Is Urinary Tumor Necrosis Factor Alpha a Predictor of Urological Abnormality in Children?

Introduction: The role of urinary Tumor Necrosis Factor Alpha (TNF-α) in the diagnosis and treatment of different disorders has been evaluated recently. This study was conducted to evaluate the correlation of urinary TNF-α with urological abnormalities in pediatric pyelonephritis.Materials and Methods: This prospective study was conducted on children with acute pyelonephritis. Urine samples were tested for TNF-α (ELISA colorimetric, SANQUINE, USA) and creatinine in study group. Renal ultrasonography and voiding cystoureterography were performed in all patients, as well.Results: One hundred pyelonephritic patients were enrolled in the study. Urinary TNF-α/Cr was in an abnormal range in 91.9% of the patients. This query revealed a significant correlation between urinary TNF-alpha and kidney ultrasound results (r=0.59) and grading of reflux in voiding cystoureterography (r=0.128). Furthermore, our study showed a significant difference between the level of urinary TNF-α/Cr in patients with and without abnormality on kidney ultrasonography (p value < 0.000).Conclusions: The results of this study indicate the efficacy of urinary TNF-α in detection of inflammatory disorders such as pyelonephritis and pediatric urological abnormalities.  Keywords: Tumor Necrosis Factor-alpha; Urologic Diseases; Child

Persistent Left Superior Vena Cava in a Hemodialysis Patient

We report a case of end-stage renal disease with a persistent left superior vena cava (PLSVC) after placement of hemodialysis (HD) catheter through the left internal jugular vein as revealed on routine post-procedure chest X-ray. The diagnosis of PLSVC was confirmed by echocardiography and thorax computed tomography. This anomaly is rather rare, and few studies have evaluated the safety of PLSVC for HD. The catheter was used for 2 months under careful continuous monitoring with no complications. Physicians who place HD catheters in the left jugular/subclavian vein should be aware of the possibility of PLSVC

