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Updated: Jun 8, 2026

Estimation of Urinary Nanocrystals in Humans using Calcium Fluorophore Labeling and Nanoparticle Tracking Analysis
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[Oxalic acid--important uremic toxin].

M Mydlík1, K Derzsiová

  • 1IV. interná klinika Lekárskej fakulty UPJS a FN L, Pasteura, Kosice, Slovenská republika.

Vnitrni Lekarstvi
|September 17, 2010
PubMed
Summary
This summary is machine-generated.

Oxalic acid is a key uremic toxin. Renal replacement therapy can temporarily lower plasma oxalic acid levels, but it is not effective for permanent reduction in chronic kidney disease patients.

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Area of Science:

  • Nephrology
  • Toxicology
  • Biochemistry

Context:

  • Oxalic acid is recognized as a significant uremic toxin contributing to the pathogenesis of uremic syndrome.
  • Elevated oxalic acid levels are implicated in the progression of chronic kidney disease (CKD) and complications post-renal transplantation.

Purpose:

  • To investigate the levels of oxalic acid in biological fluids (plasma, saliva, urine, dialysate) of patients with CKD stages 3-5 and following renal transplantation.
  • To evaluate the impact of various therapeutic interventions, including fluid diuresis, dietary modifications, furosemide administration, and different renal replacement therapies, on plasma oxalic acid concentrations.

Summary:

  • Direct correlations were observed between plasma oxalic acid and serum creatinine in CKD and post-transplant patients.
  • Salivary oxalic acid levels did not significantly differ between healthy controls and CKD patients.
  • Urinary oxalic acid excretion increased with maximal water diuresis and furosemide administration but was unaffected by high sodium chloride intake.
  • Hemodiafiltration (HDF) demonstrated the most significant reduction (63.3%) in plasma oxalic acid among renal replacement therapies.

Impact:

  • This study highlights that while renal replacement therapies can transiently decrease plasma oxalic acid, they do not offer a permanent solution for managing this uremic toxin.
  • Findings underscore the need for alternative strategies to effectively reduce persistent hyperoxalemia in patients with advanced kidney disease.