Literature DB >> 15064941

Transforming growth factor-beta in renal disease with glycogen storage disease I.

Maki Urushihara1, Shoji Kagami, Michinori Ito, Koji Yasutomo, Shuji Kondo, Akiko Kitamura, Akiyoshi Takahashi, Yasuhiro Kuroda.   

Abstract

We report a 14-year-old patient with Japanese glycogen storage disease I (GSD-I) who was found to have proteinuria. Renal biopsy revealed massive tubular atrophy and interstitial fibrosis with mononuclear cell infiltration, but the glomeruli were almost normal. The epithelial cells of tubules contained periodic acid-Schiff-positive glycogen deposits digested by diastase. In an immunohistological study, transforming growth factor (TGF)-beta expression was increased in tubular epithelial cells compared with a normal control kidney specimen. These data suggest that increased TGF-beta expression is involved in the pathophysiology of renal interstitial fibrosis in a patient with GSD-I.

Entities:  

Mesh:

Substances:

Year:  2004        PMID: 15064941     DOI: 10.1007/s00467-004-1456-6

Source DB:  PubMed          Journal:  Pediatr Nephrol        ISSN: 0931-041X            Impact factor:   3.714


  12 in total

Review 1.  TGF-beta in kidney fibrosis: a target for gene therapy.

Authors:  W A Border; N A Noble
Journal:  Kidney Int       Date:  1997-05       Impact factor: 10.612

2.  Transforming growth factor beta stimulates fibroblast-collagen matrix contraction by different mechanisms in mechanically loaded and unloaded matrices.

Authors:  Frederick Grinnell; Chin-Han Ho
Journal:  Exp Cell Res       Date:  2002-02-15       Impact factor: 3.905

Review 3.  Transforming growth factor beta in tissue fibrosis.

Authors:  W A Border; N A Noble
Journal:  N Engl J Med       Date:  1994-11-10       Impact factor: 91.245

4.  Glomerular and tubular function in glycogen storage disease.

Authors:  P J Lee; R N Dalton; V Shah; P C Hindmarsh; J V Leonard
Journal:  Pediatr Nephrol       Date:  1995-12       Impact factor: 3.714

5.  Obesity-related glomerulopathy: an emerging epidemic.

Authors:  N Kambham; G S Markowitz; A M Valeri; J Lin; V D D'Agati
Journal:  Kidney Int       Date:  2001-04       Impact factor: 10.612

6.  Polarity of stimulation and secretion of transforming growth factor-beta 1 by cultured proximal tubular cells.

Authors:  A O Phillips; R Steadman; K Morrisey; J D Williams
Journal:  Am J Pathol       Date:  1997-03       Impact factor: 4.307

7.  Tubular phenotypic change in progressive tubulointerstitial fibrosis in human glomerulonephritis.

Authors:  K Jinde; D J Nikolic-Paterson; X R Huang; H Sakai; K Kurokawa; R C Atkins; H Y Lan
Journal:  Am J Kidney Dis       Date:  2001-10       Impact factor: 8.860

Review 8.  Tubulointerstitial changes as a major determinant in the progression of renal damage.

Authors:  K A Nath
Journal:  Am J Kidney Dis       Date:  1992-07       Impact factor: 8.860

Review 9.  Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment.

Authors:  Y T Chen
Journal:  Pediatr Nephrol       Date:  1991-01       Impact factor: 3.714

Review 10.  The molecular basis of the type 1 glycogen storage diseases.

Authors:  A Burchell
Journal:  Bioessays       Date:  1992-06       Impact factor: 4.345

View more
  3 in total

Review 1.  Glycogen storage disease type I and G6Pase-β deficiency: etiology and therapy.

Authors:  Janice Y Chou; Hyun Sik Jun; Brian C Mansfield
Journal:  Nat Rev Endocrinol       Date:  2010-10-26       Impact factor: 43.330

2.  Targeted deletion of kidney glucose-6 phosphatase leads to nephropathy.

Authors:  Julie Clar; Blandine Gri; Julien Calderaro; Marie-Christine Birling; Yann Hérault; G Peter A Smit; Gilles Mithieux; Fabienne Rajas
Journal:  Kidney Int       Date:  2014-04-09       Impact factor: 10.612

3.  Angiotensin mediates renal fibrosis in the nephropathy of glycogen storage disease type Ia.

Authors:  W H Yiu; C-J Pan; R A Ruef; W-T Peng; M F Starost; B C Mansfield; J Y Chou
Journal:  Kidney Int       Date:  2007-12-12       Impact factor: 10.612

  3 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.