Comprehensive evaluation of the significance of immunofluorescent findings on clinicopathological features in IgA nephropathy.
Adult
Biomarkers
/ analysis
Biopsy
Complement C3
/ analysis
Disease Progression
Female
Fibrinogen
/ analysis
Fluorescent Antibody Technique
Glomerulonephritis, IGA
/ complications
Humans
Immunoglobulin A
/ analysis
Immunoglobulin G
/ analysis
Kidney Failure, Chronic
/ immunology
Kidney Glomerulus
/ drug effects
Male
Predictive Value of Tests
Prognosis
Risk Factors
Steroids
/ therapeutic use
Young Adult
Complement deposition
IgA deposition
IgA nephropathy
IgG deposition
Immunofluorescent study
Journal
Clinical and experimental nephrology
ISSN: 1437-7799
Titre abrégé: Clin Exp Nephrol
Pays: Japan
ID NLM: 9709923
Informations de publication
Date de publication:
Feb 2019
Feb 2019
Historique:
received:
27
03
2018
accepted:
16
07
2018
pubmed:
2
8
2018
medline:
18
6
2019
entrez:
2
8
2018
Statut:
ppublish
Résumé
The clinicopathological significance of immunofluorescent findings in IgA nephropathy remains controversial. The relations of the deposition of IgA, IgG, IgM, C3, C1q and fibrinogen (Fib) with pathological findings, baseline clinical findings, and renal outcome were evaluated in 688 patients with IgA nephropathy. Pathological features included cellular or fibrocellular crescents, endocapillary or mesangial hypercellularity, segmental or global glomerulosclerosis and the Oxford classification. The median age at biopsy was 30 years. There were 289 men. With 74 months median follow-up, 32% of patients received steroids. Twelve percent of patients developed end-stage renal disease (ESRD). The degree of IgA was closely related to the degree of C3, IgG and IgM deposition. The degree of IgA, C3, IgG and Fib deposition was significantly related to the percentage of glomeruli with crescent, endocapillary and mesangial hypercellularity. IgM deposition showed significant association with crescent, mesangial hypercellularity, segmental sclerosis, global glomerulosclerosis and tubular atrophy/interstitial fibrosis. In the patients treated with steroids, the risk for ESRD in patients with 2-3+ IgA deposition was significantly lower with reference of 1+ IgA deposition. We found the different roles of glomerular immune reactants' deposition in the inflammatory process from acute to chronic stage. IgA deposition together with IgG, Fib and C3 may produce acute inflammatory injury. IgM deposition might occur in the early stage of inflammation and remains until late sclerotic stage. The prominent deposition of IgA related to low risk for ESRD in patients who received steroids might suggest effectiveness of steroids in such patients.
Sections du résumé
BACKGROUND
BACKGROUND
The clinicopathological significance of immunofluorescent findings in IgA nephropathy remains controversial.
METHODS
METHODS
The relations of the deposition of IgA, IgG, IgM, C3, C1q and fibrinogen (Fib) with pathological findings, baseline clinical findings, and renal outcome were evaluated in 688 patients with IgA nephropathy. Pathological features included cellular or fibrocellular crescents, endocapillary or mesangial hypercellularity, segmental or global glomerulosclerosis and the Oxford classification.
RESULTS
RESULTS
The median age at biopsy was 30 years. There were 289 men. With 74 months median follow-up, 32% of patients received steroids. Twelve percent of patients developed end-stage renal disease (ESRD). The degree of IgA was closely related to the degree of C3, IgG and IgM deposition. The degree of IgA, C3, IgG and Fib deposition was significantly related to the percentage of glomeruli with crescent, endocapillary and mesangial hypercellularity. IgM deposition showed significant association with crescent, mesangial hypercellularity, segmental sclerosis, global glomerulosclerosis and tubular atrophy/interstitial fibrosis. In the patients treated with steroids, the risk for ESRD in patients with 2-3+ IgA deposition was significantly lower with reference of 1+ IgA deposition.
