Kazumoto Iijima

Kobe University, Kōbe, Hyōgo, Japan

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Publications (242)777.5 Total impact

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    ABSTRACT: Background: Vesicoureteral reflux (VUR) is associated with an increased risk of kidney disorders. It is unclear whether VUR is associated with progression from chronic kidney disease (CKD) to end-stage kidney disease (ESKD) in children with congenital anomalies of the kidney and urinary tract (CAKUT). Methods: We conducted a 3-year follow-up survey of a cohort of 447 children with CKD (stage 3-5). Rates of and risk factors for progression to ESKD were determined using the Kaplan-Meier method and Cox regression respectively. Results: Congenital anomaly of the kidney and urinary tract was the primary etiology in 278 out of 447 children; 118 (42.4 %) had a history of VUR at the start of the cohort study. There were significantly more boys than girls with VUR, whereas the proportions were similar in children without VUR. The types of urinary anomalies/complications of the two groups were significantly different. Three-year renal survival rates of the groups were not significantly different, irrespective of CKD stage. Age < 2 years and age after puberty, stage 4 or 5 CKD, and heavy proteinuria, but not history of VUR, were significantly associated with progression to ESKD. Conclusions: History of VUR at the start of follow-up was not associated with the progression of stage 3-5 CKD in children with CAKUT.
    Pediatric Nephrology 09/2015; DOI:10.1007/s00467-015-3196-1 · 2.86 Impact Factor
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    ABSTRACT: Introduction: Opsoclonus-myoclonus syndrome (OMS) is a rare neurological disorder that is associated with paraneoplastic diseases. Because OMS can frequently relapse, patients may be inflicted with neurological problems for a long time. Recently, rituximab (RTX) was introduced as a drug to treat OMS. To assess RTX treatment, we studied a patient who experienced recurrence of OMS. Case report: A 2-year-old Japanese boy, who had left adrenal neuroblastoma, suddenly showed OMS symptoms, including ataxia and opsoclonus. Surgical resection of the tumor and subsequent steroid therapy ameliorated his symptoms. When OMS relapsed during the time when prednisolone was reduced, he was treated with full-dose RTX therapy (375mg/m(2)/week) for 4 consecutive weeks. However, 1year later, he presented again with OMS symptoms. This time, we only administered an additional single dose of RTX treatment (375mg/m(2)), allowing remission of OMS symptoms. During 2years after the additional RTX treatment, OMS symptoms did not appear, even when prednisolone was reduced. He had no adverse events associated with RTX during the whole treatment period. Conclusions: An additional single-dose RTX therapy might be effective for relapsed OMS patients who were previously treated with full-dose RTX therapy.
    Brain & development 09/2015; DOI:10.1016/j.braindev.2015.09.002 · 1.88 Impact Factor
  • Koichi Kamei · Masao Ogura · Mai Sato · Mayumi Sako · Kazumoto Iijima · Shuichi Ito
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    ABSTRACT: Rituximab (RTX) is known to be effective for the treatment of refractory steroid-dependent nephrotic syndrome (SDNS). However, there are insufficient data on the risk factors for relapse and long-term outcome after RTX treatment. We administered a single dose of RTX to patients with refractory SDNS from November 2007 to December 2013 and continued with immunosuppressants. The risk factors for early relapse and long-term outcome were analyzed. Eighty-one patients were included and the observation period was 13-90 months. Seventy-six patients (94 %) discontinued steroids. Median duration of B-cell depletion was 160 days and 50 % relapse-free survival was 482 days. In multivariate analyses, only a history of steroid-resistant nephrotic syndrome (SRNS) was a statistically significant risk factor (hazard ratio, 2.44; p = 0.048). Fifty percent relapse-free survival in patients without a history of SRNS was 615 days, longer than that of patients with one relapse (393 days; p = 0.005). Fifty-one patients (63 %) received additional RTX treatments for relapses. At last observation, patients using calcineurin inhibitors decreased from 89 % to 23 %, and 12 patients (15 %) discontinued immunosuppressants. Rituximab treatment followed by immunosuppressants is an effective option for patients with SDNS, although a history of SRNS is a risk factor for early relapse.
