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Related Concept Videos

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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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In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
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Updated: May 2, 2026

In Vitro Methods for Comparing Target Binding and CDC Induction Between Therapeutic Antibodies: Applications in Biosimilarity Analysis
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Anti-complement therapy for glomerular diseases.

Andrew S Bomback1

  • 1Division of Nephrology, Department of Medicine, Columbia University Medical Center, New York, NY.

Advances in Chronic Kidney Disease
|March 8, 2014
PubMed
Summary
This summary is machine-generated.

Complement pathway components are key to understanding glomerular diseases and kidney injury. Therapies targeting complement, like C5 inhibitor eculizumab, show promise, but C3-targeted agents may be more effective for C3 glomerulopathies.

Keywords:
Anti-neutrophil cytoplasmic autoantibodyAtypical hemolytic uremic syndromeC3 glomerulopathiesComplementEculizumab

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Area of Science:

  • Nephrology
  • Immunology
  • Complement System Biology

Background:

  • Glomerular diseases are increasingly understood through the lens of complement pathway involvement in kidney injury.
  • Classification of membranoproliferative glomerulonephritis now distinguishes between immune-complex and complement-mediated lesions.
  • This focus on complement drives interest in complement-targeting therapies for disease modification.

Purpose of the Study:

  • To review the role of complement in glomerular diseases.
  • To evaluate the efficacy of complement-targeting therapies, including eculizumab.
  • To discuss the potential of novel C3-targeted therapies for C3 glomerulopathies.

Main Methods:

  • Review of current literature on complement pathways in glomerular diseases.
  • Analysis of clinical data regarding eculizumab in atypical hemolytic uremic syndrome.
  • Discussion of emerging therapeutic strategies for C3 glomerulonephritis and dense deposit disease.

Main Results:

  • Eculizumab, a C5 inhibitor, has transformed atypical hemolytic uremic syndrome treatment.
  • The efficacy of eculizumab for C3 glomerulonephritis and dense deposit disease is uncertain due to disease heterogeneity.
  • Emerging therapies targeting C3 show potential for specific treatment of C3 glomerulopathies.

Conclusions:

  • Understanding complement's role is crucial for diagnosing and treating glomerular diseases.
  • While C5 inhibition is effective for some conditions, C3-targeted therapies may offer more specific treatment for C3 glomerulopathies.
  • Further research is needed to establish the role of various complement inhibitors in different glomerular diseases.