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Vol. 97, No. 4, 2004
Issue release date: August 2004
Section title: Original Paper
Nephron Clin Pract 2004;97:c147–c153
(DOI:10.1159/000079174)

Glomerular Deposition and Urinary Excretion of Complement Factor H in Idiopathic Membranous Nephropathy

Endo M. · Fuke Y. · Tamano M. · Hidaka M. · Ohsawa I. · Fujita T. · Ohi H.
aDivision of Nephrology, Internal Medicine II, Nihon University School of Medicine, Tokyo, and bChoju Medical Institute, Fukushimura Hospital, Aichi, Japan

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 4/11/2003
Accepted: 4/2/2004
Published online: 11/17/2004

Number of Print Pages: 1
Number of Figures: 4
Number of Tables: 3

ISSN: (Print)
eISSN: 1660-2110 (Online)

For additional information: http://www.karger.com/NEC

Abstract

Background/Aims: The complement system plays an important role in the pathogenesis of membranous nephropathy (MN). In order to elucidate the regulatory mechanism of complement activation, we demonstrated glomerular deposition and urinary excretion of complement factor H, which controls the alternative pathway and the amplification loop at the C3 step, in patients with idiopathic MN. Methods: Renal biopsy specimens from 20 patients with idiopathic MN were studied immunohistochemically using monoclonal antibodies against complement components including factor H. SDS-PAGE and Western blotting analysis of urine samples were performed, and the urinary excretion of factor H and C5b-9 were measured by quantitative sandwich ELISA. Results: Intense glomerular deposition of factor H was observed with C3b·C3c and C5b-9 at an early stage of the disease. Factor H was detected in Western blots of urine samples, but factor H-like protein 1 (FHL-1) was not. The mean level of urinary factor H was elevated (86.30 ± 21.93 U/mg urinary creatinine) in comparison to that of normal controls (4.76 ± 1.03 U/mg urinary creatinine). Urinary factor H level exhibited no correlation with clinical parameters; however, a negative correlation was found between urinary C5b-9/factor H and creatinine clearance (r = 0.662, p < 0.01). Conclusion: The source of glomerular and urinary factor H is supposedly a 150-kD protein. There was no evidence to suggest that FHL-1 is synthesized at the site of inflammation. The urinary C5b-9 to urinary factor H ratio is indicative of the degree of ongoing complement activation in the glomeruli and complement-mediated renal injury. These findings suggest that factor H contributes to the control mechanism of in situ complement activation and prevents renal damage in idiopathic MN.


  

Author Contacts

Morito Endo, MD
Choju Medical Institute, Fukushimura Hospital
19-14, Yamanaka, Noyori-cho, Toyohashi
Aichi 441-8124 (Japan)
Tel. +81 532 46 7511, Fax +81 532 46 4899, E-Mail mendo@chojuken.net

  

Article Information

Received: April 11, 2003
Accepted: April 2, 2004
Number of Print Pages : 7
Number of Figures : 4, Number of Tables : 3, Number of References : 29

  

Publication Details

Nephron Clinical Practice
Founded 1964 by G. Richet and G.E. Schreiner

Vol. 97, No. 4, Year 2004 (Cover Date: August 2004)

Journal Editor: S.H. Powis, London
ISSN: 0028–2766 (print), 1660–2110 (Online)

For additional information: http://www.karger.com/nec


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 4/11/2003
Accepted: 4/2/2004
Published online: 11/17/2004

Number of Print Pages: 1
Number of Figures: 4
Number of Tables: 3

ISSN: (Print)
eISSN: 1660-2110 (Online)

For additional information: http://www.karger.com/NEC


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