Recently, a number of reports have described dominant C3 deposits in renal biopsies of patients with infection-related glomerulonephritis (GN). While acute post-infectious GN and membranoproliferative GN are commonly characterized by immune deposits containing C3 and/or C4, the absence of immunoglobulin (Ig) and/or immune complexes at light or electron microscopy is a rather unusual observation. Dominant C3 deposition is believed to result from the alternative pathway of complement activation via the C3bBb “tickover” convertase. The actual occurrence of C3 glomerulopathy could be underestimated, since infection-related GN often quickly subsides without the need for a renal biopsy. A more thorough understanding of the pathways that lead to complement assembly and deposition within the kidney is needed to support a new classification of complement-related lesions, including entities such as dense deposit disease, (atypical) hemolytic-uremic syndrome, dominant C1q, CFHR5, C4d, and C3 glomerulopathies. We will briefly review recent work in this area, focusing on GN with selective complement C3 deposits.

Dominant C3 glomerulopathy. new roles for an old actor in renal pathology / Pirozzi, Nicola; Stoppacciaro, Antonella; Menè, Paolo. - In: JN. JOURNAL OF NEPHROLOGY. - ISSN 1121-8428. - 31:4(2018), pp. 503-510. [10.1007/s40620-017-0458-y]

Dominant C3 glomerulopathy. new roles for an old actor in renal pathology

Pirozzi, Nicola
Primo
Writing – Review & Editing
;
Stoppacciaro, Antonella
Secondo
Data Curation
;
Menè, Paolo
Ultimo
Writing – Review & Editing
2018

Abstract

Recently, a number of reports have described dominant C3 deposits in renal biopsies of patients with infection-related glomerulonephritis (GN). While acute post-infectious GN and membranoproliferative GN are commonly characterized by immune deposits containing C3 and/or C4, the absence of immunoglobulin (Ig) and/or immune complexes at light or electron microscopy is a rather unusual observation. Dominant C3 deposition is believed to result from the alternative pathway of complement activation via the C3bBb “tickover” convertase. The actual occurrence of C3 glomerulopathy could be underestimated, since infection-related GN often quickly subsides without the need for a renal biopsy. A more thorough understanding of the pathways that lead to complement assembly and deposition within the kidney is needed to support a new classification of complement-related lesions, including entities such as dense deposit disease, (atypical) hemolytic-uremic syndrome, dominant C1q, CFHR5, C4d, and C3 glomerulopathies. We will briefly review recent work in this area, focusing on GN with selective complement C3 deposits.
2018
C3; complement; glomerulonephritis; immune deposits; renal biopsy; nephrology
01 Pubblicazione su rivista::01a Articolo in rivista
Dominant C3 glomerulopathy. new roles for an old actor in renal pathology / Pirozzi, Nicola; Stoppacciaro, Antonella; Menè, Paolo. - In: JN. JOURNAL OF NEPHROLOGY. - ISSN 1121-8428. - 31:4(2018), pp. 503-510. [10.1007/s40620-017-0458-y]
File allegati a questo prodotto
File Dimensione Formato  
Pirozzi_Dominant_2018.pdf

solo gestori archivio

Tipologia: Versione editoriale (versione pubblicata con il layout dell'editore)
Licenza: Tutti i diritti riservati (All rights reserved)
Dimensione 1.31 MB
Formato Adobe PDF
1.31 MB Adobe PDF   Contatta l'autore

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1072402
Citazioni
  • ???jsp.display-item.citation.pmc??? 4
  • Scopus 7
  • ???jsp.display-item.citation.isi??? 6
social impact