Neurological Manifestations of Renal Diseases in Children in Qazvin/ Iran

  How to Cite This Article: Dalirani R, Mahyar A, Ayazi P, Ahmadi Gh. Neurological Manifestations of Renal Diseases inChildren in Qazvin/ Iran. Iran J Child Neurol. Summer 2016; 10(3):24-27.AbstractObjectiveRenal diseases are one of the most common causes of referrals and admissions of children, hence it is important to know their neurological presentations. This study aimed to determine neurological presentations of renal diseases in children.Material & MethodsA total of 634 children with renal diseases, admitted to Qazvin Pediatric Hospital, Qazvin, central Iran from 2011 to 2013 were studied. Neurological presentations of patients were established and the results were analyzed using statistical tests.ResultsNeurological presentations were found in 18 (2.8%) out of 634 patients, of whom 15 had febrile seizures, two thromboembolism, and one encephalopathy. Among patients with urinary tract infection (UTI), 2.6% had febrile seizures, 11.1% of those with glomerulonephritis had encephalopathy, and 3.7% of those with nephrotic syndrome had cerebral thromboembolism.ConclusionResults showed neurological presentations in 2.8% of children with renal diseases, and febrile seizure as the most common presentation. References 1.      Elder JS. Urinary tract infection. In: Kliegman RM, Stanton RE, Schor NF, Geme III JW St, Behrman RE. Nelson Textbook of Pediatrics. 19th ed. Phila, Saunders; 2011: 1838-1846. 2.      Bhoobun S, Jalloh AA, Jacobsen KH. Cerebral venous thrombosis in a child with nephrotic syndrome: case report. Pan Afr Med J 2012;13:57. 3.      Lee P, Verrier Jones K. Urinary tract infection in febrile convulsions. Arch Dis Child 1991; 66(11):1287-90. 4.      Bensman A, Dunand O, Ulinski T: Urinary tract infection. In: Avner ED, Harman WE, Niaudet P, Yoshikawa N, Pediatric Nephrology. Berlin, Springer. 2009:1007-1025. 5.      Anochie I, Eke F, Okpere A. Childhood nephrotic syndrome: change in pattern and response to steroids. J Natl Med Assoc 2006; 98(12):1977-81. 6.      Pan GC, Avner ED. Glomerulonephritis Associated with Infections. In: Kliegman RM, Stanton RE, Schor NF, Geme III JW St, Behrman RE. Nelson Textbook of Pediatrics. 19th ed. Phila, Saunders; 2011: 1783-6. 7.      Salvadori M, Bertoni E. Update on hemolytic uremic syndrome: Diagnostic and therapeutic recommendations. World J Nephrol 2013 6; 2(3): 56-7. 8.      Shinnar S. Febrile seizures. In: Swaiman KF, Ashwal S,Ferriero DM. Pediatric neurology: principles and practice. 4th ed. Philadelphia: Mosby, 2006:1079-86. 9.      Bryce A. Kerlin, Rose Ayoob, William E. Smoyer. Epidemiology and Pathophysiology of Nephrotic Syndrome–Associated Thromboembolic Disease. Clin J Am Soc Nephrol 2012 ; 7(3): 513–520. 10.  Faigle R, Sutter R, Kaplan PW. The electroencephalography of encephalopathy in patients with endocrine and metabolic disorders. J Clin Neurophysiol 2013;30(5):10.1097. doi:10.1097/WNP.0b013e3182a73db9. 11.  Momen AA, Monajemzadeh SM, Gholamian M. The Frequency of Urinary Tract Infection among Children with Febrile Convulsions. Iran J Child Neurol 2011; 5(3): 29-32. 12.  Burn D J, Bates D. Neurology and the kidney. J Neurol Neurosurg Psychiatr 1998;65:810–821. 13.  Orth SR, Ritz E. The nephrotic syndrome. N Engl J Med 1998;338: 1202-11. 14.  Zaffanello M, Franchini M. Thromboembolism in childhood nephritic syndrome: a rare but serious complication. Hematology 2007; 12:69-73. 15.  Sébire G, Tabarki B, Saunders DE, et al. Cerebral venous sinus thrombosis in children: risk factors, presentation, diagnosis and outcome. Brain 2005; 128 (3):477–89. 16.  Joel F, Denis G, deVeber Gabrielle D V. Cerebral sinovenous thrombosis and idiopathic nephrotic syndrome in childhood: report of four new cases and review of the literature. Eur J Pediatr 2006; 165(10):709–716. 17.  Nathanson S, Kwon T, Elmaleh M et al. Acute neurological involvement in diarrhea-associated hemolytic uremic syndrome. Clin J Am Soc Nephrol 2010 ;5(7):1218-28.  

Dilated Cardiomyopathy Several Months after Hemolytic Uremic Syndrome

This is a report of a 44-month-old baby girl diagnosed as a case of atypical hemolytic uremic syndrome (aHUS) presenting with hematuria, periorbital edema, anemia, thrombocytopenia, and hypertension lacking any history of previous bloody diarrhea. She was treated with plasma infusion followed by plasmapheresis and peritoneal dialysis. After two months, she was discharged in remission undergoing periodic plasmapheresis. Four months later, she was visited for fatigue, tachypnea, and palpitation. Cardiac evaluation revealed dilated cardiomyopathy with an ejection fraction of 15-20%.  She was hospitalized and treated with inotropes and diuretics; one week later, she was discharged in a favorable condition. After six months follow-up, she showed an acceptable renal and cardiac state. It seems that cardiomyopathy can occur as a late and rare complication of HUS. We recommend cardiac evaluation for all patients with HUS at its presentation and in later follow-ups.  Keywords: Cardiomyopathy; Hemolytic Uremic Syndrome; Child

