Related Experiment Video
Updated: Jul 30, 2026
06:11
Anterior Cervical Discectomy and Fusion in the Ovine Model
Published on: October 5, 2009
13.3K
[Membranoproliferative glomerulonephritis and C3 glomerulopathy].
B Hohenstein1,2, K Amann3, J Menne4
1Nephrologisches Zentrum Villingen-Schwenningen, Albert-Schweitzer‑Str. 6, 78052, Villingen-Schwenningen, Deutschland. hohenstein@nephrologie-vs.de.
Der Internist
|March 13, 2019
Summary
C3 glomerulopathy (C3G) and immune complex-mediated membranoproliferative glomerulonephritis (IC-MPGN) share pathophysiological aspects, necessitating comprehensive diagnostic approaches including complement, antibody, and genetic analysis for effective treatment.
Area of Science:
- Nephrology
- Immunology
- Pathophysiology
Background:
- A 2010 classification introduced C3 glomerulopathy (C3G) as a subgroup of glomerulonephritis with C3 deposits.
- Immune complex-mediated membranoproliferative glomerulonephritis (IC-MPGN) and C3G are now viewed as a heterogeneous disease spectrum.
Purpose of the Study:
- To highlight shared pathophysiological aspects between IC-MPGN and C3G.
- To emphasize the importance of understanding pathophysiology for guiding diagnostic workup.
- To advocate for comprehensive diagnostic strategies in managing these conditions.
Main Methods:
- Review of recent evidence on the pathophysiology of IC-MPGN and C3G.
- Analysis of shared features including secondary causes, autoantibodies, and genetic factors.
- Discussion of diagnostic implications and treatment approaches.
Main Results:
- IC-MPGN and C3G exhibit more shared pathophysiological mechanisms than previously recognized.
- Secondary causes, autoantibodies, and genetic factors are common to both conditions.
- Current evidence supports specific diagnostic and therapeutic strategies.
Conclusions:
- Integrated understanding of IC-MPGN and C3G pathophysiology is crucial.
- Comprehensive complement, antibody, and genetic analyses are recommended for diagnosis.
- Available treatments offer a foundation for managing these progressive kidney diseases, even post-transplant.
Related Concept Videos
01:26Nephrotic Syndrome II : Assessment and Medical Management
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 any history...
01:29Acute Kidney Injury II: Pathophysiology
Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
01:27Cryptococcal Meningitis
Cryptococcal meningitis is a life-threatening opportunistic infection predominantly associated with HIV/AIDS, accounting for over 100,000 deaths annually worldwide. However, it also affects individuals with other forms of immunosuppression, including those undergoing immunosuppressive therapy, organ transplant recipients, patients with innate immunodeficiencies, and individuals with hematological disorders. The infection is caused mainly by Cryptococcus neoformans and Cryptococcus gattii,...
01:26Bacterial Meningitis II: Pathophysiology
Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
01:26Encephalitis ll: Pathophysiology
Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
01:22Cerebral Edema ll: Pathophysiology
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...