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Related Concept Videos

Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

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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...
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Acute Kidney Injury II: Pathophysiology01:29

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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 VI: Nursing Management01:22

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Acute Kidney Injury (AKI) results in an inability to maintain fluid, electrolyte, and acid-base balance. Effective nursing management is critical in improving patient outcomes and includes comprehensive patient assessment and targeted interventions.Comprehensive Patient AssessmentA detailed history collection is essential, focusing on any recent infections, nephrotoxic medication use, or chronic conditions such as hypertension and diabetes that may contribute to AKI. During the physical...
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Acute Kidney Injury V: Interprofessional Care01:20

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Acute Kidney Injury (AKI) requires a collaborative healthcare approach to restore renal function and prevent complications. Essential management strategies involve monitoring fluid and electrolyte balance, adjusting medications, initiating dialysis when necessary, and providing nutritional support.Fluid and Electrolyte ManagementFluid Monitoring: Regularly monitoring body weight, central venous pressure, and urine output helps detect fluid imbalances early. Patient intake and output are...
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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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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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Related Experiment Video

Updated: Jan 30, 2026

Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
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Targeting CDC42 Protects Mitochondrial Function through KLF2/HIF-1α/PINK1 Signaling in Acute Kidney Injury.

Xue Zhou1,2,3, Xian Fu2,3, Yi-Wen Meng2,3

  • 1Medical Examination Centre of the First Affiliated Hospital and CNTTI of College of Pharmacy, Chongqing Medical University, Chongqing 400016, China.

International Journal of Biological Sciences
|January 29, 2026
PubMed
Summary

Cell division cycle 42 (CDC42) drives acute kidney injury (AKI) by impairing mitochondrial function. Inhibiting CDC42 protects kidneys from damage and promotes recovery, offering a new therapeutic avenue for AKI.

Keywords:
acute kidney injurycell division cycle 42hypoxia-inducible factor-1alphakruppel-like factor 2mitochondrial dysfunctionoxidative stress

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Acute kidney injury (AKI) is a critical condition linked to mitochondrial dysfunction and oxidative stress.
  • Current therapies for AKI are limited, necessitating novel treatment strategies.

Purpose of the Study:

  • To investigate the role of cell division cycle 42 (CDC42) in the pathogenesis of AKI.
  • To explore CDC42 inhibition as a potential therapeutic approach for AKI.

Main Methods:

  • Analysis of human scRNA-seq data and murine AKI models (cisplatin, ischemia-reperfusion).
  • Pharmacological inhibition, knockdown, and genetic ablation of CDC42.
  • Transcriptomic analysis, bioinformatic analysis, dual-luciferase reporter assays, ChIP assays, and functional assays.

Main Results:

  • CDC42 was significantly upregulated in renal tubular epithelial cells (RTECs) during AKI.
  • CDC42 inhibition alleviated renal injury, preserved mitochondrial function, and reduced reactive oxygen species (ROS).
  • CDC42 suppression activated a KLF2/HIF-1α/PINK1 cascade, promoting mitophagy and restoring mitochondrial homeostasis.

Conclusions:

  • CDC42 is a critical mediator in AKI pathogenesis.
  • Targeting CDC42 presents a promising therapeutic strategy for AKI by mitigating mitochondrial damage and improving renal outcomes.