Feasible Relation between Glutathione Peroxidase and Febrile Seizure

How to Cite This Article: Mahyar A, Ayazi P, Dalirani R, Mohammad Hoseini B, Sarookhani MR, Javadi A, Esmaeily Sh. Feasible Relation between Glutathione Peroxidase and Febrile Seizure. Iran J Child Neurol. Winter 2017; 11(1):65-69.AbstractObjectiveWe aimed to determine the relationship between serum glutathione peroxidase and febrile seizure.Materials & MethodsIn this case-control study, 43 children with simple febrile seizure (case group) were compared with 43 febrile children without seizure (control group) in terms of serum glutathione peroxidase level, measured by ELISA method. This study was conducted in Qazvin Children Hospital, Qazvin University of Medical Sciences in Qazvin, Iran in 2012-2013. The results were analyzed and compared in two groups.ResultsFrom 43 children 24 (53%) were male and 19 (47%) were female in children with simple febrile seizure, and 26 (60%) were male and 17 (40%) were female in febrile children without seizure (control group) (P=0.827). Serum glutathione peroxidase level was 166 U/ml (SD=107) in the case group and 141 U/ml (SD=90.5) in the control group of no significant difference.ConclusionThere was no significant relationship between serum glutathione peroxidase and simple febrile seizure. Thus, it seems that glutathione peroxidase, an essential component of antioxidant system, does not play any role in the pathogenesis of simple febrile seizure.References1. Duffner PK, Baumann RJ, Berman P, Green JL, Schneider S, Hodgson ES, etal. Febrile seizures: clinical practice guideline for the long-term management of the child with simple febrile seizures. Pediatrics 2008 ;121:1281-6.Midline doi: 10.1542/peds.2008-0939.2.Shinnar S. Febrile seizures. In: Swaiman KF, Ashwal S,Ferriero DM. Pediatric neurology: principles and practice. 4th ed. Philadelphia: Mosby, 2006:1079-86.3. Mikati M A. Febrile seizures.In: Kliegman RM, Stanton B F, GemeIII J WS, Schor NF , Behrman RE. Nelson textbook of pediatrics.19th ed. Philadelphia: Saunders, 2011:2017-19. 4. Hara K, Tanabe T, Aomatsu T, Inoue N, Tamaki H, Okamoto N ,etal. Febrile seizures associated with influenza A. Brain and Development 2007;29: 30-38.5. Sugai K.Current management of febrile seizures in Japan: An overview . Brain and Development 2010; 32: 64-7. Midline doi: 10.1016/j.braindev.2009.09.019.6. Camfield P, Camfield C, Kurlemann G. Febrile seizures, epileptic syndromes in infancy, childhood, and adolescence. 3th ed. London: John Libbey & Co Ltd,2002:145–52.7. Sapir D, Leitner Y, Harel S, Kraumer U. Unprovoked seizures after complex febrile convulsions. Brain Dev 2000; 22:484–6.8. Kumari PL, Nair MK, Nair SM, Kailas L, Geetha S. Iron deficiency as a risk factor for simple febrile seizures--a case control study. Indian Pediatr 2012; 49:17-9.9. Tutuncuoglu S, Kutukculer N, Kepe L, Coker C, Berdeli A, Tekgul H. Proinflammatory cytokines, prostaglandins and zinc in febrile convulsions. Pediatr Int 2001;43:235-9.10. Ashrafi MR, Shams S, Nouri M, Mohseni M, Shabanian R, Yekaninejad MS, etal. A probable causative factor for an old problem: selenium and glutathione peroxidase appear to play important roles in epilepsy pathogenesis. Epilepsia 2007 ;48:1750-5.11. Willmore IJ, Rubin JJ. Antiperoxidant pretreatment and iron-induced epileptiform discharges in the rat: EEG and histopathologic studies. Neurology1981; 31:63–69. 12.Irshad M, Chaudhuri PS. Oxidant-antioxidant system: role and significance in human body. Indian J Exp Biol 2002 ;40:1233-9.13.Rayman MP.The importance of selenium to human health. Lancet 2000;356:233-41.14.Patel M. Mitochondrial dysfunction and oxidative stress: cause and consequence of epileptic seizures. Free Radical Biology & Medicine 2004;37:1951–1962.15.Li-Ping L, Patel M. Seizure induced changes in mitochondrial redox status. Free Radical Biology & Medicine 2006;40:316–322.16. Weber GF, Maertens P, Meng XZ, Pippenger CE. Glutathione peroxidase deficiency and childhood seizures. Lancet 1991 15; 337:1443-4.17. Sudha K, Rao AV, Rao A. Oxidative stress and antioxidants in epilepsy. Clin Chim Acta 2001; 303:19-24.18. Verrotti A, Basciani F, Trotta D, Pomilio MP, Morgese G, Chiarelli F.Serum Copper, Zinc, Selenium, Glutathione peroxidase and Superoxide dismutase levels in epileptic children before and after 1 year of sodium valproate and carbamazepine therapy. Epilepsy Res 2002;48:71-5.19. Ben-Menachem E. Kyllerman M, Marklund S. Superoxide dismutase and glutathione peroxidase function in progressive myoclonus epilepsies. Epilepsy Res 2000;40:33-9.20. Turkdogan D, Toplan S, Karakoc Y. Lipid peroxidation and antioxidative enzyme activities in childhood epilepsy. J Child Neurol 2002; 17:673-6. 21.Naziroglu M, Kutluhan S, Yilmaz M. Selenium and topiramate modulates brain microsomal oxidative stress values, Ca2+-ATPase activity, and EEG records in pentylenetetrazol-induced seizures in rats. J Membr Biol 2008;225:39-49.22.Naziroglu M. Role of selenium on calcium signaling and oxidative stress-induced molecular pathways in epilepsy. Neurochem Res 2009; 34:2181-91.Medline doi: 10.1007/s11064-009-0015-8.23.Brigelius-Flohé R, Maiorino M.Glutathione peroxidases. Biochim Biophys Acta 2013 ;1830:3289-303. 24. Harapin I, Bauer M, Bedrica L, Potoanjak D. Correlation between gluthathione peroxidase activity and the quantity of selenium in the whole blood of beef calves. Acta Vet Brno 2000; 69: 87–92.Medline. doi: 10.1016/j.bbagen.2012.11.020.25.Koller LD, South PJ, Exon JH, Whitbeck GA, Maas J. Comparison of selenium levels and glutathione peroxidase activity in bovine whole blood. Can J Comp Med 1984 ;48:431-3

