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Properdin deficiency or anti-properdin treatment ameliorates disease in the C3 gain-of-function mouse model of atypical haemolytic uraemic syndrome.

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Related Experiment Video

Updated: Sep 20, 2025

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

Atypical hemolytic uremic syndrome.

Patrick R Walsh¹, David Kavanagh¹

¹From the Complement Therapeutics Research Group, Translational and Clinical Research Institute, Newcastle University, and the National Renal Complement Therapeutics Centre, Royal Victoria Infirmary, Newcastle upon Tyne, United Kingdom.

The Journal of Allergy and Clinical Immunology

|May 28, 2025

Summary

Hemolytic uremic syndromes (HUS) involve thrombotic microangiopathy, causing organ damage. Understanding complement pathways led to C5 inhibitors, improving HUS prognosis.

Keywords:

Hemolytic uremic syndrome complement eculizumab iptacopan pegcetacoplan thrombotic microangiopathy thrombotic thrombocytopenic purpura

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Published on: June 2, 2022

Area of Science:

Nephrology
Hematology
Immunology

Background:

Hemolytic uremic syndromes (HUS) are diverse conditions characterized by thrombotic microangiopathy (TMA).
TMAs involve microangiopathic hemolytic anemia, thrombocytopenia, and often acute kidney injury due to endothelial damage.
Recent advances have elucidated various contributing pathways, including immunologic and metabolic factors.

Purpose of the Study:

To review the current understanding of HUS pathogenesis.
To differentiate between complement-dependent and non-complement-dependent TMAs.
To highlight therapeutic advancements based on pathogenetic insights.

Main Methods:

Literature review of recent research on HUS and TMA.
Analysis of immunologic, metabolic, and genetic pathways involved in HUS.
Evaluation of therapeutic strategies targeting specific HUS mechanisms.

Main Results:

Diverse pathophysiologies underlie different HUS forms.
The membrane attack complex plays a role in certain TMAs.
Pharmacologic inhibition of complement C5 has significantly improved outcomes.

Conclusions:

Understanding HUS pathogenesis is crucial for effective treatment.
Targeting complement pathways, specifically C5, offers a promising therapeutic approach for select TMAs.
Further research into non-complement-dependent TMAs is warranted.