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Related Concept Videos

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...
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...
Chronic Kidney Disease III: Interprofessional Care01:28

Chronic Kidney Disease III: Interprofessional Care

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...
Nephrotic Syndrome II : Assessment and Medical Management01:26

Nephrotic 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...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...

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Related Experiment Video

Updated: Jun 19, 2026

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

Studies on chronic membranoproliferative glomerulonephritis with hypocomplementemia.

A F Michael1, N G Westberg, A J Fish

  • 1Department of Pediatrics, University of Minnesota Medical School, Minneapolis, Minnesota 55455.

The Journal of Experimental Medicine
|October 30, 2009
PubMed
Summary

This study investigates C3 glomerulonephritis (CMPGN) with hypocomplementemia, a progressive kidney disease. Findings suggest a distinct entity possibly involving both classical and alternative complement pathways.

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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
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Last Updated: Jun 19, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

Area of Science:

  • Nephrology
  • Immunology
  • Pathology

Background:

  • C3 glomerulonephritis (CMPGN) with hypocomplementemia is a destructive kidney disease.
  • Its specific pathogenetic entity remains unproven.
  • Clinical presentations vary, including asymptomatic proteinuria/hematuria, nephrotic syndrome, or acute nephritic syndrome.

Purpose of the Study:

  • To elucidate the pathogenetic mechanisms of CMPGN with hypocomplementemia.
  • To characterize the clinical and morphological features of this glomerulonephritis.
  • To investigate the role of the complement system in CMPGN.

Main Methods:

  • Morphological studies including immunofluorescence microscopy.
  • Analysis of serum complement abnormalities using labeled isotope studies.
  • Assessment of complement regulatory proteins and enzymatic activity.

Main Results:

  • Morphology shows mesangial proliferation, increased matrix, and thickened glomerular capillaries.
  • Immunofluorescence reveals predominant peripheral lobular deposits of C3 and properdin, with less consistent immunoglobulin presence.
  • Serum analysis demonstrates C3 depression, evidence of C3 breakdown, elevated alpha(2)D, and specific complement-inhibiting factors.

Conclusions:

  • CMPGN with hypocomplementemia exhibits unique morphological and immunopathological features.
  • Findings suggest a potential role for the alternative complement pathway due to properdin deposits and terminal complement inactivation.
  • Both classical and alternative complement pathway mechanisms may contribute to immune injury in CMPGN.