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The GG genotype of the −152 G/A vascular endothelial growth factor (VEGF) polymorphism predisposes to hypertension-related chronic kidney disease

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Abstract

Our purpose was to determine whether the VEGF −152 G/A polymorphism could be associated with chronic kidney disease and endothelial dysfunction in hypertensive patients. There were 100 healthy volunteers enrolled into the control group. The group of patients was constituted by 99 consecutively admitted hypertensive patients referred to our Institution by their general practitioner. All patients were treated with anti-hypertensive polytherapy. Presented study revealed that the hypertensive patients bearing the GG genotype were characterized by the highest values of diastolic blood pressure and markers of endothelial damage such as Angiogenin, Endostatin, CRP as well as von Willebrandt factor. In addition, higher number of immature endothelial progenitor cells with CD34+CD133+, CD34+CD133- markers was observed in GG hypertensive carriers while in normotensive individuals no differences were found. Such phenomenon may indicate an increased mobilization of bone-marrow derived endothelial progenitors. It may testify to the preserved compensatory mechanism in chronic kidney disease (CKD) patients until the G3a stage of the disease. Moreover, patients with higher estimated glomerular filtration rate (eGFR) level had lower of vWf and Endostatin values, and higher level of VEGF. Taken together our findings clearly indicate the −152 GG hypertensive carriers as more prone to develop CKD. We can suspect that the VEGF −152 GG genotype is strongly associated with hypertension-dependent CKD.

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Acknowledgments

The paper was subsided by the grant of National Science Centre Nr 2011/01/B/NZ5/00345.

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Correspondence to Anna Małkiewicz.

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Małkiewicz, A., Skrzypkowska, M., Słomiński, B. et al. The GG genotype of the −152 G/A vascular endothelial growth factor (VEGF) polymorphism predisposes to hypertension-related chronic kidney disease. Mol Biol Rep 43, 967–975 (2016). https://doi.org/10.1007/s11033-016-4035-6

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