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

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

59
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...
59
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

63
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...
63
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

73
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...
73
Acute Kidney Injury V: Interprofessional Care01:20

Acute Kidney Injury V: Interprofessional Care

42
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...
42
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

53
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...
53
Acute Kidney Injury VI: Nursing Management01:22

Acute Kidney Injury VI: Nursing Management

50
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...
50

You might also read

Related Articles

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

Sort by
Same author

Neuroimmune Regulation for Acute Kidney Injury Therapy: Insights Along the Path From Bench to Bedside.

Seminars in nephrology·2025
Same author

Neuroimmune Control of Inflammation in Acute Kidney Injury and Multiorgan Dysfunction.

Journal of the American Society of Nephrology : JASN·2025
Same author

Pulsed ultrasound targeted to the spleen mitigates against kidney injury and promotes kidney repair.

American journal of physiology. Renal physiology·2025
Same author

Drivers and mechanisms of cognitive decline in chronic kidney disease.

Nature reviews. Nephrology·2025
Same author

Proximal tubule pannexin 1 contributes to mitochondrial dysfunction and cell death during acute kidney injury.

American journal of physiology. Renal physiology·2025
Same author

Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy.

Circulation research·2024
Same journal

Acute effects of exercise on the nephron index under different conditions in middle-aged males - a preliminary study.

Nephron·2026
Same journal

Lysozyme-Associated Nephropathy in Myeloid Neoplasms: A Clinicopathological and Mass Spectrometric Study of Two Cases.

Nephron·2026
Same journal

Prevalence of COVID-19 Pneumonia and Clinical Characteristics in Hemodialysis Patients During the SARS-CoV-2 Omicron Pandemic.

Nephron·2026
Same journal

Real-World Outcomes of Patients with Monoclonal Gammopathy of Renal Significance.

Nephron·2026
Same journal

Long-Term Therapy with Eculizumab Biosimilar in Patients with Atypical Haemolytic Uraemic Syndrome: Outcomes of a Prospective Observational Study.

Nephron·2026
Same journal

Kidney Organoids: Disease Modeling and Clinical Implementations for Patient Benefit.

Nephron·2026
See all related articles

Related Experiment Video

Updated: Aug 28, 2025

Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice
02:45

Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice

Published on: February 2, 2024

1.8K

Myeloid Response to Acute Kidney Injury.

William T Nash1,2, Marissa S Yee1,2, Mark D Okusa1,2

  • 1Division of Nephrology, Department of Medicine, University of Virginia, Charlottesville, Virginia, USA.

Nephron
|September 15, 2022
PubMed
Summary
This summary is machine-generated.

Understanding myeloid cell roles in kidney injury requires distinguishing between resident and infiltrating cells. Further research is needed to define their specific contributions to injury, repair, and chronic kidney disease.

Keywords:
Acute kidney injuryAcute renal failureCKDInflammationResident macrophages

More Related Videos

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
12:27

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration

Published on: June 7, 2014

50.1K
A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
09:02

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion

Published on: February 2, 2021

4.6K

Related Experiment Videos

Last Updated: Aug 28, 2025

Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice
02:45

Bilateral Renal Ischemia-Reperfusion Model for Acute Kidney Injury in Mice

Published on: February 2, 2024

1.8K
Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
12:27

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration

Published on: June 7, 2014

50.1K
A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
09:02

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion

Published on: February 2, 2021

4.6K

Area of Science:

  • Renal pathophysiology
  • Immunology
  • Cell biology

Background:

  • Myeloid cells are crucial in the response to kidney ischemia-reperfusion injury (IRI).
  • The mononuclear phagocyte system is complex, necessitating clearer definitions of distinct myeloid cell functions in the kidney.
  • Differentiating resident kidney macrophages from infiltrating monocytes is a key advance in understanding myeloid cell roles.

Purpose of the Study:

  • To highlight the need for specific analysis of resident versus recruited myeloid cells in kidney injury, repair, and chronic disease.
  • To discuss the limitations of the M1/M2 classification system for myeloid cells in kidney IRI.
  • To emphasize the importance of understanding myeloid activation states beyond M1/M2 phenotypes.

Main Methods:

  • Review of current literature on myeloid cell populations in kidney IRI.
  • Discussion of the roles of resident macrophages versus infiltrating monocytes.
  • Analysis of the M1/M2 classification system in the context of kidney myeloid responses.

Main Results:

  • Resident kidney macrophages may play a minimal role in injury but are important in recovery.
  • Myeloid cell involvement is influenced by activation states and environmental cues.
  • The M1/M2 phenotype system offers limited insight into complex myeloid responses in kidney IRI.

Conclusions:

  • Specific tools are required to rigorously define the contributions of distinct myeloid populations (resident vs. infiltrating) to kidney injury, repair, and chronic disease.
  • Further investigation into myeloid activation states beyond M1/M2 classification is essential.
  • Advances in assessing resident cells and recognizing M1/M2 system limitations are promising for kidney disease research.