Anti-factor H antibody-positive C3 glomerulonephritis secondary to poststreptococcal acute glomerulonephritis with diabetic nephropathy.
Anti-factor H antibody
C3 glomerulonephritis
Diabetes mellitus
Infection-related glomerulonephritis
Poststreptococcal glomerulonephritis
Journal
CEN case reports
ISSN: 2192-4449
Titre abrégé: CEN Case Rep
Pays: Japan
ID NLM: 101636244
Informations de publication
Date de publication:
15 Jul 2023
15 Jul 2023
Historique:
received:
11
11
2022
accepted:
05
07
2023
medline:
15
7
2023
pubmed:
15
7
2023
entrez:
15
7
2023
Statut:
aheadofprint
Résumé
Poststreptococcal acute kidney glomerulonephritis (PSAGN) has been seen in adults in recent years, especially in patients with type 2 diabetes mellitus, and the renal prognosis has not always been good. There have been cases of PSAGN in which complete remission was not achieved and hematuria and proteinuria persisted, leading to end-stage renal disease. Previous reports showed that the patients subjected to PSAGN have an underlying defect in regulating the alternative pathway of complement, and they identified that antibodies to the C3 convertase, C3 nephritic factors (C3NeF), are involved. C3NeF stabilizes C3 convertase, sustains C3 activation, and causes C3 glomerulonephritis (C3GN). On the other hand, factor H is a glycoprotein that suppresses the overactivation of the alternative pathway by decaying the C3 convertase. Anti-factor H (aFH) antibodies interfere with factor H and cause the same activation of the alternative pathway as C3NeF. However, a limited number of reports describe the clinical course of C3GN with aFH antibodies. We encountered a 49-year-old Japanese man with type 2 diabetes mellitus. He was referred to our hospital because of his elevated serum creatinine, proteinuria, hematuria, and developed edema on both legs. He was diagnosed as PSAGN at the first kidney biopsy, and his renal function improved and edema and hematuria disappeared, but proteinuria persisted after 5 months. He was diagnosed as C3GN at the second kidney biopsy. In our case, no C3NeF was detected. However, a high titer of aFH antibodies was detected in stored serum from the initial presentation, providing a unified diagnosis of aFH antibody-positive C3GN secondary to PSAGN. He progressed to end-stage renal disease (ESRD) and hemodialysis was started. The persistence of high levels of aFH autoantibodies may have caused C3GN secondary to PSAGN due to activating the alternative complement pathway, which eventually worsened the nephropathy and led to ESRD.
Identifiants
pubmed: 37452997
doi: 10.1007/s13730-023-00809-3
pii: 10.1007/s13730-023-00809-3
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2023. The Author(s).
Références
Nasr SH, Radhakrishnan J, D’Agati VD. Bacterial infection-related glomerulonephritis in adults. Kidney Int. 2013;83:792–803.
doi: 10.1038/ki.2012.407
pubmed: 23302723
Nasr SH, Fidler ME, Valeri AM, Cornell LD, Sethi S, Zoller A, Stokes MB, Markowitz GS, D’Agati VD. Postinfectious glomerulonephritis in the elderly. J Am Soc Nephrol. 2011;22:187–95.
doi: 10.1681/ASN.2010060611
pubmed: 21051737
Pickering MC,DAgati VD, Nester CM, Smith RJ, Haas M, Appel GB, Alpers CE, Bajema IM, Bedrosian C, Braun M, et al. C glomerulopathy: consensus report. Kidney Int. 2013;84:1079–89.
doi: 10.1038/ki.2013.377
pubmed: 24172683
Oda T, Yoshizawa N, Yamakami K, Sakurai Y, Takechi H, Yamamoto K, Oshima N, Kumagai H. The role of nephritis-associated plasmin receptor (NAPlr) in glomerulonephritis associated with streptococcal infection. J Biomed Biotechnol. 2012;1:417675.
Oda T, Yoshizawa N, Yamakami K, Tamura K, Kuroki A, Sugisaki T, Sawanobori E, Higashida K, Ohtomo Y, Hotta O, Kumagai H, Miura S. Localization of nephritis-associated plasmin receptor in acute poststreptococcal glomerulonephritis. Hum Pathol. 2010;41:1276–85.
doi: 10.1016/j.humpath.2010.02.006
pubmed: 20708459
Dragon-Durey MA, Blanc C, Roumenina LT, et al. Anti-factor H antibodies assay. Methods Mol Biol. 2014;1100:249–56.
doi: 10.1007/978-1-62703-724-2_20
pubmed: 24218265
Barkai LJ, Sipter E, Csuka D, Prohaszka Z, Pilely K, Garred P, Hosszufalusi N. Decreased Ficolin-3-mediated complement lectin pathway activation and alternative pathway amplification during bacterial infections in patients with type 2 diabetes mellitus. Front Immunol. 2019;10:509.
doi: 10.3389/fimmu.2019.00509
pubmed: 30949171
pmcid: 6436462
Smith RJH, Appel GB, Blom AM, Cook HT, D’Agati VD, Fakhouri F, Fremeaux-Bacchi V, Józsi M, Kavanagh D, Lambris JD, Noris M, Pickering MC, Remuzzi G, de Córdoba SR, Sethi S, Van der Vlag J, Zipfel PF, Nester CM. C3 glomerulopathy - understanding a rare complement-driven renal disease. Nat Rev Nephrol. 2019;15:129–43.
doi: 10.1038/s41581-018-0107-2
pubmed: 30692664
pmcid: 6876298
Sethi S, Fervenza FC, Zhang Y, Zand L, Meyer NC, Borsa N, Nasr SH, Smith RJ. Atypical postinfectious glomerulonephritis is associated with abnormalities in the alternative pathway of complement. Kidney Int. 2013;83:293–9.
doi: 10.1038/ki.2012.384
pubmed: 23235567
Dragon-Durey MA, Sinha A, Togarsimalemath SK, Bagga A. Anti-complement-factor H-associated glomerulopathies. Nat Rev Nephrol. 2016;12:563–78.
doi: 10.1038/nrneph.2016.99
Pilania RK, Bhattacharya D, Taneja N, Rawat A, Suri D, Ramachandran R, Tiewsoh K. Infection triggered anti complement factor H (CFH) positive atypical Hemolytic Uremic Syndrome in children: lessons for the clinical nephrologist. J Nephrol. 2021;34(3):943–7.
doi: 10.1007/s40620-020-00913-y
pubmed: 33387343