Publications (43)140.44 Total impact
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Dataset: Lipska-KI-Suppl.Mat.1
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Dataset: Lipska-KI-Suppl.Mat.2
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Article: Association of eNOS Gene Intron 4 a/b VNTR Polymorphisms in Children with Nephrotic Syndrome.
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ABSTRACT: To investigate the association of endothelial nitric oxide synthase gene intron 4 (eNOS4) polymorphisms with nephrotic syndrome, the eNOS4 genotypes were assessed in 161 children with nephrotic syndrome in comparison with 78 healthy subjects. We classified the children with nephritic syndrome into 2 groups: as steroid-sensitive nephrotic syndrome (SSNS) (n=125) and steroid-resistant nephrotic syndrome (SRNS) (n=36). The eNOS4 polymorphisms was analyzed by polymerase chain reaction. The frequencies of eNOS4 aa, ab and bb genotypes were 3%, 31%, 66% in all the nephrotic syndrome group, and 1%, 23%, 76% in the control group (x(2)=2.87, p>0.05). In addition, the frequencies of eNOS4 aa, ab and bb genotypes were 2%, 33%, 65% in SSNS group, and 5%, 28%, 67% in the SRNS group (x(2)=1.13, p=0.567). The present study is the first to investigate eNOS4 gene polymorphisms in children with SSNS and SRNS. Our data show that the eNOS4 gene polymorphisms were not associated with the development, frequent relapse and response to steroid in nephritic syndrome.Gene 04/2013; · 2.34 Impact Factor -
Article: Genetic screening in adolescents with steroid-resistant nephrotic syndrome.
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ABSTRACT: Genetic screening paradigms for congenital and infantile nephrotic syndrome are well established; however, screening in adolescents has received only minor attention. To help rectify this, we analyzed an unselected adolescent cohort of the international PodoNet registry to develop a rational screening approach based on 227 patients with nonsyndromic steroid-resistant nephrotic syndrome aged 10-20 years. Of these, 21% had a positive family history. Autosomal dominant cases were screened for WT1, TRPC6, ACTN4, and INF2 mutations. All other patients had the NPHS2 gene screened, and WT1 was tested in sporadic cases. In addition, 40 sporadic cases had the entire coding region of INF2 tested. Of the autosomal recessive and the sporadic cases, 13 and 6%, respectively, were found to have podocin-associated nephrotic syndrome, and 56% of them were compound heterozygous for the nonneutral p.R229Q polymorphism. Four percent of the sporadic and 10% of the autosomal dominant cases had a mutation in WT1. Pathogenic INF2 mutations were found in 20% of the dominant but none of the sporadic cases. In a large cohort of adolescents including both familial and sporadic disease, NPHS2 mutations explained about 7% and WT1 4% of cases, whereas INF2 proved relevant only in autosomal dominant familial disease. Thus, screening of the entire coding sequence of NPHS2 and exons 8-9 of WT1 appears to be the most rational and cost-effective screening approach in sporadic juvenile steroid-resistant nephrotic syndrome.Kidney International advance online publication, 20 March 2013; doi:10.1038/ki.2013.93.Kidney International 03/2013; · 6.61 Impact Factor -
Dataset: Supplementary appendix
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Article: Devil's Triangle in Kidney Diseases: Oxidative Stress, Mediators, and Inflammation.
