Expression of nephrin in acquired human glomerular disease

Nephrology Dialysis Transplantation

Volumn 17, Issue 3, 2002, Pages 478-484

  Huh, Wooseong ^a   Kim, Dae Joong ^a,d   Kim, Mi Kyung ^a   Kim, Yoon Goo ^a   Oh, Ha Young ^a   Ruotsalainen, Vesa ^b   Tryggvason, Karl ^c  

^a Sungkyunkwan University School of Medicine   (South Korea)

^b UNIVERSITY OF OULU   (Finland)

^c KAROLINSKA INSTITUTE   (Sweden)

^d Samsung Medical Center   (South Korea)

Author keywords

Effacement; Glomerulonephritis; Nephrin; Podocyte; Proteinuria

Indexed keywords

CORTICOSTEROID; CYCLOPHOSPHAMIDE; CYCLOSPORIN; GOLD; NEPHRIN; POLYCLONAL ANTIBODY; PROTEIN; STEROID;

ADULT; ARTICLE; CLINICAL ARTICLE; CONTROLLED STUDY; FEMALE; GLOMERULOPATHY; HUMAN; HUMAN TISSUE; IMMUNOELECTRON MICROSCOPY; IMMUNOGLOBULIN A NEPHROPATHY; KIDNEY BIOPSY; LUPUS ERYTHEMATOSUS NEPHRITIS; MALE; MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS; MEMBRANOUS GLOMERULONEPHRITIS; MINIMAL CHANGE GLOMERULONEPHRITIS; NEPHRECTOMY; PODOCYTE; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEINURIA;

EID: 0036196379     PISSN: 09310509     EISSN: None     Source Type: Journal    
DOI: 10.1093/ndt/17.3.478     Document Type: Article

References (15)

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4. Podocytic cytoskeletal disaggregation and basement-membrane detachment in puromycin aminonucleoside nephrosis
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6. Glomerular expression of nephrin is decreased in acquired human nephrotic syndrome
7. Morphometric analysis of effects of angiotensin II on glomerular structure in rats
8. Nephrin localizes at the podocyte filtration slit area and is characteristically spliced in the human kidney
9. Porous substructure of the glomerular slit diaphragm in the rat and mouse
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11. Expression of nephrin in pediatric kidney disease
12. NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome
13. Mutations in ACTN4, encoding alpha-actinin-4, cause familial focal segmental glomerulosclerosis
14. Congenital nephrotic syndrome in mice lacking CD2-associated protein
15. Nephrin redistribution on podocytes is a potential mechanism for proteinuria in patients with primary acquired nephrotic syndrome