Prevalence of Enhanced Granular Expression of Thrombospondin Type-1 Domain-Containing 7A in the Glomeruli of Japanese Patients with Idiopathic Membranous Nephropathy

PLoS One. 2015 Sep 22;10(9):e0138841. doi: 10.1371/journal.pone.0138841. eCollection 2015.

Abstract

Membranous nephropathy (MN) is a leading cause of nephrotic syndrome in adults. Autoantibodies against M-type phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-containing 7A (THSD7A), which mainly belong to the IgG4 subclass, were reported as associated antibodies for the development of MN. Although PLA2R is a major target antigen for idiopathic MN, the prevalence of MN patients seropositive for PLA2R in Japan is lower than that in other countries. In this study, we conducted immunohistochemical analysis of the presence of THSD7A and PLA2R in renal specimens of MN patients to estimate the prevalence of THSD7A/PLA2R-related idiopathic MN in Japan. Enhanced granular expression of THSD7A and PLA2R was detected in 9.1% and 52.7%, respectively, of the patients with idiopathic MN. Although none of patients with secondary MN displayed enhanced granular expression of THSD7A, 5.4% of them had enhanced granular expression of PLA2R. In conclusion, the prevalence of enhanced granular expression of THSD7A in the glomeruli of Japanese patients with idiopathic MN was higher than the prevalence of MN patients seropositive for THSD7A in USA and Europe.

MeSH terms

  • Adult
  • Aged
  • Cytoplasmic Granules / metabolism
  • Female
  • Glomerulonephritis, Membranous / epidemiology
  • Glomerulonephritis, Membranous / metabolism*
  • Humans
  • Immunoglobulin G / metabolism
  • Immunohistochemistry
  • Japan / epidemiology
  • Kidney Glomerulus / metabolism*
  • Kidney Glomerulus / pathology
  • Male
  • Middle Aged
  • Prevalence
  • Receptors, Phospholipase A2 / biosynthesis*
  • Thrombospondins / biosynthesis*
  • Young Adult

Substances

  • Immunoglobulin G
  • PLA2R1 protein, human
  • Receptors, Phospholipase A2
  • THSD7A protein, human
  • Thrombospondins

Grants and funding

The authors have no support or funding to report.