scholarly journals Minimal Change Nephrosis and Allergy

Nephron ◽  
1996 ◽  
Vol 74 (2) ◽  
pp. 422-423 ◽  
Author(s):  
Nigel Wardle
Keyword(s):  
Minimal Change ◽  
Minimal Change Nephrosis

Volume regulation in children with early relapse of minimal-change nephrosis with or without hypovolaemic symptoms

The Lancet ◽  
1995 ◽  
Vol 346 (8968) ◽  
pp. 148-152 ◽  
Author(s):  
J.G. Vande Walle ◽  
R.A.M.G. Donckerwolcke ◽  
J.W. van Isselt ◽  
J.A. Joles ◽  
H.A. Koomans ◽  
...  
Keyword(s):  
Volume Regulation ◽  
Minimal Change ◽  
Early Relapse ◽  
Minimal Change Nephrosis

scholarly journals Minimal change nephrosis and antiphospholipid antibodies: coincidental or associated?

1998 ◽  
Vol 13 (12) ◽  
pp. 3275-3276 ◽  
Author(s):  
V. C. Chitalia ◽  
A. F. Almeida ◽  
M. Krishnan ◽  
S. K. Chauhan ◽  
P. P. Khetan
Keyword(s):  
Antiphospholipid Antibodies ◽  
Minimal Change ◽  
Minimal Change Nephrosis

Frequent relapser minimal change nephrosis: An unrecognized X-linked disorder?

1989 ◽  
Vol 149 (3) ◽  
pp. 205-207 ◽  
Author(s):  
N. B. Awadalla ◽  
A. S. Teebi ◽  
A. Y. Elzouki ◽  
A. Shaltout
Keyword(s):  
Minimal Change ◽  
Minimal Change Nephrosis

Effects of Human Alpha-1-Acid Glycoprotein on Aminonucleoside- Induced Minimal Change Nephrosis in Rats

Nephron ◽  
1999 ◽  
Vol 81 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Eva-Maria Muchitsch ◽  
Ludwig Pichler ◽  
Hans Peter Schwarz ◽  
Walter Ulrich
Keyword(s):  
Minimal Change ◽  
Acid Glycoprotein ◽  
Minimal Change Nephrosis

scholarly journals Minimal change nephrosis and antiphospholipid antibodies: coincidental or associated?

1998 ◽  
Vol 13 (12) ◽  
pp. 3274-3274
Author(s):  
V. Chitalia ◽  
A. Almeida ◽  
M. Krishnan ◽  
S. Chauhan ◽  
P. Khetan
Keyword(s):  
Antiphospholipid Antibodies ◽  
Minimal Change ◽  
Minimal Change Nephrosis

scholarly journals Glomerular Expression of Dystroglycans Is Reduced in Minimal Change Nephrosis But Not in Focal Segmental Glomerulosclerosis

2000 ◽  
Vol 11 (3) ◽  
pp. 403-412 ◽  
Author(s):  
HEINRICH M. REGELE ◽  
EDITH FILLIPOVIC ◽  
BRIGITTE LANGER ◽  
HELGA POCZEWKI ◽  
ILSE KRAXBERGER ◽  
...  
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Immunoelectron Microscopy ◽  
Minimal Change ◽  
Matrix Proteins ◽  
Membrane Domains ◽  
Segmental Glomerulosclerosis ◽  
Pathologic Features ◽  
Minimal Change Nephrosis ◽  
Foot Process ◽  
Quantitative Immunoelectron Microscopy

Abstract. Extensive flattening of podocyte foot processes and increased permeability of the glomerular capillary filter are the major pathologic features of minimal change nephrosis (MCN) and focal segmental glomerulosclerosis (FSGS). Adhesion proteins anchor and stabilize podocytes on the glomerular basement membrane (GBM), and presumably are involved in the pathogenesis of foot process flattening. Thus far, α3 β1-integrin was localized to basal cell membrane domains. In this report, α- and β-dystroglycan (DG) were detected at precisely the same location by immunoelectron microscopy, and the presence of α- and β-DG chains was confirmed by immunoblotting on isolated human glomeruli. Because the major DG binding partners in the GBM (laminin, agrin, perlecan), and the intracellular dystrophin analogue utrophin are also present in glomeruli, it appears that podocytes adhere to the GBM via DG complexes, similar to muscle fibers in which actin is linked via dystrophin and DG to the extracellular matrix. As with muscle cells, it is therefore plausible that podocytes use precisely actin-guided DG complexes at their “soles” to actively govern the topography of GBM matrix proteins. Expression of the α/β-DG complex was reported to be reduced in muscular dystrophies, and therefore a search for similar pathologic alterations in archival kidney biopsies from patients with MCN (n = 16) and FSGS (n = 8) was conducted by quantitative immunoelectron microscopy. The density of α-DG on the podocyte's soles was significantly reduced to 25% in MCN, whereas it was not different in normal kidneys and FSGS. The expression of β-DG was reduced to >50% in MCN, and was slightly increased in FSGS. Levels of DG expression returned to normal in MCN after steroid treatment (n = 4). Expression of β1-integrin remained at normal levels in all conditions. These findings point to different potentially pathogenic mechanisms of foot process flattening in MCN and FSGS.

scholarly journals Expression of Nephrin in Pediatric Kidney Diseases

2001 ◽  
Vol 12 (2) ◽  
pp. 289-296
Author(s):  
JAAKKO PATRAKKA ◽  
VESA RUOTSALAINEN ◽  
ILKKA KETOLA ◽  
CHRISTER HOLMBERG ◽  
MARKKU HEIKINHEIMO ◽  
...  
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Membranous Nephropathy ◽  
Staining Pattern ◽  
Kidney Diseases ◽  
Minimal Change ◽  
Slit Diaphragm ◽  
Segmental Glomerulosclerosis ◽  
Minimal Change Nephrosis ◽  
Pediatric Kidney Diseases

Abstract. Nephrin is a podocyte cell adhesion protein located at the slit diaphragm area of the kidney glomerulus. Mutations in the nephrin gene (NPHS1) lead to congenital nephrosis, suggesting that nephrin is essential for the glomerular filtration barrier. This prompted this study of the expression of nephrin in acquired pediatric kidney diseases usingin situhybridization and immunohistochemistry.In situhybridization for nephrin mRNA was performed in biopsy samples from patients with proteinuria caused by minimal change nephrosis, focal segmental glomerulosclerosis, and membranous nephropathy. The expression of nephrin mRNA was evaluated by grading the signal intensity visually and by counting the number of grains in separate glomeruli. No significant difference was observed in these samples as compared with controls. Immunostaining for nephrin was performed using antibodies directed against extra- and intracellular parts of the molecule. Nephrin staining gave a linear pattern along the glomerular capillary loops. In minimal change nephrosis, focal segmental glomerulosclerosis, and membranous nephropathy, the distribution of nephrin was similar to that in controls. In proliferative forms of glomerulonephritides (Henoch-Schönlein nephritis, IgA nephropathy, postinfectious and membranoproliferative glomerulonephritis), crescents and sclerotic lesions were negative for nephrin, and mesangial proliferation led to a scattered and sparse staining pattern. The staining pattern of nephrin was compared to that of ZO-1, a component of the cytoplasmic face of the slit diaphragm. The distributions of these two proteins in capillary tufts were similar in all disease entities studied. In conclusion, immunohistochemistry andin situhybridization did not reveal major alterations in the expression of nephrin in proteinuric kidney diseases in children. Further studies are needed for more precise evaluation of the role of nephrin in these diseases.

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