    Pediatric Nephrology 09/2015; DOI:10.1007/s00467-015-3197-0 · 2.86 Impact Factor
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    ABSTRACT: Objectives: To assess the accuracy of transcutaneous bilirubin (TcB) measurements at 5 different body sites in Japanese very low birthweight (VLBW) infants and to determine a cut-off value of TcB to detect total serum/plasma bilirubin (TB) levels ≥10 mg/dL (171 μM). Study design: In a prospective multicenter study, 85 Japanese VLBW infants were enrolled from 5 neonatal intensive care units during the study period. A total of 383 blood samples from infants not receiving phototherapy or ≥24 hours postphototherapy were analyzed. TcB was measured at the forehead, sternum, upper back, lower abdomen, and waist within 1 hour of blood collection. Linear regression analysis and Bland-Altman plots were used to compare TcB values at each site with TB levels. The TcB cut-off value for detecting TB ≥10 mg/dL was determined by receiver operating characteristics curve analysis. Results: TcB significantly correlated with TB, but the coefficient of determination varied among the sites (forehead: 0.5294, sternum: 0.6488, upper back: 0.6321, lower abdomen: 0.5430, waist: 0.7396). At a TcB value ≥8, the sensitivity was 100% at the sternum and upper back, 85% at the waist, 84% at the forehead, and 64% at the lower abdomen to detect TB ≥10 mg/dL. Conclusions: In Japanese VLBW infants, the accuracy of TcB measurements varies according to body site. TcB ≥8 on the sternum or upper back is more reliable than that on the forehead, lower abdomen, or waist to detect TB levels ≥10 mg/dL.
    The Journal of pediatrics 09/2015; DOI:10.1016/j.jpeds.2015.08.038 · 3.79 Impact Factor
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    ABSTRACT: Glycosylphosphatidylinositol (GPI) anchors tether proteins to the extracellular face of eukaryotic plasma membranes. Defects in the human GPI anchor biosynthetic pathway cause inherited GPI deficiencies (IGDs) characterized by multiple congenital anomalies: dysmorphic faces, developmental delay, hypotonia, and epilepsy. We report the case of a 6-year-old boy with severe psychomotor developmental delay, epilepsy, and decreased granulocyte surface expression of GPI-anchored protein that suggested autosomal recessive GPI deficiency. The case underwent target exome sequencing to screen for IGDs. Target exome sequencing of the proband identified an apparently homozygous c.808T > C (p.Ser270Pro) mutation in PIGN, a gene involved in the GPI anchor biosynthetic pathway. As his parents were expecting another child, genetic carrier screening was conducted for the parents. Direct sequencing of the parents identified a heterozygous c.808T > C PIGN mutation in the father but none in the mother. To identify the mother's mutation, we performed semi-quantitative real-time PCR of the PIGN exons and long PCR, identifying a microdeletion in PIGN (del exons 2-14). The proband had inherited this microdeletion from his mother. Prenatal diagnosis of the fetus revealed that it was a heterozygous carrier of the mother's pathogenic allele. Here, we report a sporadic case of inherited GPI deficiency with a PIGN mutation and the first case of prenatal diagnosis for GPI deficiency. © 2015 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part A 09/2015; DOI:10.1002/ajmg.a.37397 · 2.16 Impact Factor
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    ABSTRACT: The nuclear pore complex (NPC) is a huge protein complex embedded in the nuclear envelope. It has central functions in nucleocytoplasmic transport, nuclear framework, and gene regulation. Nucleoporin 107 kDa (NUP107) is a component of the NPC central scaffold and is an essential protein in all eukaryotic cells. Here, we report on biallelic NUP107 mutations in nine affected individuals who are from five unrelated families and show early-onset steroid-resistant nephrotic syndrome (SRNS). These individuals have pathologically focal segmental glomerulosclerosis, a condition that leads to end-stage renal disease with high frequency. NUP107 is ubiquitously expressed, including in glomerular podocytes. Three of four NUP107 mutations detected in the affected individuals hamper NUP107 binding to NUP133 (nucleoporin 133 kDa) and NUP107 incorporation into NPCs in vitro. Zebrafish with nup107 knockdown generated by morpholino oligonucleotides displayed hypoplastic glomerulus structures and abnormal podocyte foot processes, thereby mimicking the pathological changes seen in the kidneys of the SRNS individuals with NUP107 mutations. Considering the unique properties of the podocyte (highly differentiated foot-process architecture and slit membrane and the inability to regenerate), we propose a "podocyte-injury model" as the pathomechanism for SRNS due to biallelic NUP107 mutations.
