Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Chronic Kidney Disease III: Interprofessional Care01:28

Chronic Kidney Disease III: Interprofessional Care

259
Chronic kidney disease (CKD) requires collaborative and comprehensive management. CKD progresses through stages and can lead to end-stage kidney disease (ESKD) if untreated. Interprofessional collaboration and patient education are crucial, enabling patients to manage their health and improve their quality of life.Diagnostic approach for chronic kidney diseaseThe diagnosis of CKD primarily focuses on the glomerular filtration rate (GFR), which assesses kidney function by measuring how well...
259
Nephrotic Syndrome III : Nursing Management01:24

Nephrotic Syndrome III : Nursing Management

210
Nursing management for nephrotic syndrome adapts as the disease progresses, with strategies evolving to address advancing symptoms and complications.Early-Stage Management In the early stages, nursing interventions for nephrotic syndrome resemble those used in managing acute glomerulonephritis, focusing on symptom monitoring, fluid balance, and managing mild to moderate edema.Vital Signs: Regularly monitor blood pressure, pulse, respiratory rate, and temperature to promptly identify...
210
Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

386
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...
386
Glaucoma: Overview01:25

Glaucoma: Overview

1.1K
Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
1.1K
Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

873
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.
Drugs such as carbonic anhydrase inhibitors, α2- and...
873
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

1.0K
Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
1.0K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Obinutuzumab or Tacrolimus in Primary Membranous Nephropathy.

The New England journal of medicine·2026
Same author

Pegcetacoplan Versus Iptacopan for the Treatment of Patients with C3 Glomerulopathy: Indirect Treatment Comparisons.

Advances in therapy·2026
Same author

Complement 3 Glomerulopathy (C3G) in Native and Posttransplant Kidneys: A Review.

American journal of kidney diseases : the official journal of the National Kidney Foundation·2026
Same author

Complement biomarkers during iptacopan treatment - Authors' reply.

Lancet (London, England)·2026
Same author

Shared multicellular injury programs of acute and chronic kidney disease enable mechanistic patient stratification.

medRxiv : the preprint server for health sciences·2026
Same author

Precision Diagnosis in APOL1 Kidney Disease With the p.N264K M1 Protective Variant.

JAMA network open·2026

Related Experiment Video

Updated: Dec 18, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

765

C3 Glomerulopathy: Pathogenesis and Treatment.

Syeda Behjat Ahmad1, Andrew S Bomback1

  • 1Division of Nephrology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY.

Advances in Chronic Kidney Disease
|June 20, 2020
PubMed
Summary
This summary is machine-generated.

C3 glomerulopathy (C3G) is a rare kidney disease caused by complement dysregulation. This review covers C3G pathogenesis and emerging complement inhibitor treatments for C3 glomerulonephritis and dense deposit disease.

Keywords:
ComplementDense deposit diseaseMembranoproliferative glomerulonephritis

More Related Videos

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

1.7K
Induction of Ocular Surface Inflammation and Collection of Involved Tissues
06:38

Induction of Ocular Surface Inflammation and Collection of Involved Tissues

Published on: August 4, 2022

2.6K

Related Experiment Videos

Last Updated: Dec 18, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

765
Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents
10:10

Full-Circle Cauterization of Limbal Vascular Plexus for Surgically Induced Glaucoma in Rodents

Published on: February 15, 2022

1.7K
Induction of Ocular Surface Inflammation and Collection of Involved Tissues
06:38

Induction of Ocular Surface Inflammation and Collection of Involved Tissues

Published on: August 4, 2022

2.6K

Area of Science:

  • Nephrology
  • Immunology
  • Genetics

Background:

  • C3 glomerulopathy (C3G) encompasses C3 glomerulonephritis (C3GN) and dense deposit disease, both rare kidney diseases.
  • These conditions stem from dysregulation of the complement alternative pathway, often due to genetic or acquired defects in regulatory proteins.
  • C3G presents with low serum C3 and C3-dominant immunofluorescence on kidney biopsy, but can be mistaken for other glomerulonephritides.

Purpose of the Study:

  • To review the pathogenesis of C3 glomerulonephritis (C3GN).
  • To survey current and investigational treatment options for C3G.
  • To highlight diagnostic challenges and disease recurrence after transplantation.

Main Methods:

  • Literature review of C3 glomerulopathy.
  • Analysis of complement pathway dysregulation in C3G.
  • Summary of clinical trials and approved therapies.

Main Results:

  • C3G pathogenesis involves complement alternative pathway dysregulation.
  • Both C3GN and dense deposit disease are progressive and can recur post-transplant.
  • Complement inhibitors show promise as targeted therapies.

Conclusions:

  • C3G requires understanding of complement biology for diagnosis and management.
  • Targeted complement inhibition represents a significant advancement in C3G treatment.
  • Further research is needed to optimize therapeutic strategies and address disease recurrence.