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Diabetic nephropathy (Kidney problem) 1.8 X more likely if poor Vitamin D Receptor – meta-analysis July 2017

Association between the vitamin D receptor gene polymorphisms and diabetic nephropathy risk: a meta-analysis

Nephrologiy online: 13 July 2017, DOI: 10.1111/nep.13111
Fang Yin, Jing Liu, Ming-Xiu Fan, Xiao-Li Zhou, Xiao-Ling Zhang

VitaminDWiki

Items in both categories Kidney and Vitamin D Receptor:

Items in both categories Diabetes and Vitamin D Receptor:

Items in both categories Diabetes and Kidney:

Vitamin D Receptor category has a summary table

If poor Vitamin D Receptor

Risk
increase
Health Problem
13Sepsis
9.6Chronic Periodontitis
   and smoke
7.6Crohn's disease
5.8Low back pain in athletes
5Ulcerative Colitis
5Coronary Artery Disease
4.6Breast Cancer
4polycystic ovary syndrome
3.3 Pre-term birth
3.1Lumbar Disc Degeneration
3.1Colon Cancer survival
3 Multiple Sclerosis
3Dengue
3 Waist size
3 Ischemic Stroke
3Alzheimer’s
2.8Osteoporosis if COPD
2.7Gastric Cancer
2.6Lupus in children
2.4Lung Cancer
2.3Autism
2Diabetic Retinopathy
2Parkinson's
2 Wheezing/Asthma
2 Melanoma
2Myopia
1.9Uterine Fibroids
1.9Early tooth decay
1.8Diabetic nephropathy
1.6Diabetes - Type I
1.6Prostate Cancer while black
1.5 Diabetes -Type II
1.5Pertusus
1.4 Rheumatoid arthritis
1.3Childhood asthma
1.3Tuberculosis


Aims
Diabetic nephropathy (DN) is a severe microvascular complication frequently associated with type 1 and type 2 diabetes mellitus. The objective of this study was to estimate the effect between Apa I, Bsm I, Fok I and Taq I polymorphisms of the vitamin D receptor (VDR) gene and DN susceptibility.

Methods
Eligible case–control studies published updated to March 2017 were searched. The odds ratio (OR) and 95% confident intervals (CI) were employed to calculate the strength of effect.

Results
12 articles were finally screened out, including 3954 diabetic patients and 1248 healthy controls. When compared with the diabetic patients without nephropathy, our results found that only the Bsm I polymorphism was associated with increased risk of DN under the

  • allelic model (B vs. b: OR = 1.51, 95% CI = 1.03-2.20, P = 0.04) and
  • dominant model (BB + Bb vs. bb: OR = 1.52, 95% CI = 1.00-2.31, P = 0.05).

When compared with the healthy controls, our results showed that the Bsm I polymorphism was associated with the DN susceptibility under the

  • allelic model (B vs. b: OR = 1.80, 95% CI = 1.12-2.91, P = 0.02), the
  • homogeneous model (BB vs. bb: OR = 1.43, 95% CI = 1.03-1.98, P = 0.03), and the
  • domain model (BB + Bb vs. bb: OR = 1.80, 95% CI = 1.06-3.05, P = 0.03);

the Taq I variant was associated with increased risk of DN only under the heterogeneous model (Tt vs. tt: OR = 2.29, 95% CI = 1.04-5.03, P = 0.04).

Conclusions
Our results suggested that B allele, and BB + Bb genotypes of Bsm I variant, Tt genotype of Taq I variant might be risk factors for DN. Future researches are still needed to identify our results.

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