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Related Concept Videos

Complement System01:27

Complement System

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

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Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
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Extrinsic and Intrinsic Pathways of Hemostasis01:20

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Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
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Clot Retraction and Fibrinolysis01:16

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After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
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Disorders of Hemostasis01:24

Disorders of Hemostasis

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Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
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Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
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Related Experiment Video

Updated: Apr 18, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
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Complement Factor C4d Is a Common Denominator in Thrombotic Microangiopathy.

Jamie S Chua1, Hans J Baelde2, Malu Zandbergen2

  • 1Department of Pathology and j.s.chua@lumc.nl.

Journal of the American Society of Nephrology : JASN
|January 10, 2015
PubMed
Summary

Complement factor C4d is common in thrombotic microangiopathy (TMA) kidney biopsies. Terminal complement complex (C5b-9) is also prevalent, suggesting complement inhibitors may benefit TMA patients.

Keywords:
complementhemolytic uremic syndromerenal biopsyrenal pathologyrenal transplantationthrombosis

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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

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Area of Science:

  • Nephrology
  • Immunology
  • Pathology

Background:

  • Complement activation significantly contributes to thrombotic microangiopathy (TMA), a critical condition with diverse clinical presentations.
  • Recent advancements in terminal complement-inhibiting drugs necessitate reliable biomarkers for patient stratification.
  • Understanding complement pathway involvement in TMA is crucial for targeted therapeutic strategies.

Purpose of the Study:

  • To investigate the prevalence and kidney localization of complement factor C4d in patients with TMA.
  • To identify the specific complement pathways responsible for C4d deposition in TMA.
  • To assess the presence of the terminal complement complex (C5b-9) as a consequence of complement activation in TMA.

Main Methods:

  • Analysis of 42 renal tissue sections from patients with histologically confirmed TMA.
  • Histopathological scoring of C4d, mannose-binding lectin, C1q, IgM, and C5b-9 deposits in glomeruli, peritubular capillaries, and arterioles.
  • Comparison of complement deposition patterns between TMA cases and control subjects (n=53).

Main Results:

  • C4d deposits were identified in 88.1% of TMA cases, with distinct patterns across different renal vasculature compartments.
  • Classical pathway activation was evident in 90.5% of TMA cases.
  • Terminal complement complex (C5b-9) deposits were found in 78.6% of TMA cases, compared to 39.6% in controls, with differing staining patterns.

Conclusions:

  • C4d is a frequent biomarker in TMA, irrespective of the underlying etiology.
  • The high prevalence of C5b-9 in TMA samples suggests potential therapeutic benefit from terminal complement inhibitors.
  • C4d and C5b-9 warrant further investigation as diagnostic biomarkers for complement-mediated TMA.