    The American Journal of Human Genetics 09/2015; DOI:10.1016/j.ajhg.2015.08.013 · 10.93 Impact Factor
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    ABSTRACT: Autosomal dominant hypocalcemia type 1 (ADH1) is a relatively rare endocrine disorder characterized by hypocalcemia and inadequate parathyroid hormone secretion. ADH is caused by activating mutations in the calcium-sensing receptor (CaSR) gene, CASR. CaSR plays a crucial role in calcium and magnesium homeostasis in the kidney. ADH may be accompanied by hypokalemia and metabolic alkalosis when it is classified as type V Bartter syndrome. However, the mechanism underlying hypokalemia in this disease is unclear. We investigated a 33-year-old woman with hypocalcemia and hypoparathyroidism since childhood, whose mother also had hypocalcemia and hypoparathyroidism, but with no clinical symptoms. Blood examinations showed hypokalemia and metabolic alkalosis in the patient, but not her mother. We conducted mutation analysis and diuretic tests to clarify the patient's and her mother's diagnosis and to investigate the onset mechanism of hypokalemia in ADH1. We also determined the localization of CaSR in the kidney by immunohistochemistry. We detected a known gain-of-function mutation in CASR in both the patient and her mother. Diuretic tests revealed a response to furosemide and no reaction to thiazide in the patient, although the mother responded well to both diuretics. CaSR co-localized with the Na(+)-Cl(-) cotransporter (NCCT) on distal tubular epithelial cells. These results indicate that the NCCT in the distal convoluted tubule was secondarily affected in this patient. We conclude that the main pathogenesis of secondary hypokalemia in ADH1 in this patient was secondary NCCT dysfunction.
    Clinical and Experimental Nephrology 09/2015; DOI:10.1007/s10157-015-1160-9 · 2.02 Impact Factor
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    ABSTRACT: Newborn screening for urinary cytomegalovirus (CMV) and early introduction of antiviral treatment are expected to improve neurological outcomes in symptomatic congenital CMV-infected infants. This cohort study prospectively evaluated neurological outcomes in symptomatic congenital CMV-infected infants following the introduction of hospital-based newborn urinary CMV screening and antiviral treatment. Following institutional review board approval and written informed consent from their parents, newborns were prospectively screened from 2009 to 2014 for urinary CMV-DNA by PCR within 1week after birth at Kobe University Hospital and affiliated hospitals. CMV-positive newborns were further examined at Kobe University Hospital, and those diagnosed as symptomatic were treated with valganciclovir for 6weeks plus immunoglobulin. Clinical neurological outcomes were evaluated at age ⩾12months and categorized by the presence and severity of neurologic sequelae. Urine samples of 6348 newborns were screened, with 32 (0.50%) positive for CMV. Of these, 16 were diagnosed with symptomatic infection and 12 received antiviral treatment. Four infants developed severe impairment (33%), three developed mild impairment (25%), and five developed normally (42%). This is the first Japanese report of neurological assessments in infants with symptomatic congenital CMV infection who received early diagnosis and antiviral treatment. Urinary screening, resulting in early diagnosis and treatment, may yield better neurological outcomes in symptomatic congenital CMV-infected infants. Copyright © 2015 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
    Brain & development 08/2015; DOI:10.1016/j.braindev.2015.08.003 · 1.88 Impact Factor
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    ABSTRACT: Few studies have targeted psychomotor development and associated perinatal risk factors in Japanese very low birth weight (VLBW) infants who are severely small for gestational age (SGA). A single-center study was conducted in 104 Japanese VLBW infants who were born preterm, due to maternal, umbilical cord, or placental abnormalities, between 2000 and 2007. Psychomotor development as a developmental quotient (DQ) was assessed using the Kyoto Scale of Psychological Development at 3years corrected age. Severely SGA was defined as birth weight or length below -2 standard deviation values of the mean values at the same gestation. VLBW infants were divided into 2 subgroups based on gestational age at birth: ⩾28weeks (n=64) and <28weeks (n=40). DQs of infants with severe SGA were compared with those of infants who were appropriate for gestational age (AGA). Factors associated with developmental disabilities in VLBW infants with severe SGA (n=23) were determined. In the group born at ⩾28weeks gestation, infants with severe SGA had normal DQ values and did not significantly differ from those with AGA. However, in the group born at <28weeks gestation, severe SGA infants had significantly lower postural-motor DQ values than AGA infants. Gestational age <28weeks was an independent factor for low postural-motor DQ, regardless of the cause of severe SGA or pregnancy termination. Extremely preterm newborns with severe SGA are at risk of motor developmental disability at age 3years. Copyright © 2015 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
    Brain & development 08/2015; DOI:10.1016/j.braindev.2015.07.008 · 1.88 Impact Factor
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    ABSTRACT: Pericatheter leakage is a catheter-related complication of peritoneal dialysis (PD). To prevent pericatheter leakage, a modified technique of PD catheter insertion with fibrin glue was performed in 19 children. At the time of PD catheter insertion, as much fibrin glue as possible was injected into the subcutaneous tissue along the tunneled segment of the catheter and then the skin was compressed. There was no occurrence of pericatheter leakage and full PD could be initiated 1 day (median) after implantation. This technique prevented pericatheter leakage completely even in smaller-weight infants and will enable initiation of full PD with no break-in period. Copyright © 2015 Journal of Pediatric Urology Company. Published by Elsevier Ltd. All rights reserved.
