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Related Experiment Video

Updated: Dec 3, 2025

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

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Complement in Secondary Thrombotic Microangiopathy.

Lilian Monteiro Pereira Palma¹, Meera Sridharan², Sanjeev Sethi³

¹Pediatric Nephrology, State University of Campinas (UNICAMP), Brazil.

Kidney International Reports

|October 26, 2020

Summary

This summary is machine-generated.

Thrombotic microangiopathy (TMA) involves complement system defects. Understanding complement

Keywords:

HUS autoimmune disease complement drugs hypertension thrombotic microangiopathy

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Area of Science:

Nephrology
Hematology
Immunology

Background:

Thrombotic microangiopathy (TMA) is a critical condition marked by low platelets and hemolytic anemia.
Complement system activation is a key factor in TMA pathogenesis.
TMA is categorized as primary (complement-mediated, atypical hemolytic uremic syndrome) or secondary (associated with other conditions).

Purpose of the Study:

To review the role of complement in atypical hemolytic uremic syndrome (aHUS).
To examine complement's involvement in secondary TMA forms linked to various conditions.
To propose a novel management strategy for TMA based on complement involvement.

Main Methods:

Literature review focusing on complement's role in TMA.
Analysis of genetic variants in complement genes across different TMA subtypes.
Synthesis of data to support a new management approach.

Main Results:

Genetic complement defects are prevalent in aHUS (up to 60%).
Genetic defects in secondary TMA vary, from nearly 60% in malignant hypertension-associated TMA to <10% in drug-induced TMA.
Overlap exists between primary and secondary TMA classifications due to genetic variants.

Conclusions:

Complement system dysregulation is central to TMA pathogenesis, including aHUS and secondary forms.
Identifying genetic complement defects is crucial for accurate TMA diagnosis and timely treatment.
A revised management approach is needed to address the complex role of complement in TMA.