Complement System and C4d expression in cases of Membranous nephropathy.

Autor:	Custódio FB; Universidade Federal do Triângulo Mineiro, Disciplina de Nefrologia, Uberaba - MG, Brazil., Silva CAD; Universidade Federal do Triângulo Mineiro, Serviço de Patologia Geral e Nefropatologia, Uberaba - MG, Brazil., Helmo FR; Universidade Federal do Triângulo Mineiro, Serviço de Patologia Geral e Nefropatologia, Uberaba - MG, Brazil., Machado JR; Universidade Federal do Triângulo Mineiro, Serviço de Patologia Geral e Nefropatologia, Uberaba - MG, Brazil.; Universidade Federal de Goiás, Patologia Geral, Goiânia - GO, Brazil., Reis MAD; Universidade Federal do Triângulo Mineiro, Serviço de Patologia Geral e Nefropatologia, Uberaba - MG, Brazil.
Jazyk:	English; Portuguese
Zdroj:	Jornal brasileiro de nefrologia [J Bras Nefrol] 2017 Oct-Dec; Vol. 39 (4), pp. 370-375.
DOI:	10.5935/0101-2800.20170068
Abstrakt:	Introduction: Membranous nephropathy (MN) is one of the major causes of nephrotic syndrome. The complement system plays a key role in the pathophysiology of MN. Objectives: To identify the complement pathway possibly activated in MN cases and correlate the presence of C4d with more severe clinical and histological markers. Methods: Sixty nine cases from renal biopsy with membranous nephropathy were investigated. The presence of C1q was analyzed by direct immunofluorescence; and expression of C4d by immunohistochemistry. Clinical and epidemiological data were obtained upon biopsy request. Results: The presence of focal segmental glomerulosclerosis, global glomerulosclerosis, vascular lesions and tubulointerstitial fibrosis were collected by anatomopathological report. C4d(+) was found in 58 (84%), and C1q(+) was found in 12 (17%) of the cases. Twelve patients had C4d(+)/C1q(+), 46 had C4d(+)/C1q(-), and 11 patients had C4d(-)/C1q(-), probably indicating the activation of the classical, lectin and alternative pathways, respectively. Conclusion: C4d was associated with increased interstitial fibrosis, but not with clinical markers of poor prognosis. Through the deposition of C4d and C1q we demonstrated that all complement pathways may be involved in MN, highlighting the lectin pathway. The presence of C4d has been associated with severe tubulointerstitial lesions, but not with clinical markers, or can be taken as a universal marker of all cases of MN.
Databáze:	MEDLINE
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