Abstract

Objective To evaluate the diagnostic value of pathological features of atypical membranous nephropathy (AMN). Methods Ninety-one patients with AMN diagnosed by renal biopsy during 2011 and 2017 were enrolled in this study. On the basis of M-type phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-containing 7A protein (THSD7A) by immunohistochemistry, patients were divided into AMN group (25 cases without PLA2R and THSD7A) and idiopathic membranous nephropathy (IMN) group (66 cases with positive PLA2R or THSD7A). The results of immunofluorescence (IF), light microscopy (LM) and electron microscopy (EM) of these two groups were compared, and the parameters with statistical difference were screened out in order to assess their value in the diagnosis of AMN in fourfold table. Results IF results showed that in AMN group the proportions of IgG deposition on capillary wall and mesangial area as well as positive other IgG subclasses and complement C1q but negative IgG4 were significantly higher than those in IMN group (respectively, 56.0% vs 12.1%, 44.0% vs 0, both P 0.05). LM results showed that the proportions of false double track sign on basement membrane and fuchsinophilic proteins under epithelium, endothelium, basement membrane and mesangial region in AMN group were significantly higher than those in IMN group (respectively, 36.0% vs 0, 44.0% vs 1.5%, both P 0.05). EM results showed that the rate of endothelial electron dense deposits in AMN group was significantly higher than that in IMN group (36.0% vs 1.5%, P<0.05), and its diagnostic specificity for AMN was 98.5%. Conclusions IgG deposition on both capillary wall and mesangial area, positive other IgG subclasses and C1q with negative IgG4, false-double contour sign, multi-site fuchsinophilic deposits and endothelial electron dense deposits may help for the AMN diagnosis in the absence of PLA2R and THSD7A related data. Key words: Glomerulonephritis, membranous; Immunoglobulin G; Complement C1q; Receptors, phospholipase A2; Thrombospondin type-1 domain containing 7A protein

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