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

Acute Kidney Injury II: Pathophysiology01:29

Acute 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...
Acute Pyelonephritis I: Introduction01:27

Acute Pyelonephritis I: Introduction

Pyelonephritis is a bacterial infection that primarily affects the renal parenchyma and collecting system, including the renal pelvis, tubules, and interstitial tissue of one or both kidneys. It can be classified as either acute—a sudden, severe infection—or chronic, which refers to long-term or recurrent kidney infections.The primary cause of acute pyelonephritis (APN) is bacterial infection, with Escherichia coli accounting for approximately 70-80% of cases. Other bacteria, such as Proteus,...
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...
Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

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 fluid...
Encephalitis ll: Pathophysiology01:26

Encephalitis 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...
Acute Pyelonephritis II: Diagnostic Studies and Management01:28

Acute Pyelonephritis II: Diagnostic Studies and Management

Introduction:For diagnosing acute pyelonephritis, a comprehensive patient history is collected to identify symptoms such as dysuria, frequent or urgent urination, flank pain, or costovertebral angle (CVA) tenderness that may suggest a kidney infection.Physical ExaminationDuring the physical examination, CVA tenderness is assessed. This involves gentle percussion over the costovertebral angle, where tenderness often indicates a kidney infection.Diagnostic TestsUrinalysis: Used to identify white...

You might also read

Related Articles

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

Sort by
Same author

Hematopoietic stem cell transplantation for erythropoietic porphyria-induced acute liver failure: a case report and literature review.

Clinics and research in hepatology and gastroenterology·2026
Same author

The Immune Microenvironment of Transplant Glomerulitis.

Kidney international reports·2025
Same author

Impact of Fructose-Enhanced Solid and Soft Drink Diets on Metabolism, Physiology, and Gut Microbiome in Pregnant Rats.

BioMed research international·2025
Same author

Clinicopathologic, Proteomic and Outcome Characteristics of Renal Apolipoprotein C-II Amyloidosis: A Case Series.

American journal of kidney diseases : the official journal of the National Kidney Foundation·2024
Same author

ClC-Kb pore mutation disrupts glycosylation and triggers distal tubular remodeling.

JCI insight·2024
Same author

Spatial analysis reveals targetable macrophage-mediated mechanisms of immune evasion in hepatocellular carcinoma minimal residual disease.

Nature cancer·2024
Same journal

Pathobiology and Interactions of the MiTF Signaling Pathways.

Advances in anatomic pathology·2026
Same journal

Diagnosis and Reporting of Intraductal Carcinoma of the Prostate: A Guide for Practising Pathologists With Excerpts From the Genitourinary Pathology Society and the International Society of Urological Pathology Joint Expert Consultation.

Advances in anatomic pathology·2026
Same journal

An Update on Soft Tissue Tumors of the Paratesticular Region.

Advances in anatomic pathology·2026
Same journal

Recognizing Familial Thyroid Neoplasia: The Pathologist's Role in Diagnosis and Management.

Advances in anatomic pathology·2026
Same journal

Hereditary and Familial Tumor Syndromes: When to Think of Them? The Emerging Role of Pathologists as Sentinels of Genetic Cancer Predisposition.

Advances in anatomic pathology·2026
Same journal

From Familial Clustering to a Dedicated Classification: The Historical Recognition of Hereditary Tumor Syndromes in the WHO Classification of Tumors.

Advances in anatomic pathology·2026
See all related articles

Related Experiment Video

Updated: May 19, 2026

Primed Mycobacterial Uveitis (PMU) as a Model for Post-Infectious Uveitis
10:33

Primed Mycobacterial Uveitis (PMU) as a Model for Post-Infectious Uveitis

Published on: December 17, 2021

Postinfectious glomerulonephritis.

Neeraja Kambham1

  • 1Department of Pathology, Stanford University Medical Center, Stanford, CA, USA. nkambham@stanford.edu

Advances in Anatomic Pathology
|August 14, 2012
PubMed
Summary
This summary is machine-generated.

Postinfectious glomerulonephritis (PIGN) is kidney inflammation caused by infections. While often self-limiting, especially post-streptococcal glomerulonephritis (PSGN) in children, it can lead to chronic issues and poses a public health concern globally.

More Related Videos

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Related Experiment Videos

Last Updated: May 19, 2026

Primed Mycobacterial Uveitis (PMU) as a Model for Post-Infectious Uveitis
10:33

Primed Mycobacterial Uveitis (PMU) as a Model for Post-Infectious Uveitis

Published on: December 17, 2021

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
09:43

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Area of Science:

  • Nephrology
  • Immunology
  • Infectious Diseases

Background:

  • Postinfectious glomerulonephritis (PIGN) is immunologically mediated glomerular injury.
  • Poststreptococcal glomerulonephritis (PSGN) is a classic PIGN example with specific histology and immunofluorescence findings.
  • Susceptibility to PSGN involves host and microbial factors, with identified nephritogenic antigens.

Purpose of the Study:

  • To review the understanding of PIGN, focusing on PSGN and non-streptococcal causes.
  • To highlight the changing epidemiology and clinical outcomes of PIGN.
  • To discuss the diagnostic challenges posed by the diverse morphologic changes in PIGN.

Main Methods:

  • Review of literature on PIGN, PSGN, and associated infections.
  • Analysis of histological and immunofluorescence findings in PIGN.
  • Discussion of clinical presentations, outcomes, and diagnostic criteria.

Main Results:

  • PSGN, though often self-limited in children, can cause persistent renal abnormalities.
  • PIGN in Western countries is increasingly linked to non-streptococcal infections in older adults with comorbidities, associated with poor outcomes.
  • Immunofluorescence typically shows dominant C3 staining and subepithelial humps; IgA-dominant PIGN is a recognized entity.

Conclusions:

  • PIGN presents a diagnostic challenge due to its varied morphology and association with different infections.
  • Understanding the specific causative agents and host factors is crucial for managing PIGN.
  • While PSGN incidence declines in developed nations, PIGN remains a significant concern, particularly in resource-limited settings.