Background: Vitamin D supplementation is associated with a lower incidence of diabetic nephropathy (DN); however, whether this association is causative is uncertain.
Methods: We used two-sample Mendelian randomization to examine the causal influence of vitamin D on diabetic nephropathy in 7,751 individuals with type I diabetes-related nephropathy (T1DN) and 9,933 individuals with type II diabetes-related nephropathy (T2DN). Meanwhile, we repeated some previous studies on the influence of KIM-1 (kidney injury molecule 1) and body mass index (BMI) on DN. Additionally, to test the validity of the instruments variable for vitamin D, we conducted two negative controls Mendelian randomization (MR) on breast and prostate cancer, and a positive control MR on multiple sclerosis.
Results: Results of the MR analysis showed that there was no causal association between 25(OH)D with the early/later stage of T1DN (early: OR = 0.903, 95%CI: 0.229 to 3.555; later: OR = 1.213, 95%CI: 0.367 to 4.010) and T2DN (early: OR = 0.588, 95%CI: 0.182 to 1.904; later: OR = 0.904, 95%CI: 0.376 to 2.173), nor with the kidney function of patients with diabetes mellitus: eGFRcyea (creatinine-based estimated GFR) (Beta = 0.007, 95%CI: -0.355 to 0.369)) or UACR (urinary albumin creatinine ratio) (Beta = 0.186, 95%CI: -0.961 to 1.333)).
Conclusions: We found no evidence that Vitamin D was causally associated with DN or kidney function in diabetic patients.
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http://dx.doi.org/10.1186/s12882-023-03186-2 | DOI Listing |
Int Urol Nephrol
January 2025
Department of Nephrology, Jiangxi Medical College, The Second Affiliated Hospital, Nanchang University, Nanchang, Jiangxi, China.
Purpose: To clarify the causal association between cardiovascular proteins and diabetic nephropathy (DN) in Europeans.
Methods: The large genome-wide association study data of cardiovascular proteins and DN were used for this two-sample Mendelian randomization (MR) analysis. We took the Inverse variance weighted (IVW) as the primary method.
Background: The authors aimed to explore the association of fatty acids with periodontitis and its severity and to assess causality using Mendelian randomization (MR) analyses.
Methods: Data for participants with complete data were extracted from the 2009-2014 National Health and Nutrition Examination Survey. Weighted logistic regression was used to explore the relationship between dietary fatty acids and periodontitis and its severity.
Pediatr Res
January 2025
Heart Center, Women and Children's Hospital, Qingdao University, Qingdao, China.
Background: Despite prior observational studies suggesting a link between gut microbiota to Kawasaki disease (KD), these findings remain debated. This study aimed to assess the association between gut microbiota and KD on a genetic level using a two-sample Mendelian randomization (MR) analysis.
Methods: This two-sample MR analysis utilized summary statistics from the largest genome-wide association study meta-analysis on gut microbiota conducted by the MiBioGen consortium.
Sci Rep
January 2025
Department of Urology, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, 730030, People's Republic of China.
Benign prostatic hyperplasia (BPH) is a prevalent urinary system disorder. Despite evidence of a significant genetic component from previous studies, the specific pathogenic genes and biological mechanisms are still largely unknown. The study utilized the FinnGen R10 dataset, encompassing 177,901 individuals (36,601 cases and 141,300 controls), and the GTEx v8 EQTLs files to conduct single-tissue and cross-tissue transcriptome-wide association studies (TWAS).
View Article and Find Full Text PDFSci Rep
January 2025
Division of Pancreatic Surgery, Department of General Surgery, Qilu Hospital, Shandong University, Jinan, 250012, China.
Previous studies have found that dyslipidemia is a risk factor for pancreatic cancer (PC), and that lipid-lowering drugs may reduce the risk of PC. However, it is not clear whether dyslipidemia causes PC. The Mendelian randomization (MR) study aimed to investigate the causal role of lipid traits in pancreatic cancer and to assess the potential impact of lipid-lowering drug targets on pancreatic cancer.
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