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ABSTRACT: This issue of the International Journal of Nephrology focused on kidney diseases within a devil’s triangle, oxidative stress (OS), mediators, inflammation, specifically relating to the clinical significance of identification, and prevention. Every creature in need of oxygen faces OS. It has a critical role in the molecular mechanisms of renal injury in several kidney diseases, and many complications of these diseases are mediated by OS, mediators, and inflammation. There is a complex relationship between these three; mostly they induce each other. While some of the diseases themselves can contribute to OS, reactive oxygen species (ROS) produced by activated leukocytes and endothelial cells in sites of inflammation cause tissue damage. Although inflammation looks dangerous for the organism, it is a normal reaction of organs and tissues to protect themselves against several invasion(s). It enables the immune system to remove the injurious stimuli and initiate the healing process of tissues. However, the interactions between OS, mediators, and inflammation may result in glomerular damage, proteinuria, electrolyte, and volume instabilities which cause nephron loss, on the long view. Detailed studies on this topic are included in this issue. The kidney can easily be damaged by ROS, due to the rich structure of long-chain polyunsaturated fatty acids. The article by E. Özbek summarizes the induction of OS within kidney in several conditions, including diabetes, hypertension, hypercholesterolemia, obesity, aging, urinary obstruction, environmental toxins, and molecular mechanisms of these inductions in the light of existing literature data. Diabetic nephropathy is one of the most common microvascular complications of type 1 and type 2 diabetes mellitus and the leading cause of end-stage renal disease worldwide [1]. Rojas-Rivera et al. reviewed the biological bases of oxidative stress and its role especially on diabetic nephropathy, as well as the role of the Keap1-Nrf2 pathway, and recent clinical trials targeting this pathway with bardoxolone methyl, a novel synthetic triterpenoid with antioxidant and anti-inflammatory properties. Obesity continues to be a public health problem throughout the world. Epidemiologic studies have shown that 66% of adults and 16% of children and adolescents are overweight or obese [2]. Obesity-related glomerulopathy is an increasing cause of end-stage renal diseases. J. Tang et al. stressed the chronic low-grade systemic inflammation in obesity and discussed the roles of inflammation and oxidative stress in the progression of obesity-related glomerulopathy and possible treatment modalities to prevent kidney injury in obesity, such as the usage of anti-IL-6 receptor antibody, TNF-α antagonist, adiponectin, nutritional and surgical interventions to reduce OS. Hypertension is an another important global health issue both in adults and children. It is one of the major risk factors for the progression of kidney diseases. The relationship between blood pressure and dietary sodium and salt sensitivity has been well known, and renal sodium handling is a key determinant of long-term blood pressure regulation [3]. There is a limited knowledge in the literature regarding the role of ROS-mediated fibrosis and renal proximal tubule sodium reabsorption through the Na/K-ATPase. S. Liu et al. reviewed the possible role of ROS in the regulation of Na/K-ATPase activity. The authors emphasized the importance of further researches whether ROS signaling is a link between the Na/K-ATPase/c-Src cascade and NHE3 regulation and how OS, stimulated by high salt and cardiotonic steroids, regulates Na/K-ATPase/c-Src signaling in renal sodium handling and fibrosis. Urotensin-II is the most potent mammalian vasoconstrictor identified to date, almost tenfold more potent than endothelin-I [4]. A. Balat and M. Büyükçelik discussed the role of urotensin-II on renal hemodynamics and its possible role on several kidney diseases, such as the minimal change nephrotic syndrome. The article includes a detailed discussion of urotensin-II immunoreactivity in renal biopsy specimens of children with membranoproliferative glomerulonephritis, membranous nephropathy, IgA nephropathy, Henoch-Schonlein nephritis, and focal segmental glomerulosclerosis. Because of its complex relation with OS and other mediators, authors describe it as “more than a mediator” in glomerular diseases. They briefly mention from the effectiveness of U-II antagonism, as a new promising pharmacological treatment target in some kidney diseases. Given the potential impact of OS, mediators, and inflammation trio, the importance of prevention has come into question. Strong evidence indicates the importance of new molecules that are able to diminish them which in turn may help to decrease the prevalence and/or progression of several kidney diseases. Therefore, further researches are needed to the better understanding of the molecular and clinical mechanisms of this triad. They may help to provide new therapeutical strategies to control several complications in patients with kidney diseases.International journal of nephrology. 01/2012; 2012:156286. -
Article: The Cardiovascular Comorbidity in Children with Chronic Kidney Disease (4C) study: objectives, design, and methodology.
