# Research progress on the lectin pathway of complement in IgA nephropathy

**Authors:** Xiaoqing Yu, Hui Gao, Xifeng Sun

PMC · DOI: 10.3389/fimmu.2026.1757595 · 2026-02-27

## TL;DR

This paper reviews how the lectin pathway of the complement system contributes to IgA nephropathy, a kidney disease, and its potential for new treatments.

## Contribution

The paper provides a comprehensive review of the role of the lectin pathway in IgA nephropathy and its implications for novel therapies.

## Key findings

- The lectin pathway activation is linked to IgA nephropathy progression and prognosis.
- Complement activation leads to inflammation and kidney damage in IgA nephropathy.
- Urinary complement components may serve as non-invasive biomarkers for disease monitoring.

## Abstract

As an autoimmune disease, IgA nephropathy is pathologically characterized by the deposition of immunoglobulin A (IgA) in the glomerular mesangial area. Recent research has confirmed that the activation of the lectin pathway in the complement system may be related to the development and prognosis of IgA nephropathy (IgAN). These deposited immune complexes trigger the complement cascade, generating various inflammatory mediators that directly attack glomerular mesangial cells and promote mesangial matrix proliferation and crescent formation, ultimately leading to end stage renal disease. Therefore, an in-depth understanding of complement activation pathways not only provides potential non-invasive biomarkers (such as urinary complement components) for assessing disease activity and prognosis, more importantly, establishes a theoretical foundation for developing novel anti-complement targeted therapies. This holds promise for opening new directions in the personalized precision treatment of IgA nephropathy. This article reviews the research progress on the lectin pathway and its associated components in IgA nephropathy.

## Linked entities

- **Diseases:** IgA nephropathy (MONDO:0005342), end stage renal disease (MONDO:0004375)

## Full-text entities

- **Genes:** CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}
- **Diseases:** inflammatory (MESH:D007249), autoimmune disease (MESH:D001327), end stage renal disease (MESH:D007676), IgA nephropathy (MESH:D005922)

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12982443/full.md

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Source: https://tomesphere.com/paper/PMC12982443