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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 Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

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...
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...
Acute Kidney Injury V: Interprofessional Care01:20

Acute Kidney Injury V: Interprofessional Care

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...
Acute Kidney Injury VI: Nursing Management01:22

Acute Kidney Injury VI: Nursing Management

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...
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...

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Updated: Jun 12, 2026

Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury
07:58

Nephrotoxin Microinjection in Zebrafish to Model Acute Kidney Injury

Published on: July 17, 2016

Zinc Signaling in Acute Kidney Injury.

Svetlana Lebedeva1,2, Yan Bravyy1, Anna Beknazarova1

  • 1Scientific Center of Genetics and Life Sciences, Sirius University of Science and Technology, Sirius Federal Territory 354340, Russia.

Cells
|June 11, 2026
PubMed
Summary
This summary is machine-generated.

Zinc plays a crucial role in protecting the kidneys from acute kidney injury (AKI) by modulating cellular responses to stress and inflammation. Targeting zinc signaling pathways offers potential therapeutic strategies for renoprotection.

Keywords:
acute kidney injuryhypoxiainflammationoxidative stresszinc

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Area of Science:

  • Nephrology
  • Biochemistry
  • Molecular Biology

Background:

  • Acute kidney injury (AKI) is a significant clinical problem in hospitalized patients and athletes, driven by hypoxia, oxidative stress, and inflammation.
  • Zinc is vital for cellular functions, with over 300 enzymes utilizing it as a cofactor and its signaling pathways involved in adaptive stress responses.
  • Zinc influences hypoxia-inducible factor signaling, reactive oxygen species (ROS) generation, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity.

Purpose of the Study:

  • To review the multifaceted role of zinc in the pathophysiology of AKI.
  • To explore zinc's intracellular and extracellular signaling mechanisms in kidney protection.
  • To identify therapeutic strategies targeting zinc for AKI management and risk stratification.

Main Methods:

  • Review of existing literature on zinc's role in cellular stress responses and kidney injury.
  • Analysis of molecular pathways involving zinc, including hypoxia signaling, ROS, NF-κB, and GPR39.
  • Examination of zinc's impact on inflammatory cytokine production and epigenetic regulation.

Main Results:

  • Intracellular zinc signaling modulates adaptive responses to hypoxia and oxidative stress, suppressing ROS and NF-κB.
  • Extracellular zinc, via GPR39 activation, promotes cytoprotective and anti-inflammatory effects, including A20 induction and IL-10 release.
  • Zinc's role in epigenetic control via histone deacetylases contributes to adaptive gene expression.

Conclusions:

  • Zinc signaling pathways are critical for mitigating kidney damage in AKI.
  • Targeting zinc homeostasis and signaling represents a promising therapeutic avenue for AKI renoprotection.
  • Zinc biomarkers may aid in risk stratification for patients with AKI.