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ABSTRACT: Children and adolescents with chronic kidney disease (CKD) are at high risk for cardiovascular morbidity and mortality. A systemic arteriopathy and cardiomyopathy has been characterized in pediatric dialysis patients by the presence of morphologic and functional abnormalities. The Cardiovascular Comorbidity in Children with CKD (4C) Study is a multicenter, prospective, observational study aiming to recruit more than 600 children, aged 6 to 17 years, with initial GFR of 10 to 45 ml/min per 1.73 m(2). The prevalence, degree, and progression of cardiovascular comorbidity as well as its association with CKD progression will be explored through longitudinal follow-up. The morphology and function of the heart and large arteries will be monitored by sensitive noninvasive methods and compared with aged-matched healthy controls. Multiple clinical, anthropometric, biochemical, and pharmacologic risk factors will be monitored prospectively and related to the cardiovascular status. A whole-genome association study will be performed to identify common genetic variants associated with progression of cardiovascular alterations and/or renal failure. Monitoring will be continued as patients reach end-stage renal disease and undergo different renal replacement therapies. While cardiovascular morbidity in adults is related to older age and additional risk factor load (e.g., diabetes), the role of CKD-specific factors in the initiation and progression of cardiac and vascular disease are likely to be characterized with greater sensitivity in the pediatric age group. The 4C study is expected to provide innovative insight into cardiovascular and renal disease progression in CKD.Clinical Journal of the American Society of Nephrology 09/2010; 5(9):1642-8. · 5.23 Impact Factor -
Article: Strict blood-pressure control and progression of renal failure in children.
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ABSTRACT: Although inhibition of the renin-angiotensin system delays the progression of renal failure in adults with chronic kidney disease, the blood-pressure target for optimal renal protection is controversial. We assessed the long-term renoprotective effect of intensified blood-pressure control among children who were receiving a fixed high dose of an angiotensin-converting-enzyme (ACE) inhibitor. After a 6-month run-in period, 385 children, 3 to 18 years of age, with chronic kidney disease (glomerular filtration rate of 15 to 80 ml per minute per 1.73 m(2) of body-surface area) received ramipril at a dose of 6 mg per square meter of body-surface area per day. Patients were randomly assigned to intensified blood-pressure control (with a target 24-hour mean arterial pressure below the 50th percentile) or conventional blood-pressure control (mean arterial pressure in the 50th to 95th percentile), achieved by the addition of antihypertensive therapy that does not target the renin-angiotensin system; patients were followed for 5 years. The primary end point was the time to a decline of 50% in the glomerular filtration rate or progression to end-stage renal disease. Secondary end points included changes in blood pressure, glomerular filtration rate, and urinary protein excretion. A total of 29.9% of the patients in the group that received intensified blood-pressure control reached the primary end point, as assessed by means of a Kaplan-Meier analysis, as compared with 41.7% in the group that received conventional blood-pressure control (hazard ratio, 0.65; confidence interval, 0.44 to 0.94; P=0.02). The two groups did not differ significantly with respect to the type or incidence of adverse events or the cumulative rates of withdrawal from the study (28.0% vs. 26.5%). Proteinuria gradually rebounded during ongoing ACE inhibition after an initial 50% decrease, despite persistently good blood-pressure control. Achievement of blood-pressure targets and a decrease in proteinuria were significant independent predictors of delayed progression of renal disease. Intensified blood-pressure control, with target 24-hour blood-pressure levels in the low range of normal, confers a substantial benefit with respect to renal function among children with chronic kidney disease. Reappearance of proteinuria after initial successful pharmacologic blood-pressure control is common among children who are receiving long-term ACE inhibition. (ClinicalTrials.gov number, NCT00221845.)New England Journal of Medicine 10/2009; 361(17):1639-50. · 53.30 Impact Factor -
Article: Urinary annexin V in children with nephrotic syndrome: a new prognostic marker?