    Journal of pediatric urology 08/2015; DOI:10.1016/j.jpurol.2015.07.005 · 0.90 Impact Factor
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    ABSTRACT: Some patients with childhood immunoglobulin A nephropathy (IgAN) progress to end-stage renal disease within 20 years, while others achieve spontaneous remission even without medication. Prognosis of IgAN with minimal proteinuria (MP-IgAN, <0.5 g/day/1.73 m(2)) at diagnosis seems to be generally good. However, the long-term outcome for patients with childhood MP-IgAN has not yet been determined. We retrospectively analyzed 385 children newly diagnosed with biopsy-proven IgAN between June 1976 and July 2009 whose renal biopsy specimens could be evaluated by the Oxford classification criteria. Of these 385 children with IgAN, 106 (27.5 %) were diagnosed with MP-IgAN. We compared clinical and pathological findings between the 106 patients with MP-IgAN and the remaining 279 patients to elucidate the characteristics of MP-IgAN in children. Patients with MP-IgAN were identified through a school screening program (73.6 %) or upon presentation with gross hematuria (26.4 %). Patients with MP-IgAN had significantly milder pathological symptoms than those with IgAN. The most frequently used therapeutic regimes were angiotensin converting enzyme inhibitors (30.2 %) and no therapy (36.8 %). None of the patients with MP-IgAN reached stage III chronic kidney disease within 15 years after onset. Four patients with MP-IgAN (3.8 %) received immunosuppressive therapy during the course of the disease. Our results indicate that the outcome of patients with a diagnosis of childhood MP-IgAN is good, but that careful long-term observation is required.
    Pediatric Nephrology 08/2015; DOI:10.1007/s00467-015-3176-5 · 2.86 Impact Factor
  • Natsuki Matsunoshita · Kandai Nozu · Kazumoto Iijima
    Nippon Jinzo Gakkai shi 07/2015; 57(4):743-50.
  • 06/2015; 2:15017. DOI:10.1038/hgv.2015.17
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    ABSTRACT: X-linked Alport syndrome (XLAS) is a progressive, hereditary nephropathy. Although men with XLAS usually develop end-stage renal disease before 30 years of age, some men show a milder phenotype and develop end-stage renal disease later in life. However, the molecular mechanisms associated with this milder phenotype have not been fully identified. We genetically diagnosed 186 patients with suspected XLAS between January 2006 and August 2014. Genetic examination involved: (1) extraction and analysis of genomic DNA using PCR and direct sequencing using Sanger's method and (2) next-generation sequencing to detect variant allele frequencies. We identified somatic mosaic variants in the type VI collagen, α5 gene (COL4A5) in four patients. Interestingly, two of these four patients with variant frequencies in kidney biopsies or urinary sediment cells of ≥50% showed hematuria and moderate proteinuria, whereas the other two with variant frequencies of <50% were asymptomatic or only had hematuria. De novo variants can occur even in asymptomatic male cases of XLAS resulting in mosaicism, with important implications for genetic counseling. This is the first study to show a tendency between the variant allele frequency and disease severity in male XLAS patients with somatic mosaic variants in COL4A5. Although this is a very rare status of somatic mosaicism, further analysis is needed to show this correlation in a larger population.European Journal of Human Genetics advance online publication, 27 May 2015; doi:10.1038/ejhg.2015.113.
