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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 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...
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 Pancreatitis II: Pathophysiology01:21

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The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
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 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...

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Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

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Published on: November 21, 2025

Paneth cell-mediated multiorgan dysfunction after acute kidney injury.

Sang Won Park1, Mihwa Kim, Joo Yun Kim

  • 1Department of Anesthesiology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|October 31, 2012
PubMed
Summary

Acute kidney injury (AKI) triggers Paneth cells to release IL-17A, causing organ damage. Targeting Paneth cell dysfunction may reduce AKI complications.

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

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Published on: June 7, 2014

Area of Science:

  • Nephrology
  • Gastroenterology
  • Immunology

Background:

  • Acute kidney injury (AKI) often leads to damage in other organs, such as the intestines and liver.
  • The exact mechanisms driving this extrarenal multiorgan injury following AKI are not fully understood.

Purpose of the Study:

  • To investigate if intestinal inflammation drives multiorgan injury in response to AKI.
  • To identify the specific mediators and cellular players involved in AKI-induced extrarenal damage.

Main Methods:

  • Induction of AKI in mice via renal ischemia-reperfusion or nephrectomy.
  • Analysis of IL-17A levels in the small intestine, portal circulation, and systemic circulation.
  • Assessment of intestinal apoptosis and inflammation.
  • Genetic and pharmacologic manipulation of Paneth cells and macrophages.
  • Evaluation of organ injury markers in the kidney, liver, and intestine.

Main Results:

  • AKI induced increased IL-17A synthesis and release by intestinal Paneth cells, accompanied by severe intestinal apoptosis and inflammation.
  • Elevated IL-17A levels were detected in portal and systemic circulation post-AKI.
  • Intestinal macrophages appeared to transport Paneth cell-derived IL-17A to the liver.
  • Depletion of Paneth cells or blockade of IL-17A significantly attenuated intestinal, hepatic, and renal injury.

Conclusions:

  • AKI stimulates Paneth cells to produce IL-17A, initiating intestinal and hepatic injury through macrophage-mediated IL-17A delivery.
  • Modulating Paneth cell function presents a potential therapeutic strategy to mitigate systemic complications of AKI.