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ABSTRACT: Annexin V has a molecular weight of 32-35 kDa and has been reported to possess anticoagulant activity, inhibition of phospholipase A(2), regulation of membrane transport, proliferation and signal transduction. It is reported that urinary annexin V concentration may be an indicator of apoptosis and acute renal injury related to the urinary protein level. The aim of this study was to define the role of urinary annexin V excretion and serum annexin V concentrations as new prognostic tools and follow-up criteria in children with steroid-sensitive (SSNS) and steroid-resistant nephrotic syndrome (SRNS). Annexin V concentrations were measured in serum and 24-h urine samples in 23 SSNS patients in both relapse and remission periods of each patient and in 22 SRNS patients and 22 healthy controls. Total protein, albumin, blood urea nitrogen (BUN), creatinine, total cholesterol concentrations, and 24-h urinary excretion of protein and creatinine were also measured in each patient. In the SRNS group, median 24-h urinary annexin V levels were significantly higher than for all other groups (5,048.8 ng/g creatinine vs. 2,839.5 ng/g creatinine in SSNS relapse group; 2,500.0 ng/g creatinine in SSNS remission group, and 2,018.3 ng/g creatinine in healthy control group). No significant correlation was found between urinary protein excretion and 24-h urinary annexin V levels in all subjects. Twenty-four-hour urinary annexin V excretion may be a predictor in children with SRNS, and it may be a prognostic marker in children with NS.Pediatric Nephrology 02/2008; 23(1):79-82. · 2.52 Impact Factor -
Article: NPHS2 (podicin) mutations in Turkish children with idiopathic nephrotic syndrome.
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ABSTRACT: The podocin (NPHS2) gene encodes podocin protein, which has an important role in glomerular ultrafiltration and controlling slit membrane permeability. The detection of an NPHS2 mutation affects the treatment plan for children with nephritic syndrome (NS). The frequency and spectrum of podocin mutations in the Turkish population have remained largely unknown. The aim of this study was to screen for podocin mutations in Turkish patients with steroid-resistant NS (SRNS) and to compare it with other published series. There were 295 children with SRNS, originating from Turkey, included in this study. Forty-one patients (13.8%) had familial NS and 254 patients (86.2%) had sporadic NS. Mutation analysis was performed in all eight exons of the NPHS2 gene with the direct DNA sequencing method. There were 53 different pathogenetic NPHS2 mutations detected, including 37 novel mutations. The mutation detection rate was 24.7% for all patients, 29.2% for familial, and 24% for sporadic SRNS. The most common mutated exon was exon 5 (52 allele). The presence of mutations in exon 4 was found to increase the risk of end-stage renal disease (ESRD). Among patients with mutations, the rates of renal failure and/or ESRD (26%) were significantly higher than in those without mutations (12.6%). The mean time of progression to renal failure and ESRD in patients with mutations (1.8 +/- 2.5 years) was significantly shorter than in patients without mutations (3.7 +/- 4.0 years). Additionally, in patients with heterozygote mutations, fewer cases (13.6%) progressed to renal failure and/or ESRD than in with patients who had homozygote/compound heterozygote mutations (31.3%). In conclusion, podocin mutations are responsible for some of both familial and sporadic SRNS cases in Turkey. The mutations in this gene should be searched for in every child after presentation with the first episode of NS.Pediatric Nephrology 01/2008; 22(12):2031-40. · 2.52 Impact Factor -
Article: Ambulatory blood pressure monitoring and renal functions in children with a solitary kidney.
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ABSTRACT: The aim of this study is to investigate the blood pressure (BP) profile, microalbuminuria, renal functions, and relations with remaining normal kidney size in children with unilateral functioning solitary kidney (UFSK). Sixty-six children with UFSK were equally divided into three groups: unilateral renal agenesis (URA), unilateral atrophic kidney (UAK), and unilateral nephrectomy (UNP). Twenty-two age-, weight-, and height-matched healthy children were considered as a control group. The serum creatinine level and first-morning urine microalbumin and creatinine concentrations were determined by the standard methods. Also, the BP profile was determined by ambulatory blood pressure monitoring (ABPM). We found that the serum creatinine level was higher and creatinine clearance was lower in each patient groups compared to those of the control group (p < 0.05). Compared with the controls, each group of patients had mean office, 24-h, daytime, and night-time systolic and diastolic BP values similar to those of the controls (p > 0.05). An inverse correlation was found between the renal size standard deviation scores (SDS) of normal kidneys and 24-h systolic and diastolic BP load SDS in all of the patients (p < 0.05; r = -0.372, r = -0.295, respectively). The observed relationship between renal size SDS and 24-h mean arterial pressure (MAP), systolic and diastolic BP load SDS suggests that children with UFSK should be evaluated by using ABPM for the risk of hypertension.Pediatric Nephrology 04/2007; 22(4):559-64. · 2.52 Impact Factor -
Article: Childhood vasculitides in Turkey: a nationwide survey.
