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Updated: Aug 15, 2025

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

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Thrombotic microangiopathy mediates poor prognosis among lupus nephritis via complement lectin and alternative

Binshan Zhang1, Guolan Xing1

  • 1Department of nephrology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

Frontiers in Immunology
|December 30, 2022
PubMed

Insights

Thrombotic microangiopathy (TMA) significantly worsens kidney survival in lupus nephritis (LN) patients. Complement lectin pathway (LP) and alternative pathway (AP) activation contribute to LN-associated TMA pathogenesis.

Area of Science:

  • Nephrology
  • Immunology
  • Pathology

Background:

  • Lupus nephritis (LN) pathogenesis involves complex mechanisms, including thrombotic microangiopathy (TMA).
  • The role of complement lectin pathway (LP) and alternative pathway (AP) in LN-associated TMA requires further elucidation.

Purpose of the Study:

  • To investigate the deposition of LP and AP components in renal tissues of LN patients with and without TMA.
  • To evaluate clinicopathological characteristics and identify risk factors for renal survival in LN patients with TMA.

Main Methods:

  • Retrospective cohort study of 79 LN patients with TMA and 79 matched controls without TMA.
  • Immunohistochemistry, immunofluorescence, and confocal microscopy to assess deposition of MBL, MASP1/3, CFB, CFD, C4d, VWF, C5b-9, and CD34 in renal tissues.

Main Results:

  • Patients with TMA exhibited higher incidence of acute kidney injury, acute hemodialysis, and interstitial fibrosis.
  • TMA was associated with significantly inferior 3-year renal survival rates (68% vs. 89%) and identified as an independent risk factor (HR 4.807).
  • Enhanced deposition of MBL, MASP1/3, CFB, CFD, C4d, and VWF was observed in TMA patients, alongside co-localized CD34 and C5b-9 expression in endothelial cells.

Conclusions:

  • Thrombotic microangiopathy (TMA) is an independent risk factor for renal survival in lupus nephritis (LN).
  • Lectin pathway (LP) and alternative pathway (AP) activation play a role in the pathogenesis of LN-associated TMA.
Abstract

Keywords:
alternative pathwaycomplementlectin pathwaylupus nephritisthrombotic microangiopathy

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