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

Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

796
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...
796
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

84
Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
84
Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

864
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...
864
Nephrotic Syndrome II : Assessment and Medical Management01:26

Nephrotic Syndrome II : Assessment and Medical Management

292
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...
292
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

1.2K
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...
1.2K
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

1.0K
Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...
1.0K

You might also read

Related Articles

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

Sort by
Same author

Platelet extravasation in the microvasculature: an under-appreciated role for platelets.

Frontiers in immunology·2026
Same author

LATS1/2-CD38 Metabolic Rewiring Links Senescence to Intraplaque Thrombosis.

Circulation research·2026
Same author

Platelets: the next-generation ovarian cancer biomarker?

Trends in cancer·2026
Same author

B cell depletion promotes melanoma tumor growth in a CD4+ T cell-dependent manner.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

Platelets induce VISTA expression and modulate the ovarian tumor microenvironment.

Platelets·2026
Same author

Long-term outcome and management of complement-mediated thrombotic microangiopathy/aHUS.

Hematology. American Society of Hematology. Education Program·2025

Related Experiment Video

Updated: Mar 11, 2026

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions
06:32

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions

Published on: June 13, 2025

600

Atypical hemolytic uremic syndrome.

Vahid Afshar-Kharghan1

  • 1Section of Benign Hematology, MD Anderson Cancer Center, Houston, TX.

Hematology. American Society of Hematology. Education Program
|December 4, 2016
PubMed
Summary

Atypical hemolytic uremic syndrome (aHUS), a kidney-damaging condition, requires early diagnosis for effective anticomplement therapy. Prompt identification of aHUS versus other thrombotic microangiopathies is crucial for patient outcomes and cost-effective treatment.

Area of Science:

  • Nephrology
  • Hematology
  • Immunology

Background:

  • Atypical hemolytic uremic syndrome (aHUS) is a severe thrombotic microangiopathy (TMA) primarily affecting the kidneys.
  • It stems from dysregulation of the alternative complement pathway, leading to organ damage and end-stage renal disease.
  • aHUS can manifest at any age, with frequent relapses in native or transplanted kidneys.

Purpose of the Study:

  • To emphasize the critical need for accurate and early diagnosis of aHUS.
  • To highlight the transformative impact of anticomplement therapy on aHUS management.
  • To underscore the financial and clinical importance of differentiating aHUS from other TMAs.

Main Methods:

  • Clinical observation and diagnosis of thrombotic microangiopathy (TMA).

More Related Videos

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

22.3K
Optimization of Antigen Preparation for Hemagglutination Inhibition Assay of Newcastle Disease Virus Serology
07:04

Optimization of Antigen Preparation for Hemagglutination Inhibition Assay of Newcastle Disease Virus Serology

Published on: January 24, 2025

1.3K

Related Experiment Videos

Last Updated: Mar 11, 2026

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions
06:32

Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions

Published on: June 13, 2025

600
A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

22.3K
Optimization of Antigen Preparation for Hemagglutination Inhibition Assay of Newcastle Disease Virus Serology
07:04

Optimization of Antigen Preparation for Hemagglutination Inhibition Assay of Newcastle Disease Virus Serology

Published on: January 24, 2025

1.3K
  • Assessment of complement pathway dysregulation.
  • Monitoring of patient response to anticomplement therapy.

    • Main Results:

    • Anticomplement therapy has revolutionized aHUS management, improving hematologic remission and kidney function.
    • Early diagnosis and treatment are vital for preventing progression to end-stage renal disease and graft failure.
    • Accurate differentiation from other TMAs is essential for appropriate and cost-effective therapeutic strategies.

    Conclusions:

    • Early and precise diagnosis of atypical hemolytic uremic syndrome is paramount for successful treatment with anticomplement therapies.
    • Timely intervention can significantly alter the disease course, improving renal outcomes and preventing graft loss.
    • Development of rapid diagnostic tools for complement pathway assessment is necessary for optimal aHUS patient care.