Immune-Monitoring Disease Activity in Primary Membranous Nephropathy

Paolo Cravedi, Marta Jarque, Andrea Angeletti, Àlex Favà, Chiara Cantarelli, Oriol Bestard

Research output: Contribution to journalReview articlepeer-review

17 Scopus citations

Abstract

Primary membranous nephropathy (MN) is a glomerular disease mediated by autoreactive antibodies, being the main cause of nephrotic syndrome among adult patients. While the pathogenesis of MN is still controversial, the detection of autoantibodies against two specific glomerular antigens, phospholipase A2 receptor (PLA2R) and thrombospondin type 1 domain containing 7A (THSD7A), together with the beneficial effect of therapies targeting B cells, have highlighted the main role of autoreactive B cells driving this renal disease. In fact, the detection of PLA2R-specific IgG4 antibodies has resulted in a paradigm shift regarding the diagnosis as well as a better prediction of the progression and recurrence of primary MN. Nevertheless, some patients do not show remission of the nephrotic syndrome or do rapidly recur after immunosuppression withdrawal, regardless the absence of detectable anti-PLA2R antibodies, thus highlighting the need of other immune biomarkers for MN risk-stratification. Notably, the exclusive evaluation of circulating antibodies may significantly underestimate the magnitude of the global humoral memory immune response since it may exclude the role of antigen-specific memory B cells. Therefore, the assessment of PLA2R-specific B-cell immune responses using novel technologies in a functional manner may provide novel insight on the pathogenic mechanisms of B cells triggering MN as well as refine current immune-risk stratification solely based on circulating autoantibodies.

Original languageEnglish
Article number241
JournalFrontiers in Medicine
Volume6
DOIs
StatePublished - 8 Nov 2019

Keywords

  • PLAR
  • THSD7A
  • autoreactive B cells
  • glomerulonephritis recurrence
  • membranous nephropathy

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