C3 glomerulopathy and current dilemmas View Full Text


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Article Info

DATE

2016-11-23

AUTHORS

Naoko Ito, Ryuji Ohashi, Michio Nagata

ABSTRACT

C3 glomerulopathy (C3G) is a recently identified disease entity caused by dysregulation of the alternative complement pathway, and dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) are its components. Because laboratory detection of complement dysregulation is still uncommon in practice, “dominant C3 deposition by two orders greater than that of immunoglobulins in the glomeruli by immunofluorescence”, as stated in the consensus report, defines C3G. However, this morphological definition possibly includes the cases with glomerular diseases of different mechanisms such as post-infectious glomerulonephritis. In addition, the differential diagnosis between DDD and C3GN is often difficult because the distinction between these two diseases is based solely on electron microscopic features. Recent molecular and genetic advances provide information to characterize C3G. Some C3G cases are found with genetic abnormalities in complement regulatory factors, but majority of cases seem to be associated with acquired factors that dysregulate the alternative complement pathway. Because clinical courses and prognoses among glomerular diseases with dominant C3 deposition differ, further understanding the background mechanism, particularly complement dysregulation in C3G, is needed. This may resolve current dilemmas in practice and shed light on novel targeted therapies to remedy the dysregulated alternative complement pathway in C3G. More... »

PAGES

541-551

References to SciGraph publications

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  • 2010-03-11. A case of dense deposit disease associated with a group A streptococcal infection without the involvement of C3NeF or complement factor H deficiency in PEDIATRIC NEPHROLOGY
  • 1977-03. Basement membrane changes in membranoproliferative glomerulonephritis in VIRCHOWS ARCHIV A PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY
  • 2011-11-22. Clinical features and outcomes of 98 children and adults with dense deposit disease in PEDIATRIC NEPHROLOGY
  • 2015-05-19. Successful therapy of C3Nef-positive C3 glomerulopathy with plasma therapy and immunosuppression in PEDIATRIC NEPHROLOGY
  • 2012-10-02. Pathogenesis of the C3 glomerulopathies and reclassification of MPGN in NATURE REVIEWS NEPHROLOGY
  • 2011-12-20. A case of idiopathic membranoproliferative glomerulonephritis with a transient glomerular deposition of nephritis-associated plasmin receptor antigen in CLINICAL AND EXPERIMENTAL NEPHROLOGY
  • 2012-10-02. Use of eculizumab for atypical haemolytic uraemic syndrome and C3 glomerulopathies in NATURE REVIEWS NEPHROLOGY
  • 2014-12-02. Histopathology of MPGN and C3 glomerulopathies in NATURE REVIEWS NEPHROLOGY
  • 2010-08-19. Complement: a key system for immune surveillance and homeostasis in NATURE IMMUNOLOGY
  • 1992-03. Treatment of mesangiocapillary glomerulonephritis with alternate-day prednisone —a report of The International Study of Kidney Disease in Children in PEDIATRIC NEPHROLOGY
  • 2002-07-01. Uncontrolled C3 activation causes membranoproliferative glomerulonephritis in mice deficient in complement factor H in NATURE GENETICS
  • 2007-03-30. Dense deposit disease is not a membranoproliferative glomerulonephritis in MODERN PATHOLOGY
  • 2009-05. An update on acute postinfectious glomerulonephritis worldwide in NATURE REVIEWS NEPHROLOGY
  • 2001-05. Structure and composition of drusen associated with glomerulonephritis: Implications for the role of complement activation in drusen biogenesis in EYE
  • 2014-01-10. Rituximab fails where eculizumab restores renal function in C3nef-related DDD in PEDIATRIC NEPHROLOGY
  • 2010-07-06. C3 glomerulopathy: a new classification in NATURE REVIEWS NEPHROLOGY
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s10157-016-1358-5

    DOI

    http://dx.doi.org/10.1007/s10157-016-1358-5

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27878657


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