Evidence map›Paper›PMID 42886391›Full record

ArticleMolecular biology reports2026

Serum vitamin D and VDR genetic variation in kidney stone disease: haplotype and gene-environment interaction analyses in a genetically homogeneous population.

Sanjenbam Yaiphaba Meitei, Malvika Yumnam, Aheibam Robertson Singh, Erika Pebam, Henry Konjengbam, Nameirakpam Shantajit, Somorendro Singh Paonam

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Article in Molecular biology reports, 2026. 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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7 authors.

Sanjenbam Yaiphaba MeiteiDepartment of Anthropology, Manipur University, Imphal, Manipur, 795003, India. yaiphabameitei@manipuruniv.ac.in.
Malvika YumnamDepartment of Anthropology, Manipur University, Imphal, Manipur, 795003, India.
Aheibam Robertson SinghDepartment of Anthropology, Manipur University, Imphal, Manipur, 795003, India.
Erika PebamDepartment of Anthropology, Manipur University, Imphal, Manipur, 795003, India.
Henry KonjengbamDepartment of Anthropology, Rajiv Gandhi University, Doimukh, 791112, Arunachal Pradesh, India.
Nameirakpam ShantajitRaj Medicity, North AOC, Imphal, Manipur, 795001, India.
Somorendro Singh PaonamShija Hospitals and Research Institute, Langol, Imphal, Manipur, 795004, India.

Funding

Science and Engineering Research Board CRG/2020/004697
6 · The paper itself

Abstract

backgroundSerum vitamin D status and vitamin D receptor (VDR) genetic variation may contribute to kidney stone disease (KSD) susceptibility, although their combined effects remain poorly understood. This study investigated the independent and combined effects of serum vitamin D status and VDR genetic variation on KSD susceptibility in a genetically homogeneous population.

methodsA case-control study was conducted on 267 KSD patients and 296 metabolically screened controls. Serum 25-hydroxyvitamin D was measured, and VDR ApaI, TaqI, and FokI polymorphisms were genotyped by PCR-RFLP. Haplotype, linkage disequilibrium, ROC, and additive gene-environment interaction analyses were performed.

resultsIndividual VDR polymorphisms were not significantly associated with KSD. However, elevated serum vitamin D was strongly associated with disease risk (OR = 12.55, 95% CI: 4.70-33.54; p < 0.001). ROC analysis identified an optimal vitamin D cut-off of 35.84 ng/mL (AUC = 0.816). Haplotype analysis identified GCC as a risk haplotype (OR = 4.08, 95% CI: 2.47-6.72), whereas GCT (OR = 0.21, 95% CI: 0.10-0.46) was protective. Additive interaction analyses demonstrated positive interactions between elevated serum vitamin D and the ApaI GT and FokI CC/CT genotypes, while TaqI variants showed antagonistic interactions.

conclusionThe study highlights that VDR haplotypes and serum vitamin D-VDR genotype interactions substantially modified disease risk, suggesting that integrating biochemical and genetic markers may improve KSD risk assessment and support precision prevention strategies.

Indexed as

Kidney CalculiReceptors, CalcitriolVitamin DAdultCase-Control StudiesFemaleGene-Environment InteractionGene FrequencyGenetic Predisposition to DiseaseGenotypeHaplotypesHumansLinkage DisequilibriumMaleMiddle AgedPolymorphism, Single Nucleotide25-hydroxyvitamin DReceptors, CalcitriolVDR protein, humanVitamin DGene-Environment InteractionHaplotypeSerum vitamin DVDR polymorphism

Identifiers

PMID42886391

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