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Related Concept Videos

Acute Kidney Injury I: Introduction01:22

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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 II: Pathophysiology01:29

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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 VI: Nursing Management01:22

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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 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 III: Clinical Manifestations01:29

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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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Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

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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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Related Experiment Video

Updated: Feb 13, 2026

Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
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Rab27a Deficiency Mitigates Mitochondrial Damage by Upregulating PPAR-γ in Sepsis Associated Acute Kidney Injury.

Haifeng Mao1, Yang Ji1, Xinran Meng2

  • 1Department of Emergency Medicine, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|February 12, 2026
PubMed
Summary

Rab27a is identified as a key factor in sepsis-associated acute kidney injury (SA-AKI). Silencing Rab27a protected kidney cells from injury and mitochondrial dysfunction, suggesting a therapeutic target for SA-AKI.

Keywords:
PPAR‐γRab27amitochondrial dysfunctionrenal tubular epithelial cellsepsis‐associated acute kidney injury

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Sepsis-associated acute kidney injury (SA-AKI) is a major cause of mortality in sepsis patients.
  • The underlying mechanisms of SA-AKI are not fully understood.
  • Identifying key molecular players is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the role of Rab27a in the pathogenesis of SA-AKI.
  • To explore the molecular mechanisms by which Rab27a influences kidney injury.
  • To determine potential therapeutic targets for SA-AKI.

Main Methods:

  • In vitro and in vivo models of SA-AKI were used.
  • Rab27a expression levels were analyzed.
  • The effects of Rab27a knockdown on kidney cell injury, mitochondrial function, and cell migration were assessed.
  • Interactions between Rab27a, PPAR-γ, and AMPK-α1 were investigated.

Main Results:

  • Rab27a expression was upregulated in SA-AKI models.
  • Rab27a silencing mitigated LPS-induced kidney cell injury and mitochondrial dysfunction.
  • Knockdown of Rab27a enhanced cell migration and functional recovery.
  • The protective effects of Rab27a knockdown were dependent on PPAR-γ.
  • An interaction between PPAR-γ and AMPK-α1 was observed after Rab27a knockdown.

Conclusions:

  • Rab27a is a critical mediator in the development of SA-AKI.
  • Targeting Rab27a may offer a therapeutic strategy for SA-AKI.
  • Rab27a influences RTEC function and mitochondrial integrity through pathways involving PPAR-γ and AMPK-α1.