Comprehensive evaluation of the significance of immunofluorescent findings on clinicopathological features in IgA nephropathy.


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
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

169-181

Références

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

Auteurs

Ritsuko Katafuchi (R)

Kidney Unit, National Fukuoka-Higashi Medical Center, 1-1-1, Chidori, Koga, Fukuoka, 811-3195, Japan. rkatafuchi@jcom.home.ne.jp.

Hiroshi Nagae (H)

Kidney Unit, National Fukuoka-Higashi Medical Center, 1-1-1, Chidori, Koga, Fukuoka, 811-3195, Japan.

Kosuke Masutani (K)

Division of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.

Kazuhiko Tsuruya (K)

Department of Nephrology, Nara Medical University, Nara, Japan.

Koji Mitsuiki (K)

Kidney Unit, Fukuoka Red Cross Hospital, Fukuoka, Japan.

Articles similaires

[Redispensing of expensive oral anticancer medicines: a practical application].

Lisanne N van Merendonk, Kübra Akgöl, Bastiaan Nuijen
1.00
Humans Antineoplastic Agents Administration, Oral Drug Costs Counterfeit Drugs

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male

Classifications MeSH