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A study on the improvement of the immunofluorescence classification of membranoproliferative glomerul-onephritis like lesion |
LI Chang1, 2, ZHU Shuang1, HUANG Zhaoxing1. |
1.Department of Nephrology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015; 2.Department of Nephrology, Cangnan
Hospital Affiliated to Wenzhou Medical University, Wenzhou, 325800 |
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Cite this article: |
LI Chang,ZHU Shuang,HUANG Zhaoxing.. A study on the improvement of the immunofluorescence classification of membranoproliferative glomerul-onephritis like lesion[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2018, 48(9): 646-651,656.
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Abstract Objective: To explore the improvement of immunofluorescence (IF) classification of membranoproliferative glomerulonephritis (MPGN) like lesion, to understand the etiology of MPGN like lesions and the prevalence of idiopathic MPGN. Methods: MPGN like lesions were diagnosed by optical microscopic examination of renal biopsy tissues in 118 patients from January 1994 to April 2018 in the First Affiliated Hospital of Wenzhou Medical University. All these cases were studied by a modified method of IF classification based on IF classification which had been suggested by SETHI and FERVENZA, and combined with electron microscopic examination and clinical retrospective etiological analysis. Results: A total of 118 cases of MPGN like lesions, with an average age of 39.8±17.2 years old, including 12 cases of idiopathic MPGN and 9 738 cases of renal biopsy in the same period. Idiopathic MPGN accounted for 0.12% of the total cases of renal biopsy. According to the improved IF classification, immune-complex (IC) mediated MPGN accounted for 78.8% (93/118), monoclonal immunoglobulin related MPGN accounted for 5.9% (7/118), C3 glomerulopathy and non immuno-mediated MPGN like lesions accounted for 8.5% (10/118) and 6.8% (8/118) respectively. Etiological classification: idiopathic MPGN accounted for 10.2% (12/118), the cases with secondary causes accounted for 89.8% (106/118), the most common secondary cause was systemic lupus erythematosus (SLE) which accounted for 34.7% (41/118), followed by hepatitis B virus (HBV) infection which accounted for 12.7% (15/118). Electron microscopy revealed 77 cases of MPGN like lesions, including 73 cases of MPGN and 4 cases of MPGN like lesions. The most frequent pathological type of MPGN was I type, accounting for 56.2% (41/73), followed by III type 41.1% (30/73). Secondary MPGN was 78.1% (32/41) and 90% (27/30) in type I and III respectively. Conclusion: The prevalence of idiopathic MPGN in Wenzhou is extremely low. Most of the cases with MPGN like lesions have secondary etiology which are common caused by SLE and HBV infection, and in which MPGN is the most common mediated by IC. The modified method of IF classification can lead to an improved understanding of the pathogenic mechanism in MPGN, and may be more helpful to the etiological identification of MPGN like lesions.
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Received: 21 March 2018
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[1] FAKHOURI F, FRÉMEAUX-BACCHI V, NOËL L H, et al.
C3 glomerulopathy: a new classification[J]. Nat Rev Nephrol,
2010, 6(8): 494-499.
[2] SETHI S, FERVENZA F C. Membranoproliferative glomerulonephritis: pathogenetic heterogeneity and proposal for a new classification[J]. Semin Nephrol, 2011, 31(4): 341-348.
[3] ALCHI B, JAYNE D. Membranoproliferative glomerulone-phritis[J]. Pediatr Nephrol, 2010, 25(8): 1409-1418.
[4] SETHI S, FERVENZA F C. Membranoproliferative glomerulonephritis——a new look at an old entity[J]. N Engl J Med, 2012, 366(12): 1119-1131.
[5] COOK H T, PICKERING M C. Histopathology of MPGN and C3 glomerulopathies[J]. Nat Rev Nephrol, 2015, 11(1): 14-22.
[6] SETHI S, FERVENZA F C, RAJKUMAR S V. Spectrum of manifestations of monoclonal gammopathy-associated renal lesions[J]. Curr Opin Nephrol Hypertens, 2016, 25(2): 127-137.
[7] SERVAIS A, NOËL L H, ROUMENINA L T, et al. Acquired and genetic complement abnormalities play a critical role in dense deposit disease and other C3 glomerulopathies[J]. Kidney Int, 2012, 82(4): 454-464.
[8] BRIDOUX F, LEUNG N, HUTCHISON C A, et al. Diagnosis of monoclonal gammopathy of renal significance[J]. Kidney Int, 2015, 87(4): 698-711.
[9] Chung J, Bemstein J, Glassock R J. World Health Organization (WHO) Monograph[M]. Renal Disease, 2nded, Tokyo: Lgaku-Shoin, 1995: 1-541.
[10] 邹万忠. 肾活检病理诊断标准指导意见[J]. 中华肾脏病杂志, 2001, (4): 270.
[11] PICKERING M C, D’AGATI V D, NESTER C M, et al. C3 glomerulopathy: consensus report[J]. Kidney Int, 2013, 84 (6): 1079-1089.
[12] SETHI S, HAAS M, MARKOWITZ G S, et al. Mayo clinic/renal pathology society consensus report on pathologic classification, diagnosis, and reporting of GN[J]. J Am Soc Nephrol, 2016, 27(5): 1278-1287.
[13] LU Y, SHEN P, LI X, et al. Re-evaluation of the classification system for membranoproliferative glomerulonephritis [J]. Contrib Nephrol, 2013, 181: 175-184.
[14] AGRAWAL V, KAUL A, RANADE R S, et al. Immunoglobulin A dominant membranoproliferative glomerulonephritis in an elderly man: A case report and review of the lit-erature[J]. Indian J Nephrol, 2015, 25(3): 168-170.
[15] FERVENZA F C, SETHI S, GLASSOCK R J. Idiopathic membranoproliferative glomerulonephritis: does it exist?[J]. Nephrol Dial Transplant, 2012, 27(12): 4288-4294.
[16] LARSEN C P, MESSIAS N C, WALKER P D, et al. Membranoproliferative glomerulonephritis with masked monotypic immunoglobulin deposits[J]. Kidney Int, 2015, 88(4): 867-873. |
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