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ABSTRACT: The aims of this study were to evaluate the characteristics of childhood vasculitides and to establish the first registry in Turkey, an eastern Mediterranean country with a white population. A questionnaire was distributed to the main referral centers asking for the registration of the Henoch-Schönlein purpura (HSP) patients in the last calendar year only and 5 years for other vasculitides. Demographic, clinical, and laboratory data were assessed. Vasculitic diseases were registered from 15 pediatric centers. These centers had a fair representation throughout the country. In the last calendar year, incidences were as follows: HSP 81.6%, Kawasaki disease (KD) 9.0%, childhood polyarteritis nodosa (C-PAN) 5.6%, Takayasu arteritis (TA) 1.5%, Wegener's granulomatosis 0.4%, and Behçet disease 1.9%. There was no clear gender dominance. The mean age was 11.05+/-4.89 years. Acute phase reactants were elevated in almost all, highest figures being in C-PAN. Renal involvement was present in 28.6% of HSP and 53% of the C-PAN patients. Abdominal aorta was involved in all TA patients. Among the C-PAN patients, 25% had microscopic PAN with necrotizing glomerulonephritis; antineutrophil cytoplasmic antibody was positive in those who were studied. Among the patients, 12.5% and 15% had classic PAN and cutaneous PAN, respectively. The remaining majority were classified as systemic C-PAN diagnosed with biopsies and/or angiograms demonstrating small to midsize artery involvement. The overall prognosis was better than reported in adult series. This is the largest multicenter study defining the demographic data for childhood vasculitides. The distribution of childhood vasculitides was different in our population where KD is much less frequent, whereas HSP constitutes an overwhelming majority. C-PAN was more frequent as well.Clinical Rheumatology 03/2007; 26(2):196-200. · 2.00 Impact Factor -
Article: Changes in osmolal gap and osmolality in children with chronic and end-stage renal failure.
Nephron Physiology 02/2007; 105(2):p19-21. · 2.55 Impact Factor -
Article: Reduced systolic myocardial function in children with chronic renal insufficiency.
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ABSTRACT: Increased left ventricular (LV) mass in children with chronic renal insufficiency (CRI) might be adaptive to sustain myocardial performance in the presence of increased loading conditions. It was hypothesized that in children with CRI, LV systolic function is impaired despite increased LV mass (LVM). Standard echocardiograms were obtained in 130 predialysis children who were aged 3 to 18 yr (59% boys) and had stages II through IV chronic kidney disease and in 130 healthy children of similar age, gender distribution, and body build. Systolic function was assessed by measurement of fractional shortening at the endocardial (eS) and midwall (mS) levels and computation of end-systolic stress (myocardial afterload). The patients with CRI exhibited a 6% lower eS (33.1 +/- 5.5 versus 35.3 +/- 6.1%; P < 0.05) and 10% lower mS (17.8 +/- 3.1 versus 19.7 +/- 2.7%; P < 0.001) than control subjects in the presence of significantly elevated BP, increased LVM, and more concentric LV geometry. Whereas the decreased eS was explained entirely by augmented end-systolic stress, mS remained reduced after correction for myocardial afterload. The prevalence of subclinical systolic dysfunction as defined by impaired mS was more than five-fold higher in patients with CRI compared with control subjects (24.6 versus 4.5%; P < 0.001). Systolic dysfunction was most common (48%) in patients with concentric hypertrophy and associated with lower hemoglobin levels. CRI in children is associated with impaired intrinsic LV contractility, which parallels increased LVM.Journal of the American Society of Nephrology 02/2007; 18(2):593-8. · 9.66 Impact Factor -
Article: Endothelial nitric oxide synthase gene intron 4 a/b VNTR polymorphism in children with APSGN.
