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Updated: Jan 18, 2026

Estimation of Urinary Nanocrystals in Humans using Calcium Fluorophore Labeling and Nanoparticle Tracking Analysis
Published on: February 9, 2021
Origin of monosodium urate Randall's plaques
Els Van de Perre1,2, Elise Maréchal3, Karl Martin Wissing4,5
1Department of Nephrology and Arterial Hypertension, Universitair Ziekenhuis Brussel (UZ Brussel), Vrije Universiteit Brussel (VUB), Brussels, Belgium. els.vandeperre@uzbrussel.be.
Monosodium urate deposits in Randall's plaques are linked to distinct patient characteristics, including older age and hyperuricemia. This suggests different kidney stone formation mechanisms may be involved, potentially treatable with uric acid-lowering therapies.
Area of Science:
- Nephrology
- Urology
- Biochemistry
Background:
- Randall's plaques are implicated in kidney stone formation.
- A subset of Randall's plaques contain monosodium urate (NaUr pos RP), with unknown formation mechanisms and patient characteristics.
- Classical Randall's plaques lack monosodium urate (NaUr neg RP).
Purpose of the Study:
- To investigate the clinical and biochemical differences between patients with kidney stones associated with monosodium urate-containing Randall's plaques (NaUr pos RP) and those with classical Randall's plaques (NaUr neg RP).
- To explore potential differences in the formation mechanisms of these two types of Randall's plaques.
Main Methods:
- Retrospective analysis of clinical and biochemical data from patients with kidney stone formation.
- Comparison of urinary calcium, magnesium, uric acid excretion, and urinary pH between NaUr pos RP and NaUr neg RP groups.
- Assessment of patient demographics, comorbidities, and serum creatinine levels.
Main Results:
- The NaUr neg RP group showed significantly higher urinary calcium and magnesium excretion.
- The NaUr pos RP group tended towards higher rates of hyperuricemia, were more frequently male, older, and had higher serum creatinine levels.
- A higher prevalence of hypertension, dyslipidemia, cardiovascular disease, and gout was observed in the NaUr pos RP group.
Conclusions:
- Distinct formation mechanisms are likely involved in NaUr pos RP and NaUr neg RP associated kidney stones.
- Interstitial monosodium urate precipitation, driven by high serum uric acid, is hypothesized for NaUr pos RP formation.
- Xanthine oxidase inhibitors may reduce recurrent stone formation in NaUr pos RP cases.
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