    European journal of human genetics: EJHG 05/2015; DOI:10.1038/ejhg.2015.113 · 4.35 Impact Factor
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    ABSTRACT: Phenotypic overlap exists among type III Bartter syndrome (BS), Gitelman syndrome (GS), and pseudo-BS/GS (p-BS/GS), which are clinically difficult to distinguish. We aimed to clarify the differences between these diseases, allowing accurate diagnosis based on their clinical features. A total of 163 patients with genetically defined type III BS (n = 30), GS (n = 90), and p-BS/GS (n = 43) were included. Age at diagnosis, sex, body mass index, estimated glomerular filtration rate, and serum and urine electrolyte concentrations were determined. Patients with p-BS/GS were significantly older at diagnosis than those with type III BS and GS. Patients with p-BS/GS included a significantly higher percentage of women and had a lower body mass index and estimated glomerular filtration rate than did patients with GS. Although hypomagnesemia and hypocalciuria were predominant biochemical findings in patients with GS, 17 and 23% of patients with type III BS and p-BS/GS, respectively, also showed these abnormalities. Of patients with type III BS, GS, and p-BS/GS, 40, 12, and 63%, respectively, presented with chronic kidney disease. This study clarified the clinical differences between BS, GS, and p-BS/GS for the first time, which will help clinicians establish differential diagnoses for these three conditions.Genet Med advance online publication 16 April 2015Genetics in Medicine (2015); doi:10.1038/gim.2015.56.
    Genetics in medicine: official journal of the American College of Medical Genetics 04/2015; DOI:10.1038/gim.2015.56 · 7.33 Impact Factor
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    ABSTRACT: Attention Deficit/Hyperactivity Disorder (ADHD) is a common neurobehavioral problem in children throughout the world. The Stroop test has been widely used for the evaluation of ADHD symptoms. However, the age-related change of the Stroop test results has not been fully clarified until now. Sixty-five ADHD and 70 age-matched control children aged 6-13 years were enrolled in this study. ADHD was diagnosed based on DSM-IV criteria. We examined the completion time and error rates of the Congruent Stroop test (CST) and Incongruent Stroop test (IST) in ADHD and control children. No significant difference was observed in the completion time for CST or IST between the ADHD and control children at 6-9 years old. However, ADHD children at 10-13 years old showed significantly delayed completion time for the CST and IST compared with controls of the same age. As for the error rates of the CST and IST, ADHD and control children at 6-9 years old showed no difference. However, error rates of CST and IST in the ADHD children at 10-13 years were significantly higher than those of control of the same age. Age may influence the results of Stroop test in ADHD children. For the ages of 10-13 years old, the Stroop test clearly separates ADHD children from control children, suggesting that it may be a useful screening tool for ADHD among preadolescent children.
    The Kobe journal of medical sciences 04/2015; 61(1):E19-26.
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    ABSTRACT: The dystrophin gene, which is mutated in Duchenne muscular dystrophy (DMD), comprises 79 exons that show multiple alternative splicing events. Intron retention, a type of alternative splicing, may control gene expression. We examined intron retention in dystrophin introns by reverse-transcription PCR from skeletal muscle, focusing on the nine shortest (all <1000 bp), because these are more likely to be retained. Only one, intron 40, was retained in mRNA; sequencing revealed insertion of a complete intron 40 (851 nt) between exons 40 and 41. The intron 40 retention product accounted for 1.2% of the total product but had a premature stop codon at the fifth intronic codon. Intron 40 retention was most strongly observed in the kidney (36.6%) and was not obtained from the fetal liver, lung, spleen or placenta. This indicated that intron retention is a tissue-specific event whose level varies among tissues. In two DMD patients, intron 40 retention was observed in one patient but not in the other. Examination of splicing regulatory factors revealed that intron 40 had the highest guanine-cytosine content of all examined introns in a 30-nt segment at its 3' end. Further studies are needed to clarify the biological role of intron 40-retained dystrophin mRNA.Journal of Human Genetics advance online publication, 2 April 2015; doi:10.1038/jhg.2015.24.
