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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...
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Estimation of Urinary Nanocrystals in Humans using Calcium Fluorophore Labeling and Nanoparticle Tracking Analysis
07:45

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Published on: February 9, 2021

Stroke in primary hyperoxaluria type I.

Neal M Rao1, Anil Yallapragada, Kellen D Winden

  • 1David Geffen School of Medicine at UCLA, Los Angeles, CA.

Journal of Neuroimaging : Official Journal of the American Society of Neuroimaging
|April 5, 2013
PubMed
Summary
This summary is machine-generated.

A young man experienced multiple strokes due to undiagnosed kidney disease. High serum oxalate levels and circulating microemboli suggest a novel mechanism for stroke in primary oxalosis.

Keywords:
Strokegeneticshyperoxalurianeuroimagingprimary oxalosistranscranial Doppler

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Area of Science:

  • Nephrology
  • Neurology
  • Vascular Medicine

Background:

  • Cerebrovascular infarction in young adults necessitates investigation beyond common etiologies.
  • Primary oxalosis is a rare metabolic disorder characterized by oxalate deposition, potentially affecting multiple organs.

Observation:

  • A 27-year-old male presented with multiple cerebrovascular infarctions despite negative workup for traditional stroke causes.
  • Transcranial Doppler revealed circulating microemboli (14/hour), and elevated serum oxalate exceeded calcium oxalate supersaturation.
  • Imaging showed rapid mineralization in infarcted brain regions.

Findings:

  • The absence of conventional stroke risk factors points to an alternative etiology.
  • Elevated serum oxalate and detected microemboli suggest oxalate crystals as a source of cerebrovascular events.
  • Rapid mineralization of infarcts indicates ongoing pathological processes.

Implications:

  • Circulating oxalate precipitate is proposed as a novel mechanism for stroke in primary oxalosis.
  • This case highlights the importance of considering metabolic disorders in cryptogenic strokes.
  • Early detection and management of hyperoxaluria may prevent cerebrovascular complications.