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Related Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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

Acute Kidney Injury IV: Diagnostic Studies and Prevention

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

Acute Kidney Injury III: Clinical Manifestations

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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...
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Related Experiment Video

Updated: Dec 12, 2025

Forward Genetics Screens Using Macrophages to Identify Toxoplasma gondii Genes Important for Resistance to IFN-γ-Dependent Cell Autonomous Immunity
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Endothelial dysfunction in acute acquired toxoplasmosis.

Azhar H Al-Kuraishi1, Salah D Al-Windy1, Hayder M Al-Kuraishy1

  • 1Department of Pharmacology, Toxicology and Medicine, College of Medicine Almustansiriya University, Baghdad, Iraq.

Tropical Parasitology
|August 11, 2020
PubMed
Summary

Acute toxoplasmosis (AT) is linked to oxidative stress and inflammation, causing endothelial dysfunction (ED). Elevated immunoglobulin, IL-6, ET-1, and MDA levels were observed in AT patients, highlighting these biomarkers in disease progression.

Keywords:
Endothelial dysfunctionToxoplasma gondiiendothelin-1

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Area of Science:

  • Immunology
  • Pathophysiology
  • Biochemistry

Background:

  • Acute toxoplasmosis (AT), caused by *Toxoplasma gondii*, triggers pro-inflammatory and oxidative stress responses via host immune activation.
  • Understanding the mechanisms linking AT to systemic changes is crucial for patient management.

Purpose of the Study:

  • To investigate endothelial dysfunction (ED) and oxidative stress markers in patients diagnosed with acute toxoplasmosis.
  • To correlate specific immune and oxidative stress biomarkers with the clinical presentation of AT.

Main Methods:

  • A comparative study involving 21 AT patients and 20 healthy controls.
  • Serum levels of immunoglobulins (IgM, IgG, IgA), Interleukin-6 (IL-6), endothelin-1 (ET-1), and malondialdehyde (MDA) were quantified.

Main Results:

  • AT patients exhibited significantly elevated IgM, IgG, IgA, IL-6, MDA, and ET-1 levels compared to controls (P < 0.01).
  • A strong positive correlation was found between IgM levels and other immunoglobulins, as well as oxidative stress and ED biomarkers in AT patients (P = 0.0001).

Conclusions:

  • Acute toxoplasmosis is associated with significant oxidative stress and pro-inflammatory alterations.
  • These combined factors contribute to the development of endothelial dysfunction in AT patients.