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Updated: Jun 14, 2026
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Estimation of Urinary Nanocrystals in Humans using Calcium Fluorophore Labeling and Nanoparticle Tracking Analysis
Published on: February 9, 2021
The initial and subsequent inflammatory events during calcium oxalate lithiasis
John W M Yuen1, Mayur-Danny I Gohel, Ngork-Wah Poon
1Department of Health Technology & Informatics, The Hong Kong Polytechnic University, Hung Hom, Kowloon, Hong Kong.
Summary
Kidney stone formation begins with calcium oxalate crystal nucleation on proximal tubule cells. These cells internalize crystals, causing damage and an inflammatory response involving hyaluronan (HA) synthesis.
Area of Science:
- Nephrology
- Urology
- Cell Biology
Background:
- Urolithiasis, or kidney stone formation, is initiated by crystal crystallization.
- The precise location of initial crystal nucleation within the nephron remains unclear.
Purpose of the Study:
- To investigate direct nucleation of calcium oxalate crystals on human proximal tubular cells.
- To examine subsequent events including crystal internalization, cellular damage, and hyaluronan expression.
Main Methods:
- Utilized a two-compartment culture system with intact human proximal tubular HK-2 cell monolayers.
- Exposed cells to hypercalciuric and hyperoxaluric conditions to induce calcium oxalate dihydrate (COD) nucleation.
- Assessed crystal binding, internalization, cellular damage, and hyaluronan (HA) synthesis via microscopy and molecular analysis.
Main Results:
- COD crystals nucleated and adhered to the apical surface of HK-2 cells.
- Cells internalized some COD crystals and exhibited mild cellular damage within 18 hours.
- Prolonged incubation led to monolayer disruption, and hyaluronan disaccharides were detected with associated HAS-3 mRNA expression.
Conclusions:
- Human proximal tubule cells can internalize nucleated COD crystals, leading to cellular damage.
- This process triggers HAS-3 specific hyaluronan synthesis, indicating an inflammatory response.
- Proximal tubule cells play a key role in urolithiasis by facilitating crystal endocytosis and promoting an inflammatory environment.
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