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ABSTRACT: The role of endothelial nitric oxide synthase gene intron 4 a/b (eNOS4a/b) variable number of tandem repeats (VNTR) polymorphism in various renal diseases was investigated. We investigated whether the eNOS4a/b VNTR polymorphism is associated with susceptibility to acute poststreptococcal glomerulonephritis (APSGN) and its clinical features. Endothelial NOS4a/b VNTR polymorphism is determined by the polymerase chain reaction in 60 children with APSGN, and 66 healthy controls. The genotype distribution of eNOS4 does not differ between the patients and the controls (X(2)=5.1, p=0.079). However, the frequency of eNOS4a (eNOS4a/a and eNOS4a/b) genotype is higher in the patients than in the controls (X(2)=4.5, p=0.046). In the APSGN group we performed renal biopsy on eight patients because of nephrotic syndrome accompanies acute nephritic syndrome or glomerular filtration rate (GFR) is lower than 50% of normal, and found that to carry a/a and a/b genotypes were a significant risk factor for this type presentation (OR=17.3, 95% CI:1.95-152.67, p=0.03). Mean serum creatinine values are found statistically significantly higher in a/a and a/b genotypes when compared with b/b genotypes (p=0.022). Children carrying the "aa" and "ab" genotype or "a" allele of eNOS4 have a greater tendency to develop and clinical presentation of APSGN.Pediatric Nephrology 12/2006; 21(11):1661-5. · 2.52 Impact Factor -
Article: ACE gene polymorphism in Turkish children with nephrotic syndrome.
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ABSTRACT: Since 1990, the role of angiotensin converting enzyme (ACE) gene polymorphism in various renal and cardiac diseases is still debated. This study comprised 71 pediatric patients with nephrotic syndrome, 47 males (66%) and 24 females (34%) with a mean age of 57.4 +/- 37.6 months, and a control group of 83 healthy males (59%) and 57 healthy females (41%) with a mean age of 505 +/- 160.5 months. The distribution of the ACE genotype in the control group was II, 11%; ID, 53%; and DD, 36%, and the nephrotic syndrome was II, 4%; ID, 78%; and DD, 18%. Angiotensin-converting enzyme genotypes were significantly different between patients and control groups (p<0.05). The study groups consisted of 52 (73%) with steroid-sensitive nephrotic syndrome (SNSS) and 19 (27%) with steroid-resistant nephrotic syndrome (SRNS). The distribution of the ACE genotype was II, 6%; ID, 75%; and DD, 19% in the SSNS population and ID, 84% and DD, 16% in the SRNS population. No statistically significant difference was found between steroid sensitivity and ACE genotypes (p=0.5). The results show that ACE I/D polymorphism does not contribute to the steroid resistance, even though this study indicates that the presence of the I/D genotype has a much higher risk--approximately 2.8 times--of having nephrotic syndrome. Further studies with a larger number of patients are needed.Renal Failure 02/2006; 28(5):401-3. · 0.82 Impact Factor -
Article: An unusual cause of pleural effusion, urinothorax in a child with urinary stone disease.
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ABSTRACT: The association of obstructive uropathy with ascites has been known since 1863 and with pleural effusion since 1954. Urinothorax is a rare complication of blunt renal trauma, ureteral instrumentation or ureteral surgery. Leakage from the urinary tract may cause urinoma, retroperitoneal collection of fluid, which can lead to urinothorax. This case report describes a child with a massive right-sided pleural effusion that was caused by same-sided renal calculi. The effusion disappeared within a few days after adequate urinary drainage had been established.Pediatric Nephrology 11/2005; 20(10):1487-9. · 2.52 Impact Factor -
Article: Acute renal failure after overdose of colloidal bismuth subcitrate.
