Proteinuria in Frasier Syndrome


Creative Commons License

Peco-Antic A., ÖZALTIN F., Parezanovic V., Milosevski-Lomic G., Zdravkovic V.

SRPSKI ARHIV ZA CELOKUPNO LEKARSTVO, vol.141, pp.685-688, 2013 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 141
  • Publication Date: 2013
  • Doi Number: 10.2298/sarh1310685p
  • Journal Name: SRPSKI ARHIV ZA CELOKUPNO LEKARSTVO
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.685-688
  • Keywords: steroid resistant nephrotic syndrome, Wilms' tumour suppressor gene (WT1), angiotensin converting enzyme (ACE) inhibitor, angiotensin receptor blocker, indomethacin, FOCAL SEGMENTAL GLOMERULOSCLEROSIS, CONGENITAL NEPHROTIC SYNDROME, SPLICE-SITE MUTATION, WILMS-TUMOR-1 GENE, STEROID-RESISTANT, RENAL-FAILURE, WT1 MUTATIONS, INDOMETHACIN, NEPHROPATHY, PREVALENCE
  • Hacettepe University Affiliated: Yes

Abstract

Introduction Frasier syndrome (FS) is a genetic form of glomerulopathy, which results from mutations in the Wilms' tumour suppressor gene (WT1). Proteinuria in FS has been traditionally considered unresponsive to any medication and FS inevitably progresses to end stage renal failure.