Evidence map›Paper›PMID 39198784›Full record

ArticleBMC urology2024

Mendelian randomization study of urolithiasis: exploration of risk factors using human blood metabolites.

Dekai Hu, Jiashan Pan, Anqi Deng, Defeng Ge, Rui Yao, Bingbing Hou, Zongyao Hao

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Article in BMC urology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Dekai Hu *Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Jiashan Pan *Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Anqi Deng *Anhui Medical University, Hefei, Anhui, China.
Defeng GeDepartment of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Rui YaoDepartment of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Bingbing HouDepartment of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China. binggoaza@163.com.
Zongyao HaoDepartment of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China. haozongyao@ahmu.edu.cn.

Funding

National Natural Science Foundation of China 82070724National Natural Science Foundation of China,China 82370768
6 · The paper itself

Abstract

backgroundUrolithiasis is a highly prevalent global disease closely associated with metabolic factors; however, the causal relationship between blood metabolites and urolithiasis remains poorly understood.

methodIn our study, we employed a bi-directional two-sample Mendelian randomization (MR) analysis to investigate the causal associations between urolithiasis and metabolites. The random-effects inverse-variance weighted (IVW) estimation method was utilized as the primary approach, complemented by several other estimators including MR-Egger, weighted median, colocalization and MR-PRESSO. Furthermore, the study included replication and meta-analysis. Finally, we conducted metabolic pathway analysis to elucidate potential metabolic pathways.

resultsAfter conducting multiple tests for correction, glycerol might contribute to the urolithiasis and dehydroisoandrosterone sulfate (DHEA-S) might inhibit this process. Furthermore, several blood metabolites had shown potential associations with a causal relationship. Among the protective metabolites were lipids (dehydroisoandrosterone sulfate and 1-stearoylglycerol (1-monostearin)), amino acids (isobutyrylcarnitine and 2-aminobutyrate), a keto acid (acetoacetate) and a carbohydrate (mannose). The risk metabolites included lipids (1-palmitoylglycerophosphoethanolamine, glycerol and cortisone), a carbohydrate (erythronate), a peptide (pro-hydroxy-pro) and a fatty acid (eicosenoate). In reverse MR analysis, urolithiasis demonstrated a statistically significant causal relationship with butyrylcarnitine, 3-methyl-2-oxobutyrate, scyllo-inositol, leucylleucine and leucylalanine. However, it was worth noting that none of the blood metabolites exhibited statistical significance after multiple corrections. Additionally, we identified one metabolic pathway associated with urolithiasis.

conclusionThe results we obtained demonstrate the causal relevance between two metabolites and urolithiasis, as well as identify one metabolic pathway potentially associated with its development. Given the high prevalence of urolithiasis, further investigations are encouraged to elucidate the mechanisms of these metabolites and explore novel therapeutic strategies.

Indexed as

Mendelian Randomization AnalysisUrolithiasisDehydroepiandrosterone SulfateGlycerolHumansMolecular EpidemiologyDehydroepiandrosterone SulfateGlycerolGenetic epidemiologyMendelian randomization studyMetabolitesUrolithiasis

Identifiers

PMID39198784
PMCPMC11350957

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