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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 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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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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Using an Integrated -Omics Approach to Identify Key Cellular Processes That Are Disturbed in the Kidney After Brain

M Z Akhtar1,2, H Huang2,3, M Kaisar2,3

  • 1Centre for Cellular and Molecular Physiology, Oxford University, Oxford, UK.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|November 26, 2015
PubMed
Summary
This summary is machine-generated.

Brain death causes kidney dysfunction by altering metabolism and mitochondrial function. Interventions targeting donor metabolism may prevent this kidney injury, improving transplant viability.

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Area of Science:

  • Nephrology
  • Organ Transplantation
  • Metabolomics

Background:

  • Increasing reliance on older donors for kidney transplantation necessitates understanding brain death's impact on kidney viability.
  • Brain death significantly compromises kidney function, posing a challenge for organ transplantation.
  • Identifying mechanisms of kidney injury post-brain death is crucial for improving graft outcomes.

Purpose of the Study:

  • To investigate the cellular and metabolic changes in kidneys following brain death using a rodent model.
  • To delineate key cellular processes perturbed in the kidney after brain death.
  • To explore potential therapeutic strategies for mitigating brain death-induced kidney injury.

Main Methods:

  • Utilized a rodent model of hemorrhagic stroke to induce brain death.
  • Employed next-generation proteomic and metabolomic technologies for comprehensive analysis.
  • Performed pathway analysis on kidney proteomic signatures.

Main Results:

  • Identified large-scale alterations in mitochondrial proteins, linked to impaired mitochondrial activity and injury.
  • Observed an increase in glycolytic proteins and lactate production, indicating a shift to anaerobic metabolism.
  • Detected elevated succinate levels and increased oxidative stress markers in brain-dead kidneys.

Conclusions:

  • Brain death induces significant metabolic disturbances and mitochondrial dysfunction in the kidney.
  • These alterations, including oxidative stress, contribute to cellular injury.
  • Metabolic conditioning of organ donors may offer a novel approach to prevent brain death-induced kidney injury and enhance transplant quality.