Frequency of Massive Proteinuria in Childhood Pyelonephritis and the Response to Antibiotic Therapy

Introduction: Urinary tract infection (UTI) is one of the most common bacterial infections in childhood which can contribute to high blood pressure and renal failure later in life. There are diffident methods for evaluation of a child with UTI for differentiation of cystitis from acute pyelonephritis. One of which is measuring protein in urine. The aim of this study is to investigate the role of UTI in provoking proteinuria.Material and Methods: This is Quasi- experimental study, before and after, in patients with acute pyelonephritis in Mofid Children's Hospital during 2004-2006. All pyelonephritic patients were treated by intravenous ceftriaxone for at least for 10 days. Random urine samples were taken from all patients at the onset of admission before starting the antibiotic and at the ninth day of treatment for the evaluation of urine protein and creatinine.Results: 152 children between 1 to 2 years of age entered the study. The prevalence of proteinuria in the acute phase of pyelonephritis was 94.8%. According to our study the prevalence of proteinuria during pyelonephritis is higher in children less than 2 years old (97.3%) and 20% of patients showed nephrotic range of proteinuria. In all cases random urine samples were normal after completion of treatment (p<0.005). Conclusions: the results of this study illustrate that proteinuria has a high frequency during UTI and acute pyelonephritis. Proteinuria during pyelonephritis may be massive and in the nephrotic range but should not be the cause of concern because in the majority of cases it disappears following treatment. Keywords: Pyelonephritis; Proteinuria; Antibiotics; Child