ArticleBMC urology2026
Genetically predicted urinary sodium excretion and urolithiasis risk: a two-sample mendelian randomization study.
Article in BMC urology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigh sodium intake has been linked to kidney stone formation in many observational studies, but these findings may be influenced by dietary habits and fluid intake. Whether urinary sodium itself plays a causal role in urolithiasis remains unclear.
methodsWe performed a two-sample Mendelian randomization analysis to examine the association between urinary sodium excretion and urolithiasis risk. Genetic instruments for urinary sodium were obtained from large genome-wide association studies based on the UK Biobank and EBI databases (N > 300,000). Summary statistics for urolithiasis were derived from the FinnGen R12 dataset. The primary analysis was conducted using the inverse variance weighted method, with additional sensitivity analyses including MR-Egger, weighted median, and MR-PRESSO.
resultsHigher genetically predicted urinary sodium excretion was associated with an increased risk of urolithiasis (IVW OR = 2.49, 95% CI: 1.45-4.29, P= 0.00099). Similar results were observed in an independent replication dataset (OR = 2.66, 95% CI: 1.39-5.07, P= 0.0029). There was no evidence of horizontal pleiotropy (MR-Egger intercept P= 0.523), and heterogeneity was low. MR-PRESSO did not detect any significant outliers.
conclusionsOur findings provide supportive genetic evidence suggesting that higher urinary sodium excretion may contribute to an increased risk of urolithiasis. These results align with current recommendations for dietary sodium restriction in stone prevention.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.