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ABSTRACT: Bismuth salts are widely used to treat peptic ulcers. Acute toxicity with colloidal bismuth subcitrate overdose causes nephrotoxicity. There have been numerous reports of encephalopathy after long-term consumption of bismuth salts, but only a few cases of nephrotoxicity (adult and pediatric) have been documented to date. This report presents a case of acute renal failure due to colloidal bismuth subcitrate overdose in adolescent. A 16-year-old girl presented with complaints of nausea, vomiting, and facial paresthesia. Ten days earlier she had tried to commit suicide by taking 60 tablets of De-nol (colloidal bismuth subcitrate 18 g). The physical examination findings on admission indicated minimal fluid overload but no signs of encephalopathy. Laboratory tests on admission showed blood urea nitrogen 102 mg/dl, serum creatinine 19.9 mg/dl, and serum bismuth level 495 microg/l. The patient was started on appropriate fluid therapy and penicillamine as a chelating agent and then began hemodialysis on alternate days. The patient's renal function gradually returned to normal over 9 weeks and by 64 days after the overdose her serum bismuth level had fallen to almost half the level detected 2 days after admission. The patient made a complete recovery. The case demonstrates that acute renal failure can develop as a manifestation of acute toxicity from colloidal bismuth ingestion, and that the prognosis may be favorable if the patient receives appropriate supportive treatment and dialysis.Pediatric Nephrology 10/2005; 20(9):1355-8. · 2.52 Impact Factor -
Article: Aggressive angiomyxoma in a child with chronic renal failure.
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ABSTRACT: Aggressive angiomyxoma (AAM) is a rare and nonmetastasizing soft-tissue tumor predominantly found in the female pelvis and perineum. It has a high risk of local recurrence. We report the unusual case of a 15-year-old boy with an AAM presenting as a slowly enlarging scrotal mass. The patient had had chronic renal failure since 1997 and had needed hemodialysis for the previous 11 months. He presented with a 12-month history of a nontender soft mass in the right scrotum. Ultrasound examination revealed a solid mass in the scrotum. After surgical resection, pathological analysis disclosed spindle-shaped neoplastic cells widely separated by a myxoid stroma rich in collagen fibers and prominent irregularly shaped blood vessels; the histological examination confirmed an AAM.Pediatric Surgery International 08/2005; 21(7):563-5. · 1.25 Impact Factor -
Article: Glycosaminoglycans in childhood urinary tract infections.
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ABSTRACT: It has been suggested that urinary glycosaminoglycans (GAGs) form a natural defense mechanism against urinary tract infections (UTIs). This study investigated whether urinary GAGs play a role in pediatric UTIs, and whether urinary GAG level can be used to differentiate upper UTI from lower UTI. Forty-one children with UTIs (33 girls and eight boys; mean age 5.4+/-3.7 years) and 46 age- and sex-matched healthy children (35 girls and 11 boys; mean age 6.6+/-3.9 years) were included in the study. Urinary GAG levels were measured at the onset of acute infection and after a 10-day course of antibiotic treatment. Group GAG findings were compared, and comparisons were also made with the patients divided according to sex and according to UTI type (upper versus lower). The mean urinary GAG level in the patient group at the onset of acute infection (pretreatment) was significantly higher than the mean level in the control group (132.2+/-104.8 mg/g vs 42.2+/-27.1 mg/g creatinine, respectively; P <0.01). In the patient group, the mean urinary GAG level after antimicrobial therapy was significantly lower than the pretreatment level (75.9+/-52.1 mg/g vs 132.2+/-104.8 mg/g creatinine, respectively; P <0.01). However, the mean post-treatment level was still higher than the mean level in the controls ( P <0.05). There was no significant difference in urinary GAG levels when patients were categorized as upper versus lower UTI ( P >0.05). The study results suggest that GAGs play an important role in the pathogenesis of UTIs in children, and that measurement of urinary GAGs may be a valuable noninvasive method for evaluating UTIs in this patient group. However, this assay cannot be used to differentiate upper UTI from lower UTI in children.Pediatric Nephrology 08/2005; 20(7):937-9. · 2.52 Impact Factor
Top co-authors
Top Journals
Institutions
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2013
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Universität Heidelberg
Heidelberg, Baden-Wuerttemberg, Germany
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1998–2013
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Çukurova Üniversitesi
- • Division of Pediatric Urology
- • Department of Nuclear Medicine
Adana, Adana, Turkey
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2002–2012
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University of Gaziantep
- Division of Pediatric Nephrology
Gaziantep, Gaziantep, Turkey
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2010
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Charité Universitätsmedizin Berlin
- Department of Pediatrics, Division of Nephrology
Berlin, Land Berlin, Germany
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2007
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Università degli Studi di Napoli Federico II
Portici, Campania, Italy
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