between 1 January 2010 and 31 December 2012 were selected. We calculated the incidence and prevalence of RRT per million population (pmp) and the 3-, 12-and 24-month patient survival using the Kaplan-Meier method and Cox regression.ResultsThere were 5985 prevalent patients on RRT on 31 December 2012 (131.2 pmp). Mean age was 46.5 ± 13.8 years, 56 men and 74 received haemodialysis (HD), while peritoneal dialysis and kidney transplantation both represented 13. The most common cause of end-stage renal disease was glomerulonephritis (51), while only 12 had diabetes. In 2012, 1129 patients started dialysis (incidence 24.8 pmp), with 80 on HD. Mean age was 48 ± 14 years, 58 men and 20 had diabetes. Three, 12-and 24-month patient survival on dialysis was 95.1, 86.0 and 76.4, respectively. The transplant rate in 2012 was 2.1 pmp.ConclusionsThe incidence and prevalence of RRT and the transplantation rate in Ukraine are among the lowest in Europe, suggesting that the need for RRT is not being met. Strategies to reduce the RRT deficit include the development and improvement of transplantation and home-based dialysis programmes. Further evaluation of the quality of Ukrainian RRT care is needed. © 2014 The Author 2014.


ABSTRACT: To investigate whether myofibrillogenesis regulator 1 (MR-1) attenuates renal ischemia/reperfusion (I/R) injury via inhibiting phosphorylated Akt (p-Akt) mitochondrial translocation-mediated opening of the mitochondrial permeability transition pore (mPTP), we injected adenovirus containing MR-1 gene or its siRNAs to the left kidney subcapsular areas of Sprague-Dawley rats, which subsequently underwent experimental renal I/R injury. Renal functions and the severity of the tubular injury were evaluated by the serum creatinine and blood urea nitrogen levels and the pathological scores. We also examined the mitochondrial morphology and functions. Total/p-Akt were assessed by western blot using the mitochondrial and the cytosolic fractions of cortex of renal tissue, respectively. We found that mitochondrial and cytosolic MR-1 levels and mitochondrial p-Akt decreased, and cytosolic p-Akt increased after reperfusion. Subcapsular injection of adenovirus led to higher MR-1 expression in the mitochondria/cytosol, inhibited mPTP opening, and alleviated renal I/R injury; adenovirus injection also up-regulated mitochondrial total and p-Akt levels more prominently compared to the normal saline (NS) group. Subcapsular injection of MR-1 siRNAs significantly lowered MR-1 expression and induced renal injury, with increased mPTP opening and mitochondrial damage, similar to I/R injury. MR-1 interacted with Akt in renal cortex homogenate. Wortmannin, a phosphatidylinositol 3 kinase (PI3K) inhibitor, abolished both mitochondrial p-Akt recruitment and the protective effect of MR-1 overexpression on I/R injury. To conclude, MR-1 protects kidney against I/R injury through inhibiting mPTP opening and maintaining mitochondrial integrity, through the recruitment of PI3K-dependent p-Akt to the mitochondria. MR-1 could be a new therapeutic strategy for renal I/R injury. © 2016 by the Shock Society


Yamamoto T.,Institute of Nephrology
Advances in Chronic Kidney Disease | Year: 2010

Databases which are useful for proteomic analysis of human kidney tissue and urine have been discussed in this article. Integration of the gene-centric and protein-centric general databases with those of human kidney tissue and urine proteomes may open a new window for research in nephrology. Proteins present in the kidney and urine provide basic tools for investigation of kidney function and disease. By comparing such databases between the healthy and diseased populations, we may be able to identify the following: proteins involved in the development of renal disease, proteins involved in progression of CKD, or new biomarker candidate proteins for either the development of renal disease or the progression of CKD. © 2010 National Kidney Foundation, Inc.

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