Related Experiment Video

Updated: Aug 27, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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Phospholipase A2 receptor is associated with hypercoagulable status in membranous nephropathy: a narrative review

Xu Lu1, Chao Kan1, Rui Zhang2

  • 1Department of Clinical Medicine, Changchun University of Chinese Medicine, Changchun, China.

Annals of Translational Medicine
|September 29, 2022
PubMed
Abstract

Insights

Membranous nephropathy patients face high thrombotic risks. Secretory phospholipase A2 (sPLA2) and arachidonic acid (AA) may link phospholipase A2 receptor (PLA2R) to hypercoagulability in PLA2R-related MN.

Area of Science:

  • Nephrology
  • Immunology
  • Hematology

Background:

  • Membranous nephropathy (MN) is a leading cause of thrombotic events in nephrotic syndrome (NS).
  • The precise mechanisms linking MN to thrombosis remain incompletely understood.
  • Elevated phospholipase A2 receptor (PLA2R) antibodies correlate with proteinuria and reduced remission rates in PLA2R-associated MN, factors also associated with thrombotic risk.

Purpose of the Study:

  • To elucidate the relationship between PLA2R and hypercoagulability in MN patients.
  • To explore the potential roles of secretory phospholipase A2 (sPLA2) and arachidonic acid (AA) in regulating blood lipids and coagulation in PLA2R-positive MN.

Main Methods:

  • Literature retrieval from China National Knowledge Infrastructure (CNKI) and PubMed.
  • Systematic review and classification of retrieved abstract and introduction information.
  • Summarization of key findings to formulate a novel theoretical standpoint.

Main Results:

  • Discussed the involvement of PLA2R antibodies and sPLA2 in MN-related hypercoagulability.
  • Analyzed four proposed mechanisms: sPLA2-PLA2R binding inducing podocyte apoptosis, sPLA2 promoting anti-PLA2R antibody production, sPLA2 mediating AA release, and AA-induced platelet aggregation.

Conclusions:

  • PLA2R may contribute to the exacerbation of hypercoagulability in PLA2R-related MN.
  • Secretory phospholipase A2 (sPLA2) appears to play a significant role in this pro-thrombotic process.
Keywords:
Arachidonic acid (AA)coagulation disordermembranous nephropathy (MN)phospholipase A2 receptor (PLA2R)secretory phospholipase A2 (sPLA2)

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