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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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Renal Corpuscle01:20

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The glomerulus and Bowman's capsule are two essential components of the nephron, which is the functional unit of the kidney. These microscopic structures play a critical role in the process of blood filtration to produce urine.
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Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of...
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Nephrotic Syndrome II : Assessment and Medical Management01:26

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IntroductionNephrotic syndrome is a kidney disorder marked by excessive protein loss in the urine, leading to various systemic complications. This condition often results from damage to the glomeruli—the kidney's filtering units—causing proteinuria, low blood protein levels, and fluid retention. Understanding the assessment, diagnosis, and management of nephrotic syndrome is essential for effective treatment and prevention of further kidney damage.AssessmentPatient History: Document...
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Hypersensitivity Reactions: Immune-Complex Reactions01:19

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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum...
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Nephrotic Syndrome III : Nursing Management01:24

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Related Experiment Video

Updated: Mar 16, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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Complement in Lupus Nephritis: New Perspectives.

Lihua Bao1, Patrick N Cunningham1, Richard J Quigg2

  • 1Section of Nephrology, Department of Medicine, University of Chicago, Chicago, Ill., USA.

Kidney Diseases (Basel, Switzerland)
|August 19, 2016
PubMed
Summary
This summary is machine-generated.

Systemic lupus erythematosus (SLE) involves the complement system in dual roles. Complement deficiencies increase SLE risk, while its activation drives disease, suggesting complement-targeted therapies are promising for SLE treatment.

Keywords:
Animal modelComplementLupus nephritisSystemic lupus erythematosusTherapy

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Area of Science:

  • Immunology
  • Autoimmunity
  • Complement System Biology

Background:

  • Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by loss of self-tolerance, autoantibody production, and immune complex deposition.
  • Lupus nephritis is a severe complication of SLE, involving multiple organs and immune-mediated tissue damage.
  • The complement system, crucial for immune responses, is implicated in SLE pathogenesis but its precise role remains complex.

Purpose of the Study:

  • To elucidate the dual role of the complement system in the pathogenesis of Systemic Lupus Erythematosus (SLE).
  • To review the evidence supporting complement involvement in SLE, from genetic deficiencies to therapeutic interventions.
  • To assess the potential of complement-targeted therapies for managing SLE and its complications like lupus nephritis.

Main Methods:

  • Review of literature on complement system components (C1q, C4, CFH, DAF) and their association with SLE.
  • Analysis of experimental models of lupus nephritis in genetically modified mice.
  • Examination of clinical trial data for complement-targeted drugs (e.g., eculizumab, TP10) in SLE and related conditions.

Main Results:

  • Hereditary deficiencies in classical complement pathway components (C1q, C4) are linked to an increased risk of developing SLE.
  • Immune complex-mediated complement activation is evident in affected tissues in both experimental and human SLE.
  • Genetic studies show that deficiencies in complement inhibitors (CFH, DAF) accelerate lupus nephritis, while inhibitors ameliorate disease.
  • Clinical trials demonstrate that complement-targeted drugs can safely inhibit complement activation and are under investigation for various conditions.

Conclusions:

  • The complement system plays a dichotomous role in SLE pathogenesis, exhibiting both protective and detrimental functions.
  • Evidence from experimental models and clinical studies supports the therapeutic potential of targeting the complement system in SLE.
  • Complement-targeted therapies represent a promising strategy for managing SLE and its severe manifestations, including lupus nephritis.