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

92
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...
92
Acute Kidney Injury I: Introduction01:22

Acute Kidney Injury I: Introduction

80
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...
80
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

59
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...
59
Acute Kidney Injury III: Clinical Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

97
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...
97
Acute Kidney Injury VI: Nursing Management01:22

Acute Kidney Injury VI: Nursing Management

67
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...
67
Acute Kidney Injury V: Interprofessional Care01:20

Acute Kidney Injury V: Interprofessional Care

48
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...
48

You might also read

Related Articles

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

Sort by
Same author

Notch signaling pathway mediates anti-inflammatory effects of vagus nerve stimulation during lipopolysaccharide-induced acute kidney injury.

Communications biology·2026
Same author

Kidney Biorepositories: Valuable Tools Advancing Acute Kidney Injury Research.

Kidney360·2025
Same author

Remembering Fred S. Wright, M.D. (1937-2023).

Kidney360·2025
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

Clinical uptake of an antigen-based approach to membranous nephropathy: a survey of general nephrologists and glomerular disease experts.

Journal of nephrology·2025
Same author

Drivers and mechanisms of cognitive decline in chronic kidney disease.

Nature reviews. Nephrology·2025

Related Experiment Video

Updated: Sep 16, 2025

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

50.2K

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

Eibhlin Goggins1, Hiro Inoue, Mark D Okusa

  • 1Division of Nephrology and Center for Immunity, Inflammation, and Regenerative Medicine, University of Virginia, Charlottesville, Virginia.

Journal of the American Society of Nephrology : JASN
|July 7, 2025
PubMed
Summary

The neuroimmune axis regulates inflammation in acute kidney injury (AKI) and organ dysfunction. Targeting neural circuits, like the cholinergic anti-inflammatory pathway (CAP), offers new therapeutic strategies for AKI.

Keywords:
AKI and critical careacute renal failureischemia-reperfusionischemic renal failurekidneymacrophages

More Related Videos

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
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

9.0K

Related Experiment Videos

Last Updated: Sep 16, 2025

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

50.2K
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
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

9.0K

Area of Science:

  • Neuroimmunology
  • Renal Physiology
  • Inflammation Biology

Background:

  • Bidirectional communication between nervous and immune systems is crucial for physiological regulation and disease.
  • The neuroimmune axis modulates inflammation in acute kidney injury (AKI) and multiorgan dysfunction.
  • The inflammatory reflex pathway, involving sensory and motor arcs, is central to this regulation.

Purpose of the Study:

  • To review the neuroimmune axis, focusing on the inflammatory reflex pathway and cholinergic anti-inflammatory pathway (CAP).
  • To discuss the role of neuroimmune communication in AKI, multiorgan dysfunction, and sepsis.
  • To explore potential therapeutic strategies targeting neural circuits for AKI.

Main Methods:

  • Review of existing literature on neuroimmune interactions in inflammation and organ injury.
  • Discussion of the cholinergic anti-inflammatory pathway (CAP) mechanisms, including vagus nerve activation and receptor signaling.
  • Analysis of organ-specific neuroimmune communications and their impact on systemic inflammation.

Main Results:

  • The CAP suppresses inflammation via vagus nerve activation and signaling in macrophages.
  • Vagus nerve stimulation and pulsed ultrasound activate the CAP, attenuating inflammation and protecting against AKI.
  • Pulsed ultrasound before ischemia-reperfusion injury preserves kidney function in a CAP-dependent manner.

Conclusions:

  • Targeting neuroimmune pathways, including the CAP and sympathetic nervous system, offers novel therapeutic potential for AKI.
  • Understanding multiorgan neuroimmune communications is vital for managing systemic inflammatory conditions like sepsis.
  • Neural circuit modulation presents a promising avenue for treating AKI and related multiorgan failures.