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Related Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

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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 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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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 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 VI: Nursing Management01:22

Acute Kidney Injury VI: Nursing Management

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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 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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Related Experiment Video

Updated: Aug 19, 2025

Standardized Colon Ascendens Stent Peritonitis in Rats - a Simple, Feasible Animal Model to Induce Septic Acute Kidney Injury
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HYDROCORTISONE, ASCORBIC ACID, AND THIAMINE THERAPY DECREASE RENAL OXIDATIVE STRESS AND ACUTE KIDNEY INJURY IN MURINE

John Kim1, Allan Stolarski2, Qiuyang Zhang1

  • 1Departments of Pathology and Laboratory Medicine.

Shock (Augusta, Ga.)
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This study found that septic mice predicted to die showed significant kidney injury and oxidative stress. Hydrocortisone, ascorbic acid, and thiamine (HAT) therapy improved physiological parameters and reduced kidney damage in these critical sepsis patients.

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Area of Science:

  • Critical care medicine
  • Sepsis pathophysiology
  • Renal injury mechanisms

Background:

  • Acute kidney injury (AKI) is common in sepsis and linked to higher mortality.
  • Previous clinical trials on hydrocortisone, ascorbic acid, and thiamine (HAT) therapy for sepsis have yielded mixed results.
  • Stratification of septic patients based on predicted mortality may help identify candidates for therapy and elucidate organ injury mechanisms.

Purpose of the Study:

  • To test if predicted non-survivors (P-Die) in a sepsis model exhibit greater kidney injury than predicted survivors (P-Live).
  • To determine if HAT therapy can correct physiological deterioration and organ injury in P-Die septic mice.
  • To investigate the mechanisms of kidney injury, including inflammation, oxidative stress, and endothelial cell damage in sepsis.

Main Methods:

  • Sepsis was induced via cecal ligation and puncture (CLP) in mice.
  • Mice were stratified into P-Live and P-Die groups based on heart rate 6 hours post-CLP.
  • Stratified mice received either HAT or vehicle treatment 7 hours post-CLP, with physiological and biochemical assessments at 24 hours.

Main Results:

  • P-Die mice showed significant declines in heart rate, cardiac output, breath rate, and temperature, which were reversed by HAT therapy.
  • Ascorbic acid levels were depleted in P-Die mice and restored by HAT.
  • HAT therapy reduced elevated inflammatory markers (IL-6, KC, MIP-2, IL-1RA), endothelial injury markers (glypican 1 & 4), and renal oxidative stress in P-Die mice.
  • Kidney injury markers (BUN, cystatin C) were elevated in P-Die mice and reduced by HAT, while hepatic parameters remained normal.

Conclusions:

  • Septic mice predicted to die (P-Die) exhibit increased inflammation, oxidative stress, and kidney injury.
  • HAT therapy administered after the onset of sepsis-induced physiological changes effectively decreased renal oxidative stress and injury in P-Die mice.
  • Mortality stratification can identify septic patients who may benefit from specific therapies like HAT, targeting key injury pathways.