    Journal of Human Genetics 04/2015; 60(6). DOI:10.1038/jhg.2015.24 · 2.46 Impact Factor
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    ABSTRACT: CDKL5-related encephalopathy is an X-linked dominantly inherited disorder that is characterized by early infantile epileptic encephalopathy or atypical Rett syndrome. We describe a 5-year-old Japanese boy with intractable epilepsy, severe developmental delay, and Rett syndrome-like features. Onset was at 2months, when his electroencephalogram showed sporadic single poly spikes and diffuse irregular poly spikes. We conducted a genetic analysis using an Illumina® TruSight™ One sequencing panel on a next-generation sequencer. We identified two epilepsy-associated single nucleotide variants in our case: CDKL5 p.Ala40Val and KCNQ2 p.Glu515Asp. CDKL5 p.Ala40Val has been previously reported to be responsible for early infantile epileptic encephalopathy. In our case, the CDKL5 heterozygous mutation showed somatic mosaicism because the boy's karyotype was 46,XY. The KCNQ2 variant p.Glu515Asp is known to cause benign familial neonatal seizures-1, and this variant showed paternal inheritance. Although we believe that the somatic mosaic CDKL5 mutation is mainly responsible for the neurological phenotype in the patient, the KCNQ2 variant might have some neurological effect. Genetic analysis by next-generation sequencing is capable of identifying multiple variants in a patient. Copyright © 2015 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
    Brain & development 03/2015; 37(9). DOI:10.1016/j.braindev.2015.03.002 · 1.88 Impact Factor
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    ABSTRACT: Antisense oligonucleotide (AO)-mediated exon skipping is the most promising way to express internally deleted dystrophin in Duchenne muscular dystrophy (DMD), by correcting the reading frame of dystrophin mRNA. An antisense chimeric oligonucleotide consisting of 2´-O-methyl RNA and ethylene-bridged nucleic acid (ENA), targeting exon 45 of the dystrophin gene, AO85, has been shown to induce exon 45 skipping efficiently. Since phosphorothioate (PS)-modification of AO85 has never been explored, we produced a PS-modified AO85 (AO88) and examined its exon skipping capability and cytotoxicity. Exon 45 skipping activity was examined in primary muscle cells established from a DMD patient carrying a deletion of dystrophin exon 44. Cytotoxicity was assessed by MTT assay. AO88 induced dystrophin exon 45 skipping from 50 nM. More than 90% of products lacked exon 45 at 400 nM. AO88 showed significantly higher exon skipping activity than AO85. The EC50 of AO88 was 94.8 nM, while EC50 of AO85 was 66.7 nM. Cytotoxicity was lower for AO88 than for AO85. the PS-modified RNA/ENA chimera displayed stronger exon skipping activity and lower cytotoxicity than the phosphodiester-RNA/ENA chimera. AO88 has better potential for clinical use than AO85.
    The Kobe journal of medical sciences 03/2015; 60(4):E86-94.
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    ABSTRACT: Uromodulin-associated kidney disease (UAKD) is an autosomal dominant disease caused by a mutation in the uromodulin (UMOD) gene, leading to end-stage renal disease. We herein report the case of a family with UAKD caused by a novel mutation (C135G) in the UMOD gene. A 31-year-old woman had a low estimated glomerular filtration rate (59.7 mL/min per 1.73 m(2)). Her father, grandfather and paternal aunt had received maintenance hemodialysis therapy since their 40's. This case underscores the importance of performing genetic testing in young patients even in cases involving only moderate abnormalities in the kidney function.
    Internal Medicine 03/2015; 54(6):631-5. DOI:10.2169/internalmedicine.54.3151 · 0.90 Impact Factor

Publication Stats

3k Citations
777.50 Total Impact Points


  • 2000–2015
    • Kobe University
      • Division of Pediatrics
      Kōbe, Hyōgo, Japan
    • Osaka Rosai Hospital
      Ōsaka, Ōsaka, Japan
  • 2012
    • Aichi Children's Health and Medical Center
      Nagoya, Aichi, Japan
  • 2005–2011
    • Wakayama Medical University
      • Department of Pediatrics
      Wakayama, Wakayama, Japan
  • 2002–2010
    • National Center for Child Health and Development
      Edo, Tōkyō, Japan
  • 2003–2007
    • Tokyo Metropolitan Children's Medical Center
      Edo, Tōkyō, Japan
  • 1999
    • University of Shizuoka
      • Department of Biochemistry
      Sizuoka, Shizuoka, Japan
  • 1998
    • Hyogo Prefectural Amagasaki Hospital
      Amagasaki, Hyōgo, Japan