CONCLUSION
CONCLUSIONS
We found the different roles of glomerular immune reactants' deposition in the inflammatory process from acute to chronic stage. IgA deposition together with IgG, Fib and C3 may produce acute inflammatory injury. IgM deposition might occur in the early stage of inflammation and remains until late sclerotic stage. The prominent deposition of IgA related to low risk for ESRD in patients who received steroids might suggest effectiveness of steroids in such patients.
Identifiants
pubmed: 30066158
doi: 10.1007/s10157-018-1619-6
pii: 10.1007/s10157-018-1619-6
doi:
Substances chimiques
Biomarkers
0
C3 protein, human
0
Complement C3
0
Immunoglobulin A
0
Immunoglobulin G
0
Steroids
0
Fibrinogen
9001-32-5
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
169-181Références
Kidney Int. 2000 Aug;58(2):598-606
pubmed: 10916083
Am J Nephrol. 2002 Sep-Dec;22(5-6):480-6
pubmed: 12381947
Am J Kidney Dis. 2003 May;41(5):972-83
pubmed: 12722031
J Am Soc Nephrol. 2006 Jun;17(6):1724-34
pubmed: 16687629
Nephrol Dial Transplant. 2008 Dec;23(12):3915-20
pubmed: 18644797
Nephrol Dial Transplant. 2009 Mar;24(3):886-91
pubmed: 18842673
Kidney Int. 2009 Sep;76(5):546-56
pubmed: 19571790
Kidney Int. 2009 Sep;76(5):534-45
pubmed: 19571791
Nephrology (Carlton). 2010 Dec;15(8):747-54
pubmed: 21175960
Nephrol Dial Transplant. 2011 Aug;26(8):2533-6
pubmed: 21273233
Clin Exp Nephrol. 2013 Feb;17(1):73-82
pubmed: 22752397
PLoS One. 2012;7(7):e40495
pubmed: 22792353
Clin Nephrol. 2013 Aug;80(2):98-104
pubmed: 23587123
Clin Exp Immunol. 2013 Oct;174(1):152-60
pubmed: 23750697
J Nephropathol. 2013 Jul;2(3):190-5
pubmed: 24475448
Clin J Am Soc Nephrol. 2014 May;9(5):897-904
pubmed: 24578331
Clin Exp Immunol. 2015 Feb;179(2):354-61
pubmed: 25267249
J Nephrol. 2015 Aug;28(4):441-9
pubmed: 25585823
J Am Soc Nephrol. 2015 Jul;26(7):1503-12
pubmed: 25694468
Mod Pathol. 2016 Jul;29(7):743-52
pubmed: 27102346
J Am Soc Nephrol. 2017 Feb;28(2):691-701
pubmed: 27612994
Kidney Int. 2017 May;91(5):1014-1021
pubmed: 28341274
Am J Kidney Dis. 1988 Nov;12(5):348-52
pubmed: 3142256
Nihon Jinzo Gakkai Shi. 1987 Sep;29(9):1181-8
pubmed: 3694897
Am J Nephrol. 1986;6(4):246-52
pubmed: 3777033
Medicine (Baltimore). 1985 Jan;64(1):49-60
pubmed: 3880853
Am J Nephrol. 1985;5(3):150-7
pubmed: 4014321
Nephron. 1983;34(3):146-53
pubmed: 6348567
Contrib Nephrol. 1984;40:167-73
pubmed: 6388997
Contrib Nephrol. 1984;40:99-106
pubmed: 6389003
Contrib Nephrol. 1978;9:88-100
pubmed: 668392
Histopathology. 1981 Sep;5(5):469-90
pubmed: 7026405
Acta Med Scand. 1981;210(5):363-72
pubmed: 7039240
Clin Nephrol. 1998 Jan;49(1):1-8
pubmed: 9491278