{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,28]],"date-time":"2025-10-28T05:48:03Z","timestamp":1761630483611},"reference-count":30,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2008,1,16]],"date-time":"2008-01-16T00:00:00Z","timestamp":1200441600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pediatric Transplantation"],"published-print":{"date-parts":[[2008,5]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> Recurrent FSGS is a major challenge in the field of nephrology. To clarify the role of <jats:italic>NPHS2<\/jats:italic> defects in the pathogenesis of FSGS recurrence, we sequenced all eight exons of <jats:italic>NPHS2<\/jats:italic> in 11 Japanese pediatric FSGS patients with or without post\u2010transplant recurrence. All patients had biopsy\u2010proven primary FSGS, had no family history of renal diseases or consanguinity, were steroid\u2010resistant, and received living\u2010related renal transplantation. The mean age at onset was 5.0\u2003\u00b1\u20033.1\u2003yr and mean age at renal transplantation was 10.4\u2003\u00b1\u20034.1\u2003yr. Mutational analysis of <jats:italic>NPHS2<\/jats:italic> was performed using polymerase chain reaction and direct sequencing. We found a synonymous T\/C polymorphism at alanine 318 (GC<jats:styled-content>C<\/jats:styled-content> to GC<jats:styled-content>T<\/jats:styled-content>) in seven of 11 patients but no other causative <jats:italic>NPHS2<\/jats:italic> mutations. FSGS recurred immediately after transplant in seven patients, while the remaining four patients had no recurrence for 3.2\u20135.8\u2003yr. There were no differences between recurrent and non\u2010recurrent patients in the onset age and the interval from onset to ESRD. In conclusion, we detected no causative <jats:italic>NPHS2<\/jats:italic> mutations in Japanese pediatric FSGS patients with or without post\u2010transplant recurrence. Further studies on the involvement of other genes are required to better understand recurrent FSGS.<\/jats:p>","DOI":"10.1111\/j.1399-3046.2007.00752.x","type":"journal-article","created":{"date-parts":[[2008,4,24]],"date-time":"2008-04-24T02:34:09Z","timestamp":1209004449000},"page":"341-346","source":"Crossref","is-referenced-by-count":8,"title":["Clinical features and mutational survey of <i>NPHS2<\/i> (podocin) in Japanese children with focal segmental glomerulosclerosis who underwent renal 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